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Transcript
Doctor-Patient Confidentiality
Quote:
Originally Posted by Anonymous
Hi marianco,
I was wondering if the dr-patient confidentiality applies if I wanted something withheld
from one doctor to another.
Whenever my GP referes me to a specialist he will put in the letter that "I have a history
of anxiety problems" or "I am obsessed with the need for testosterone replacement" and it
is out of context with the rest of the letter and in some cases even irrelevant, and I find it
negatively influences the way I am treated by the specialists.
Is there anything I can do about this(not legally of course) like ask my GP to be
completly confidential about certain things or not include what may be personal opinions
in referal letters?
Thanks.
Yes.
One should be able to tell their doctor to withhold information if this would impair the assessment
of the consultant.
Particularly when it comes to psychological or mental health issues, it is important to leave much
of this out to prevent the consultant from becoming blinded or prejudiced by the information.
For example, when it comes to physical problems presenting with mental symptoms, up to 25% of
the time the diagnosis is missed if the physician focuses primarily on the possibility of a mental
illness. For example, when patients with chest pain and panic attacks come to the emergency
room, up to 25% of the time, they really have a heart attack.
As another example, often times, physicians get frustrated when patients come in with
"somatization disorder" - meaning that the physician can't find anything physically wrong with
them, so they say it is all in the patient's head. When such a physician comes to me asking what
they should do, I usually tell them to keep doing testing to make sure no stone has been unturned
to find out if there is a physical problem occurring. When I see such a patient, I many often find
something wrong with them that the physician missed and it is not just fabricated by the patient. It
was missed because the physician didn't have the skills or did the right tests to find out what was
happening. For example, I had a patient who was unable to work for years by severe fatigue and
depression. A string of doctors could not find out what is wrong. I found that her temperature was
mildly elevated and her pulse was high. I also did not think she had a psychological reason to be
severely depressed. I thought she had some soft of infection that was not yet found. A bone scan
reveased she had a dental infection that got into her nasal bones. After removal of the infected
bone and with antibiotic treatment, her depression and fatigue went away. Thus a string of
doctors could not find the cause of her problem and they attributed it to depression. If any one of
them could have kept going and not dismissed her problem as only depression, and do further
testing, he or she may have found the nasal bone infection that caused her problem. Luckily for
her, someone finally did.
If the doctor doesn't recognize or is open to the possibility of prejudice from the inclusion of
certain information and goes ahead and adds this information - causing prejudice to the patient in
the subsequent evaluation - I would change doctors.
The problem is that physicians can be all too human. And if they are not sensitive to a person's
mental health, they can be instead prejudiced by it in evaluating a patient. It is all too easy to
blame the patient for one's inability to find the cause of a person's problems.
__________________
Any statement I make on this site is for educational purposes only and will change as medical knowledge progresses. It does not
constitute medical advice, does not substitute for proper medical evaluation from physician, does not create a doctor/patient
relationship or liability. If you would like medical advice, please make an appointment. Thank you.
Nolvadex and Arimidex and decreased sex drive.
Quote:
Originally Posted by Anonymous
Nolvadex and Arimidex and decreased sex drive.
Is it possible that the usage of nolva (10mg/day) in combination with arimidex 0.25mg
reduce sex drive?
If yes, what to do?
And for how long can both of these drugs be used?
The use of Tamoxifen (Nolvadex) in combination with Arimidex can reduce sex drive - depending
on what pathways are being affected in a particular person. Each person can be different in their
response to these two medications.
What can be useful to help determine what is happening is to do both blood tests of hormones,
lipids, etc and 24-hour urine tests of hormones and their metabolites to determine what is being
changed by the addition of Tamoxifen and Arimidex. This will then help determine the course of
action. This cah be expensive. The 24-hour comprehensive urine tests can run $400 each time
done, for example.
Both medications can be used indefinitely so long as their use and the patient's condition are
being monitored by a physician. Both do have adverse effects (e.g. blood clots from Tamoxifen,
elevated cholesterol and impaired hormone production with Arimidex, etc.) which can cause
serious long-term problems if not monitored and steps taken to help improve long-term safety.
=========================================================================
================================================
Hypogonadism from taking steroids
Quote:
Originally Posted by Anonymous
"If the guru himself prescribes me a type of recovery program should i go for it or
continue my natural route. Past 3 months I've grown more facial hair and quicker,
although theyre not strong i have had morning erections on probably half(or a little less
than half) the days in each month. Balls seem around 1.5 - 1.7 inches that might be a
little less than normal. Last test results total t= 315ng/dl LH = 2.1 (the first time in 3
years it's gone above 1.0) FSH= 1.7? . Doing anything naturally is always better than
doing something chemically, so I wonder is it possible I recover naturally on my own
despite being shut down for 3 years or should I give Dr. Shippens protocol for me a shot?
What I'm most worried about is having his program disrupt my natural recovery(if its
even possible). Just a reminder my case is secondary hypogonadal as a result of taking
steroids at age 17 (i'm now 20). Also what do you guys think he might recommend for
me?"
I'm not an expert in Anabolic Steroid Induced Hypogonadism (ASIH) and I have not yet treated
someone with such a problem, nor have I read extensive literature on it and it's treatment. John
Crisler, D.O., has much more experience in this regard, since he has treated so many patients
who have had ASIH.
As far as I know, it may take a long time for the hypothalamus and pituitary glands of the brain to
recover from being suppressed so long by elevated anabolic steroids. It would be like trying to
restart the adrenal glands after having used high dose prednisone for years - it can take many
years to get it toward recovery. The various treatments on the surface appear designed to
accelerate this process of recovery by causing the brain to think it has even less estrogens and/or
testosterone than it already has (e.g. using Tamoxifen).
I am not familiar with Dr. Shippen's protocol so cannot comment or speculate on it.
__________________
Any statement I make on this site is for educational purposes only and will change as medical knowledge progresses. It does not
constitute medical advice, does not substitute for proper medical evaluation from physician, does not create a doctor/patient
relationship or liability. If you would like medical advice, please make an appointment. Thank you.
Re: Hypogonadism from taking steroids
Quote:
Originally Posted by BigAk
Dr. Marianco... I'm currently supplementing with 25mg of DHEA daily after my latest
bloodwork revealed levels a bit below normal range. I'm not on any form of TRT or
anything. In your opinion, do you think DHEA supplementation at this dose would cause
any negative impact or shut down of my HPTA?
As usual, we do appreciate your expertise and tremendous help to our community.
p.s. I'm 40 year old former ASIH patient currently on 10mg of Tamoxifen only.
I do not know how any individual person would respond to 25 mg of DHEA without an exam or
test to see where it is going.
DHEA at 25 mg a day could stay as is - which tends to occur with most patients who are low on
DHEA - i.e. have lower adrenal function/adrenal fatigue/aging, etc.
DHEA in some can turn into testosterone.
DHEA in some can turn into estrogens.
If DHEA does these two, then it could reduce LH/FSH production.
There are many directions for it go to.
If unwanted pathways are a concern, then one would have to be on the lookout for adverse
effects (e.g. gynecomastia from excess estrogen activity) or get lab testing. Currently, the best
way I have found is to do 24-hour urine tests for steroid hormones and their metabolites. It is
complicated to read but does help more than others in determining where a particular treatment is
going - particularly when one is concerned about adverse effects.
In general, for most people, I would stick with lab tests since insurance can pay for them, but in
some cases, the specialized testing is valuable.
__________________
Any statement I make on this site is for educational purposes only and will change as medical knowledge progresses. It does not
constitute medical advice, does not substitute for proper medical evaluation from physician, does not create a doctor/patient
relationship or liability. If you would like medical advice, please make an appointment. Thank you.
==================================================================================================
=================================================================
Glucose resistance? help please!!
Quote:
Dr Marianco, Ive read ur posts about if the patient isnt feeling good and throd, adrenals,
and test is fine, glucose and stuff like that should be tested. i had mine tested and it was
smack dab in the middle, but whenever i take in a high amount of carbs like 100 grams of
it in one of my weight gainer shakes, i get tired after! what could this mean and how do
you test for insulin insensitivity or whatever the condition is called? glucose resistance?
To test for insulin resistance, a person does the 3-hour glucose tolerance test. This test has a
person fast for 12 hours. Then the person's blood glucose and insulin level are tested at hour-0.
The person then ingests 75 grams of glucose. Thereafter, the person's bloog glucose and insulin
are measured at 1-hour intervals for the next 3 hours. If the glucose levels do not fall
appropriately, then a person has insulin resistance. If the insulin levels are much higher than
usual, then the person has insulin resistance. The person taking the test usually feels sick after
ingesting 75 grams of glucose.
The problem of ingesting the 100 or so grams of carbs in a weight gainer shake is that such a
shot of carbohydrates causes the brain to think the adrenal glands have done their job too well.
The brain then shuts down signals to the adrenal glands, essentially worsening adrenal function
over the next several hours. If a person has adrenal fatigue, this worsens the situation. The carbs
will temporarily give a person energy, but once the carbs are absorbed and stored, the person is
left with slowed adrenal glands for hours - which means fatigue for hours.
One study found kids who eat high processed carbonhydrates for breakfast - cereal, juice,
breads, etc. - have a much lower energy level than kids who eat a higher proportion of protein
and fat for breakfast - e.g. ham and eggs - thus did not perform as well in school. The shot of
sugar gives them initial energy. But then when the sugar is absorbed and stored, they are left with
lower adrenal function, resulting in lower abilitly to generate energy, concentration problems,
possible irritability and agitation, etc. - symptoms similar to adrenal fatigue - the rest of the day.
Since the after-workout meal often is a weight-gainer shake, I wonder if it would be better overall
to eat frequently through the day - with complex carbs such as vegetables and proteins - to be
able to maintain a more consistent source of energy - then keep the after-workout meal
something like a protein shake without as much sugar - to avoid shutting down the adrenals along with a complex carbohydrate product - to better maintain health.
The addition of glucose or other sugar to the weight gainer shakes is a short-cut attempt to speed
up muscle growth. The body releases more insulin in response to the surge of sugar. Insulin can
be anabolic. The surge of glucose may be stored in the muscles helping muscle growth after
exercise.
The problem is what does a person sacrifice in health from doing this?
Insulin is in the long run an inflammatory hormone. High insulin levels increases the risk of cancer
and heart disease, and tends to shorten a person's lifespan. High insulin levels reduce
testosterone production - leading to hypogonadism and sexual problmes. If a person has insulin
resistance, then high glucose levels are toxic to the pancreas - eventually killing the beta cells
that make insulin - turning a condition that is treatable in many circumstances with diet, lifestyle,
and exercise management to a life-long need for insulin injections. High insulin levels increase
the risk of Alzheimer's disease. Etc. Etc.
=========================================================================
==================================================
Glucose resistance? help please!!
Quote:
Originally Posted by ironaddict69
so after this 3 hour test, if the person shows up positive and has it, what do they treat it
with?
If a person has frank diabetes, then it is treated.
If a person has insulin resistance - unfortunately it is not often treated until too late - i.e. a person
has a heart attack, stroke, diabetes, cancer, hypogonadism, obestiy, hypertension, etc.
Treatments for insulin resistance include:
Hormones IF needed:
1. Thyroid hormone
2. Testosterone
3. DHEA
4. Progesterone - to help improve thyroid hormoen effectivness
5. Insulin - in some cases
6. etc.
Medications IF needed:
1. Metformin - if a person doesn't have adrenal fatigue.
2. Avandia, Actos
3. etc.
Nutrition options:
1. Paleolithic or Diabetic diet - meats and vegetables and fruits, minimizing processed
carbohydrates and sugars.
2. Alpha Lipoic Acid
3. Chromium Picolinate
4. Fish Oil
5. Magnesium
6. etc. etc. Too many to list - nutrients (not herbs) - which can help reduce insulin resistance.
Herbal products IF needed:
1. You'll have to look them up. Herbs are like medications, and I prefer nutritional interventions
when possible.
Exercise:
1. Moderate aerobic exercise plus or minus moderate anerobic exercise can help improve insulin
sensitivity.
Weight loss IF needed:
1. at least a 7 pound weight loss when over 7 pounds overweight.
Treatment of problems stemming from insulin resistance (also called Metabolic Syndrome X):
1. hypertension
2. cholesterol problems
3. obesity
4. heart disease
5. atherosclerosis
6. hypogonadism
7. dementia
8. mood disorders
9. etc. etc.
There should be a physician's supervision in the treatment.
=========================================================================
===================================================
DHT and Testosterone
Quote:
Originally Posted by drp90210
May I bother you with a question? The testosterone cream I am using gets my total and
free testosterone to middle levels (600-700 total test and 10-20 free test), but my DHT is
through the roof at 240 (normal is 17-66). Reducing the skin area of application has not
improved the DHT problem. I do not want lose any more hair, which is a big issue for
me. Do you know how I could get my DHT down? Would injectible testosterone
significanty reduce DHT versus creams? And would there be a problem with using
SMALL amounts of Propecia (like a 1/4 tablet a day) to simply get my DHT to the top of
the normal range? Any thoughts would be greatly appreciated. If you prefer, you can
email me directly or simply post to the group. Many thanks and best regards.
High DHT can occur with transdermal testosterone.
It is a concern in regard to hair loss, possible abdominal fat increases, and other negative effects
of DHT when it is at too high a level.
Possible ways to maintain control over DHT include:
1. High potency testosterone gels or creams allowing reduced skin area of application.
2. Alpha-reductase inhibitors like Finasteride or Saw Palmetto - to reduce DHT production. The
dose and potency have to be considered since alpha-reductase activity is important for brain
function. Saw Palmetto would probably be the safest of the alternatives. It is not as potent as
finasteride, and hasn't been shown to grow hair like finasteride. But it can reduce DHT levels.
Low dose Finasteride is a viable option - so long as one monitors for side effects.
3. Scalp application of an alpha-reductase inhibitor to avoid systemic alpha-reductase inhibition
(which can cause cognitive problems, sexual problems, etc.), while reducing hair loss at the scalp
itself. These included compounded lotions and shampoos containing products such as azelaic
acid or saw palmetto. ucprx.com (University Compounding Pharmacy) and minoxidil.com are
examples of compounding pharmacies that carry products like this.
4. If a man was progesterone deficient, rubbing a compounded progesterone cream into the scalp
is an option - progesterone being an alpha-reductase inhibitor.
5. Injection of a testosterone ester - e.g. depo-testosterone, testosterone enanthate, testosterone
cypionate, when done twice a week, help reduce DHT production. When injections are done once
every two weeks, DHT production can also be high, due to the higher peak levels of testosterone
obtained.
6. etc.
DHT and Testosterone and Testocreme vs. injections.
Quote:
Originally Posted by drp90210
Many thanks. Would once-a-week injections of testosterone cause an unwanted DHT
spike? The thought of doing IM shots twice a week is not appealing.
Injections twice a week aren't so bad considering that the dose is half the size.
A smaller gauge needle can be used.
At around 25 gauge and smaller - plus the smaller dose - pain is much less or non-existant.
The ventrogluteal site is the least painful site - it has fewer nerves and blood vessels than the
dorsogluteal or lateral thigh (vastus lateralis muscle)
Realize that if one was on growth hormone, then one would be doing daily injections. If one was
on insulin for diabetes, one would be doing even more frequent injections - plus the needles
involved for monitoring blood sugar.
If one wants zero pain, then transdermal testosterone is the best.
Testocream is one version of a compounded PLO, oil-based testosterone cream which may
minimize DHT production compared to other creams and gels since it seems to have lower
storage in skin fat. Rather, the pharmacokinetics indicate most of the testosterone goes directly
into the intracellular space then into the blood stream. It also has an aromatase as a component.
One can Google to find it.
Dopamine
Quote:
I sometimes have difficulty in formulating very specific questions, but here's one :
In anyone complaining of low sex drive, is it indisputable that that individual has a
dopamine deficiency, whatever the underlying cause ? I mean, whether it is from low
Testosterone, low cortisol, low thyroid etc..
Clearly, low dopamine can have many origins, sometimes taking the form of low T,
while low cortisol is also likely, I read it causes increased Norepi. which in turn causes
the brain to decrease DA.
I take it that's cause Norepi. is synthesized from DA, thus if there's more stress it requires
more conversion of DA to Norepi. leaving less DA to do perform others functions.
Lately, I've focused on dopamine, not because I think it's doing it's job alone, but because
I want to make sure I know what it does as a neurotransmitters. But of course like you so
often say, the neurotransmitter, immune, and hormone form a 3-dimensional web, which
turns out to be one large network.
When one has low sex drive one can have low or normal or high dopamine levels. Which
situation may be present depends on each individual.
Low sex drive most commonly involves a group of neurotransmitter, hormone, and cytokine
problems - not a single isolated problem.
Commonly, I find thyroid and adrenal problems as causes of low sex drive. Next, are low
testosterone levels. However, quite a a number of times, in men who complain about low sex
drive, their testosterone levels turned out to be sky high - in the 800-1000 without TRT.
Dopamine itself is extremely difficult to manipulate in isolation from other chemical messengers.
The treatments which affect dopamine always invariably have significant side effects (e.g.
amphetamines which can increase dopamine through reuptake inhibition, can eventually cause
adrenal fatigue from also increasing norepinephrine. The adrenal fatigue may eventually result in
lowering dopamine production).
By improving the other systems which are easier to manipulate without too many bad side effects
and interactions - e.g. testosterone, estrogens, thyroid, DHEA and other adrenal hormones, etc. then dopamine can itself improve given the linkage in function. In a way, then, dopamine
abnormalities can be considered often as a marker of problems in other systems. Improvements
in those systems can be expressed as an improvement in dopamine levels.
In my experience, If we're lucky, then a single intervention - such as adding testosterone - will
solve their problem. However, I do often get the more complex, treatment resistant patients,
referred from neuroendocrinologists or other hormone specialists, when conventional treatment is
not working.
More often, than not, I find it necessary to do a complex treatment addressing as many
imbalances as I can find in order to improve a person's ability to function - tuning up a person's
ability to function - so to speak. This may involve neurotransmitter interventions (e.g. psychiatric
medications), hormones, and/or nutritional interventions, customized to what the patient needs.
The more things a person takes, the more complex the treatment becomes. Even with nutrients,
this is the case.
For example, with Vitamin C, I have to think about the possibility of developing a copper
deficiency if too high a dose of Vitamin C is used. Zinc and copper are linked. Various minerals
and Vitamins are linked in function. Vitamin B12 itself can have toxicity at too high a dose. It also
has interactions with some minerals and other nutrients.
Vitamin B12
Quote:
Originally Posted by DrmChld
I'm curious about this also. I thought B vitamins were water soluable and whatever our
body didn't need we would just piss it out.
The B Vitamins are water soluble.
But not all of them are "just pissed out".
Vitamin B12 is one of them. Vitamin B12 is stored in the liver. Usually a person in good health
can store about 10 or more years worth of B12 in the liver.
Generally, B12 has very low toxicity. There isn't a upper limit noted for it. It is a very important
vitamin involved in many processes in the body.
However under relatively rare circumstances, an excess can cause problems.
This may include:
1. spasms of the arteries - contributing to chest pain or mild-stroke-like symptoms - primarily with
injected B12
2. rapid heartbeat
3. anxiety
4. hypokalemia
5. skin problems - itching, rash, urticaria, rosacea
6. increased return of coronary artery blockage in patients after angioplasty with stents receiving
a combination of folic acid, B6, and B12.
7. diarrhea
8. peripheral vascular thrombosis
9. hiding the presence of polycythemia vera
10. gout
11. hiding the presence of folic acid deficiency
12. rapid optic nerve atrophy in patients with Leber's diease
13. etc.
Admittedly, these are fairly rare when taking B12. But when confronted with symptoms and a
person is taking B12, it should be taken into account.
Dythymia
Quote:
Would you be so kind as to tell me what exactly is dysthymia.
I mean I read that this can happen in middle-aged man, because of T deficiency, but it
also seem to exist from a neurotransmitter point of view.
Worded differently, Is DD more rooted in hormones imbalances or neurotransmitters ?
Psychiatric Diagnoses tend to avoid determination of the cause.
It some ways, it is because if a psychiatric diagnosis has a "physical cause", then a psychiatrist
tends to give up and refer the patient to the patient's primary care provider or other specialist even if these other physicians cannot do a good job in treating the person - e.g. they have no idea
of optimizing mental health in the face of hypothyroidism or other hormonal, neurotransmitter
problem.
Psychiatrists also tend to not do lab tests because the tests they were told to do in residency tend
to be "normal", and thus they have given up in finding something abnormal. Unfortuantely, they
were taught the wrong tests to look for. And unfortunately, they and other physicians and nearly
every other health care provider tend to be poorly trained in reading lab tests. They cannot
understand the process of determining the lab results, nor critically assess the meaning of the lab
results. Rather they too often read anything that is within the reference range as "normal".
Further, psychiatrists and other physicians were not trained in the physical diagnostic skills
involved to adequately determine hormonal or neurotransmitter problems. Psychiatrist, further,
have tended to give up doing physical exams - a serious problem - leaving the task to a nurse
practitioner or primary care provider - who usually has no clue what to look for in a mentally illl
person - thus completely missing the associated problems, further usually having no clue as to
optimal treatment.
Oh well.
Now to your question:
Dysthymia is a mild chronic depressive state, where a person never regains a normal mood.
It lasts at least 2 years (an arbitrary length of time to allow it to be distinguished from major
depressive disorder or adjustment disorders).
It can be attributed to psychological, stress, and/or physical health problems.
Thus, dysthymia may occur in neurotransmitter and hormone problems.
This includes conditions with one OR more of the following (oversimplified descriptions):
1. Low Serotonin
2. Low Dopamine
3. Low Norepinephrine or high Norepinephrine
4. Low Testosterone
5. Low Estrogen
6. Low DHEA
7. Low Cortisol
8. Low Progesterone
9. Low Thyroid
10. High Insulin
11. etc. etc.
Since these neurotransmitters and hormones are very tightly knit in activities and functions, one
cannot separate them and say that dysthymia is due mostly to one or the other.
For example, is one is low in dopamine, then one can be low in thyroid, low in testosterone, low in
estrogen, low in cortisol, and/or low in DHEA, etc. In another example, iIf one is low in Cortisol,
then one can be high in norepinephrine, low in dopamine, low in serotonin, etc.
Thus dysthymia tends to be both a neurotransmitter and hormonal problem - together.
Re: Dythymia
[quote=Naturdoc]
Quote:
Originally Posted by marianco
Marianco
I would appreciate hearing what physical exams you try to accomplish in a visit. Even in
a 1.5 hr visit I feel I am unable to do all that I would like for P.E. and there are no
references that I have seen as to which exams would be most useful from the view of
screening for physical etiology of mental problems. Thanks
You have to know what your are looking for in order to focus the physical exam. You may already
be doing what you need to do.
In training, my attending cardiologist told me he doesn't need a fancy stethoscope - just a basic
one. The main difference between he and I was that he knows what to listen for. For example, if
he was thinking of mitral regurgitation, he would envision whan he would hear, then would listen
to the patient's heart and can find it or not. Since I did not know what to listen for - whatever
sound I hear I would have to compare to a large database of possible sounds - which would make
it more difficult to determine what I am listening to.
Since mental problems can often have a physical etiology, it is important to think first of the
possible condition (e.g. hypothyroidism) which is causing the mental illness, to help focus the
physical exam.
For example, with hypothyroidism, what does one expect in the physical exam?
1. dry skin - to the point sometimes of hyperkeratosis with cracked lines or a sandpaper texture
2. hair loss
3. decreased deep tendon reflexes
4 . bradycardia
5. thickened skin due to myxedema (mucin deposition) - I use a skin caliper
6. swelling of the eyelids
7. cold hands and feet (which can be hidden by high norepinephrine levels causing warmness of
the skin with sweating)
8. low body temperature
9. etc. etc.
With each hormone deficiency, a list of physical signs can be made. One would gain an
expectation of what hormone deficiency is occurring from the history, then look for verification on
the physical exam.
The same thing is present for some neurotransmitter problems and nutritional deficiencies - which
can cause mental illness.
There is no textbook on this. The information already exists but occurs in disparate areas.
Hopefully the book I am writing will pull it most if this together.
Re: Dythymia
Quote:
Originally Posted by chip douglas
Is the book you're writing the first one ? I'd like to purchase any that you have published,
if any other of course.
I wasn't aware that you were in the process of writing a book.
I'm going to try and revolutionize psychiatry - perhaps save the field. Interestingly, if psychiatry
becomes integrated into the rest of medicine, it would be the top integrated specialty. No other
integrated medicine field can more closely bind mind and body than psychiatry can.
The book will probably take 2-3 years to write. A colleague is writing a book on diabetes by
himself. He has been working until 2 AM every night over the past 2 years so that it can be
released this year. Since my book is far more extensive, it will take at least that long if not longer.
Another physician author friend who wrote a book on hormones wanted me to collaborate with
other psychiatrists who do some hormone research. However, I am too far advanced of them
already to be able to do a collaborative book. Collaborative work would also lose the integrated
point of view of what I want to do.
Re: Dythymia
[quote=marianco]
Quote:
Originally Posted by Naturdoc
You have to know what your are looking for in order to focus the physical exam. You may
already be doing what you need to do.
In training, my attending cardiologist told me he doesn't need a fancy stethoscope - just a
basic one. The main difference between he and I was that he knows what to listen for. For
example, if he was thinking of mitral regurgitation, he would envision whan he would
hear, then would listen to the patient's heart and can find it or not. Since I did not know
what to listen for - whatever sound I hear I would have to compare to a large database of
possible sounds - which would make it more difficult to determine what I am listening to.
Since mental problems can often have a physical etiology, it is important to think first of
the possible condition (e.g. hypothyroidism) which is causing the mental illness, to help
focus the physical exam.
For example, with hypothyroidism, what does one expect in the physical exam?
1. dry skin - to the point sometimes of hyperkeratosis with cracked lines or a sandpaper
texture
2. hair loss
3. decreased deep tendon reflexes
4 . bradycardia
5. thickened skin due to myxedema (mucin deposition) - I use a skin caliper
6. swelling of the eyelids
7. cold hands and feet (which can be hidden by high norepinephrine levels causing
warmness of the skin with sweating)
8. low body temperature
9. etc. etc.
With each hormone deficiency, a list of physical signs can be made. One would gain an
expectation of what hormone deficiency is occurring from the history, then look for
verification on the physical exam.
The same thing is present for some neurotransmitter problems and nutritional
deficiencies - which can cause mental illness.
There is no textbook on this. The information already exists but occurs in disparate
areas. Hopefully the book I am writing will pull it most if this together.
For many sections of the physical exam, most of them are already done even before the formal
physical exam is done.
For example, a good neurologist can usually complete almost all of the neurological exam before
the patient steps into the office by just observing the patient in the waiting room and as they walk
to the office.
An internist friend told me that when a person complains about chest pain he only needs to
examine three things to verify a heart attack - the whole physical exam doesn't need to be done.
Looking at the ears, etc. wouldn't be necessary under those circumstances to address the
patient's concerns.
The mental status exam is pretty much complete as the history is taken from the patient by
observing the patient as they respond.
A lot of the dermatological and body habitus exam can occur from just looking at the exposed
parts of a patient's body, by the initial handshake that occurs when one greets a patient.
During the history, I develop a differential diagnosis - a list of possible diagnoses the person has,
including alternative diagnoses. The diagnosis is not only a psychiatric diagnosis but what the
underlying mechanism or pathophysiology may be occurring that causes the symptoms the
patient is experiencing. It is the pathophysiology (e.g. thyroid problems, adrenal problems,
gonadal problems, insulin resistance, neurotransmitter problems, lipid problems) which gives a
list of expected signs on the physical exam. The physical exam becomes then a focused exam to
determine which of those signs are present to help verify the pathophysiology.
If one did not do a focused physical exam, then the physical exam can take forever - the usual
medical student exam - since it is too extensive - covering areas which are not so necessary to
know in managing the person's immediate problems.
As one family doctor told me 20 years ago: don't try to solve every problem the patient has in one
appointment. Focus on the immediate problem that caused the patient to present. The other
problems can be dealt with as necessary on follow ups - including the part of the exam that is
necessary for each of the other problems.
Men vs. Women's Dosing
Quote:
My wife is suffering from low test verified from lab results, the doctors were
unsympathetic and she decided to take matters in her own hands. She requested that I
give her some type of test that would boost her sex drive. She feels totally helpless and
this has become a major issue in our marriage. Prior to the birth of out 3y.o. daughter we
had a frequently wild sex life during which she iniated sex. Now she has literally cried to
me that her body just doesn't react. She lacks wetness and the desire for sex. She has been
a trooper and accomodates me most of the time and almost always climaxes during
intercourse, so I think it's safe to say everything is operating fine except the chemicals
that get things going. I have opted based on some research to give her 25mg of cypinate
injected 1x a week. My question is is cypinate o.k. and is the dosage sufficient and
frequent enough to have any affect. She is 35 y.o. 5'3" 120lbs excellent health. I also
know that cypinate is long acting and would stay in her system longer, hense the 1x a
week dose. If I sound totally ignorant or uneducated I appologize, I'm just trying to make
the best out of a desperate situation. Please help me any way you can, I truly appreciate it.
I have access to high quality steroids and can change the type if you are so inclined to
advise me. Thank you very much,...
I cannot give you advice because you are not a patient.
From an educational point of view, as rules of thumb:
1. Women tend to have 1/7th to 1/10th the testosterone of men. The upper range is generally
around 75 ng/dl for total testosterone. I tend to like a level around 50-75 ng/dl so long as side
effect don't occur - e.g. hair loss, more male characteristics, acne, etc., to help improve memory,
sex drive, concentration, mood, bone density, etc.
2. It would be important to monitor labs to verify the dosing.
3. Testosterone cypionate is an option in women - though not commonly used. (Depo-estradiol is
also an option in women as well as transdermals. Avoiding the oral route helps improve response
to growth hormone and reduces the increase in inflammatory cytokines (and C-reactive protein)
that occurs with the higher concentrations in the liver of estrogen from oral estrogen).
4. Women tend to have twice the half-life of men when it comes to medications.
5. Oral compounded testosterone is a viable route for women - as opposed to men. It usually is
the most convenient route for testosterone in women - and from some compounding pharmacies such as the Women's International Pharmacy - it is very inexpensive.
6. In a woman, low testosterone can also be a sign of adrenal fatigue - particularly in
perimenopausal and menopausal women.
7. Multiple hormones affect sex drive in Women - not just testosterone - just as in men.
Dr. M
Quote:
Originally Posted by JustOne
Its nice to have you posting here again Doctor.
In men, besides estrogens, testosterone and DHT, what other hormones are responsable
for libido?
The hormones that can influence libido directly or indirectly include:
Testosterone
Dihydrotestosterone
Estradiol and other estrogens
Progesterone
DHEA
Cortisol
Aldosterone
Pregnenolone
Thyroid Hormones
Insulin
Glucagon
IGF-1
Growth Hormone
Melatonin
Vasopressin
Calcitonin
TSH
LH
FSH
GHRH
Prolactin
CRH
ACTH
TRH
Epinephrine
Norepinephrine
Dopamine
Serotonin
Oxytocin
Endorphins
Somatostatin
Renin
EPO
Angiotensins
etc.etc. (practically every hormone)
Of course, some have greater influence than others. But all are involved in a tight mesh of
function. Abnormalities in one can permeate the entire system, causing problems with the others.
A question about HGH
Quote:
Originally Posted by anonymous
This seems to be a hard one to find an answer to. I have seen a couple references on the
internet about hgh raising prolactin and reducing dopamine. Are there any studies to
back this up?
Thanks
Anonymous
I can't quote you studies since that is too much work for this forum.
You can find studies yourself on Medline. A free link to Medline is at
http://www.ncbi.nlm.nih.gov/pubmed
Some references on the internet may refer to the practitioner's clinical experience rather than
studies themselves.
Realize that studies are very expensive to do. A good study may run millions of dollars. This is
why bringing a new drug to FDA approval in the U.S. costs a drug company at least $250 million.
There are many things which therefore have no studies. For example, studies on children and
women (particularly pregnant women) tend to be few compared to studies on men - particularly
when a medication may cause fertility or developmental problems.
This is where "evidenced-based" medicine fails - when the physician has to go past what is in the
literature - to customize a treatment in the patient's best interest. This often occurs in psychiatry.
An example is the use of more than one antidepressant, mood stabilizing medicationi, or
antipsychotic medication at a time. This is a standard of practice but has little data in the literature
to back it up.
Realize that drug companies do not want to sponsor studies with two medications since that may
be free advertisement for their competitor's product.
Dr. M
Add
Quote:
Originally Posted by Anonymous
Quote:
Originally Posted by marianco
Quote:
Originally Posted by Anonymous
I have Inattentive type ADD and will be seeing my GP for this soon. I have tried
Adderall and do not like the wired feeling and clammy hands and feet. I am
interested in seeing what you think about Concerta and/or Wellbutrin for the ADD
and a mild lift from winter blues. I do not metabolise stimulants very well unless
taken early in the day.
My hormones have been optimized.
Thoughts or suggestions?
Methylphenidate (as in Concerta) increases norepinephrine less than amphetamines
(such as Adderall). Both increase dopamine - which helps improve mood and attention.
Norepinephrine improves attention and alertness but also can burn out the adrenal
glands - thus the clammy hands and feet as possible side effects. Wellbutrin increases
only norepinephrine. It is a problem when a person has impaired adrenal function.
When a person has side effects from a stimulant, then a lower dose may be useful.
Thyroid and adrenal function are both stressed by winter - particularly with colder
weather. This is a highly important factor when one has ADD, thyroid or adrenal
problems since a stronger treatment may be needed.
Thanks Marianco,
I have been taking 18 and 36 mg of Concerta with the only side effect being headache at
36mg. My mood, motivation, and energies are good, but attention is only slightly
improved.
In short, I like the Concertas mild positive effects except I cannot feel my prefrontal
cortex being activated like I do from Adderall. Perhaps the Adderall XL version is what I
need. I wonder if running Concerta concurrent with Wellbutrin or with Adderal XL might
be the answer. Do you do this with some patients?
Knowing I suffer from Adrenal Insufficiency, can I use Adderall or Wellbutrin as long as
I supplement with 20mg of Hydrocortisone?
I had a urinary neurotransmitter test done and it revealed the following:
Low in: NorEpinephrine, Serotonin, Glycine (suboptimal)
Elevated in: Dopamine, Histamine, GABA, Glutamate
Normal: PEA, Taurine
The panel was done by NeuroScience Labs, with explainations at Neurorelief.com. An
amino acid product called ExcitoPlus has been recommended along with a product
called AdrenoCor which over timeis supposed to elevated my deficient NeuroHormones.
If one has adrenal insufficiency, the hormones are not optimized.
I wonder what other hormone problems are present - e.g. hypothyroidism, etc.
What other substances are being taken, besides Methylphenidate that can contribute to the
neurotransmitter profile described.
And why are there mood problems - the condition is then much more complex than Attention
Deficit/Hyperactivity Disorder alone.
A seasonal affective disorder is actually not really related to light levels. I think it is related to the
higher demands made on the thyroid and adrenal glands to maintain energy levels. One finding in
seasonal affective disorder is the presence of photophobia. This happens to be also a symptom
of adrenal fatigue.
Treatment of ADHD is often done using medications such as the stimulants, which increase
dopamine and norepinephrine. Wellbutrin only increases norepinephrine significantly in humans.
Strattera primarily increases norepinephrine - though has mild increases in serotonin and
dopamine.
A problem of increasing norepinephrine is that it can cause - and often not realized by
conventional psychiatrists - adrenal fatigue. This leads to the mood problems found in ADHD thought to be a feature of the illness or a side effect of treatment. Unfortunately, often this is
treated with an antipsychotic such as Risperdal, to knock down the mood symptom, at the
expense of risking serious side effects such as diabetes or cholesterol problems or neurological
problems.
To keep treatment going, it is then important to institute a treatment for adrenal fatigue to
maintain adrenal function. This may include hydrocortisone and other treatments, including
nutritional treatments.
When it comes to neurotransmitter profiles, the most reliable sign of a pure attention deficit
disorder is a increased amount of dopamine. This is a genetic form of attention
deficit/hyperactivity disorder, where there is dopamine resistance and the brain compensates by
producing more dopamine to get the same effect.
In other neurotransmitter profiles, where serotonin and other neurotransmitters are affected, I
would also look for other underlying problems which may be the actual cause of attentional
problems - for example, depression, anxiety disorders, hypothyroidism, adrenal fatigue, bipolar
disorder, etc. A stimulant may be used in treatment, but more caution may be necessary to avoid
worsening the underlying problem. For example, in bipolar disorder, a stimulant may worsen the
person's condition.
It is possible to use a stimulant along with Wellbutrin to try and improve attention by increasing
primarily norepinephrine. The usual warning about worsening adrenal fatigue applies.
It is possible to mix stimulants. However, In more than 14 years of practice, I have not found a
need to do so, nor have a seen another psychiatrist do so. Other concurrent conditions may be in
play to reduce the effectiveness of a stimulant. For example, once adrenal fatigue sets in, all
stimulants stop working, since the lack of adequate cortisol production will impair concentration
itself and worsen mood, motivation, etc.
Blocking Histamine
Quote:
Originally Posted by anonymous
Hi Marianco I am going to start experimenting with drugs that block histamine. I belive this is why
Serzone worked for me.
For the past year, benadryl has done me wonders almost makes me feel 100% free of
anxiety symptoms.. If i take it before bed my sleep is much more restfull.
Whats your thoughts on this, and are there any drugs I should try.
I'm wondering if the root of my issue is an allergy problem.
I'm going to give Cyproheptadine hydrochloride a try and see if i get any benefits from
it..
I recently saw my old psyc doc and he mentioned me trying the bipolar med Lamictal. I
am using the starter pack for a month to see if it works at.. I'm just about done with week
2 and uping the dosage tonight... i doubt it will work for me though...
Thanks man..
Serzone has multiple mechanisms of action, which makes it difficult to find a substitute once it
was taken off the Market. Trazodone is its sister medication - however the risk for priapism and
loss of the penis is significant when one's testosterone level is high (such as in young men). It
looks ugly when it happens - notwithstanding the death of one's penis. For those who are brave
enough to take the risk. Trazodone may potentially be useful as a substitute for Serzone. When
Serzone first came out, it was essentially Trazodone without the oversedation and dizziness.
Anti-histamines which penetrate the blood-brain barrier have traditionally been also used as antianxiety and sleep medications.
Lamictal does not affect histamine significantly. It may help reduce depression and anxiety in
some people.
Cyproheptadine blocks histamine receptors, blocks serotonin receptors, reduces CRH leading to
reduction in ACTH and Cortisol production, reduces prolactin production via thyroid-releasing
hormone mechanisms, and blocks muscarinic acetylcholine receptors. (as far as I recall off the
top of my head). It is very sedating and can increase appetite. It is a very complex moledule, and
is not just an antihistamine.
Valium Problem
Quote:
Hi there Marianco, i have stupidly been takign valium again on and off for the last 6
months increasingly, to the point of about 20mg 5 times a week the last few months.
I dont drink and take disulfuram to stop me which is why i started taking the valium to
cope with dating situations - i have a bit of a serial dating/sex addicition, which doesnt go
well with social anxiety hence drink in the past and now valium.
for 4 days now im stablising on 5mg 11am and 11pm and was going to cut down 1mg a
week so im off it in 10 weeks, as im suffering from mental and phsyical sides depression, paranoia, anxiety, physically numbness in my hands and feet. not good.
Now i have a sales job where i need to be very confident, and stopping cold turkey id
need 2 weeks off from past experience, so thats not an option.
i have spoke to people at benzo helplines who advised coming off 10% every 3 weeks so
30 weeks to come off but id rather more discomfort and be done. BUT they also said
SSRIs etc havent been shown to help with the anxiety, feelings of guilt and agoraphobia
etc in withdrawal i have felt.
Is there anything i can do to make this easier as my job is performance related and i must
be a high flyer.
I am currently pursuing CBT for social anxiety and the serial dating pathology i have, but
my doc doesnt know of the benzos tho i am going to see an addiction clinic next week (
who were of limited help talking about alcohol - as i was a binge drinker i felt i didnt
warrant attention and i couldnt talk about feelings about women to a woman and there are
no men there)
thanks for any advice bro
I can't give you advice since you are not a patient.
Some general thoughts:
1. A psychiatrist would be better capable of providing medical solutions to problems with anxiety
than a primary care provider.
2. Anticonvulsant medications, such as gabapentin or lamotrigine, have been used as alternatives
to benzodiazepines in regard to withdrawal symptoms and as treatment itself for anxiety.
3. SSRIs are often the first choice in reducing anxiety.
4. Adequate testosterone levels (in balance with estrogen, DHT) may help reduce social anxiety.
5. Treatment of adrenal fatigue, when present, may improve a person's ability to adapt to stress including reduction of anxiety symptoms and difficulty in social situations.
6. Long-term benzodiazepine use is an option - though difficult when a person tends to overuse
sedatives or have a history of alcoholism. In the appropriate case, maintenance treatment may be
considered with a benzodiazepine.
7. Therapy with a good marriage-family-therapist or psychologist is highly useful to address
psychological issues that contribute to anxiety, self-esteem, and relationship problems.
SHBG low ; what can it indicate ?
Quote:
Originally Posted by chip douglas
My latest SHBG was :
SHBG 17 ( 10 - 73 )
But I have low Total T, therefore what can this low SHBG can reveal in terms of
relationship to other hormones such as Estrogens and insulin ?
SHBG is reduced by: high insulin (insulin resistance/diabetes), low thyroid, high testosterone,
high DHEA, high growth hormone, low estrogens, low progesterone, high dihydrotestosterone
SHBG is increased by: low insulin, high thyroid, high estrogens, high progesterone, low
testosterone, low DHEA, low growth hormone, low Dihydrotestosterone.
Low SHBG increases Free Testosterone.
High SHBG reduces Fress Testosterone
The hormone with the strongest effect on SHBG is insulin.
Low SHBG is most often strongly correlated with diabetes or insulin resistance.
High androgen levels such as the use of supraphysiologic doses of testosterone can also drive
SHBG down.
Most cases of insulin resistance/type II diabetes start with hypothyrodism (low thyroid hormone
levels). Treating thyroid hormone deficiency can prevent the development of insulin resistance
and diabetes. Once the horse is out of the barn - and diabetes type II is present, increasing
thyroid hormone alone may not always reverse insulin resistance since other hormone
imbalances may occur to perpetuate insulin resistance (e.g. testosterone deficiency or adrenal
fatigue - which in turn worsens conversion of T4 to T3, etc.) or end-organ damage may occur
which may be irreversible. Insulin resistance itself can worsen thyroid function - thus causing a
positive feedback loop or death spiral - by causing loss of zinc and iodine and by causing nervous
system damage. This is where the relationships between hormone systems and nutrition become
highly intricate and undoing problems can become complex.
Re: Lab concerns - attn: Marianco and Headdoc
Anabolic steroid induced hypogonadism is a possible outcome from the use of supraphysiologic
doses of anabolic steroids.
As a person in the medical field yourself, it is highly important to educate yourself highly before
taking risks with your health. I recall one of the top knowledgeable moderators on the steroid
forum stating that the use of anabolic steroids is not for the uninformed or beginners. Extensive
education is imperative given the risks involved.
What are you trying to accomplish in your life?
Your discussion is also lacking in detail as to the problem you want to solve. It would also be
helpful to avoid using acronyms to help clarify what substance, supplement, etc. you are using.
In regard to iron, excessive iron can be dangerous in men because there isn't a way to get rid of
excess iron if an otherwise healthy man. This risks problems including liver damage. This is why
men usually do not need to take additional iron supplements.
Re: Blood tests again... still confused!!! help!
Quote:
Originally Posted by hartmann_gr
My blood test 3 months ago was the following:
Estradiol: 50.4 (5.0-70) pg/ml
FSH: 3.1 (3.4-20.5) mIU/ml
LH: 5 (1.6-8.0) mIU/ml
SHBG: 34.0 (10-70) nmol/l
Total test: 4.85 (3.0-11) ng/dl
Free test: 10.7 (13-41) pg/ml
I generally experienced a low sex drive.
So I run an aromatse inhibitor, and specifically 6-OXO.
n the first week, sex drive really hit the sky! Morning woods were awesome and sex drive
fantastic! From week 2 to the end of the treatement week 6 sex drive was not so evident
with not so many mornign woods
3 weeks after finishing the 6-OXO treatement I run blood tests again. Here are the
results:
Estradiol: 30 (5.0-70) pg/ml
FSH: 2.6 (3.4-20.5) mIU/ml
LH: 2.7 (1.6-8.0) mIU/ml
SHBG: 23.0 (10-70) nmol/l
Total test: 4.31 (3.0-11) ng/dl
Free test: 9.54 (13-41) pg/ml
Prolactin: 17.8 (0.2-12)ng/ml
I feel dispaired....
When one is not doing well, it is usetul to do labs to find out what is happening.
When one is doing well during the course of a treatment, it is useful to do labs to find out what
state one is in that caused that sense of well-being.
The two labs appear to be taken at the person was not doing well. The labs are also not
extensive enough to help determine what is happening.
If a problem with sex drive is occurring, then multiple systems may be at play to cause the
problem with sex drive.
SHBG is determined by numerous hormones (e.g. testosterone, progesterone, thyroid, estrogens,
growth hormone, insulin, DHEA, etc.). Thus without these other measurements, SHBG may tell
very little. A low SHBG may correlate best with insulin levels - i.e. diabetes or insulin resistance and is thus most useful for screening for diabetes.
Free Testosterone is determined primarily by SHBG, and is thus determined by the same multiple
hormones as SHBG. It is not a useful determinant of sexual function - not as useful as total
testosterone. One can easily have high free testosterone and zero sex drive for example. it isn't
useful in determining the dose of testosterone replacement to use. And too often, Free
Testosterone is not a reliable or accurate lab test. The primary reason I would obtain free
testosterone is that it is often part of a panel which includes Total Testosterone and SHBG for the
same price as Total Testosterone alone - thus I would get SHBG as a freebie. This would then
allow calculation of bioavailable testosterone which some practitioners like using in place of total
testosterone.
A blood test indicates the status of a person at a single moment in time.
Some levels such as estradiol and prolactin can vary a lot from moment to moment. Estradiol
itself can vary a lot depending on whether a man has or has not had sex during the day before
the test, for example - many times it can be high after having sex. Before deciding on the use of
an aromatase inhibitor, it therefore is important to perhaps take a few more tests of estradiol to
determine if a high level is consistent and thus can be a problem rather than jumping ahead and
taking the aromatase inhibitor - particularly if no significant estrogenic effects are present - such
as gynecomastia.
Similarly, Prolactin can go up and down. After an orgasm, Prolactin levels can go up, for example,
and may thus be a normal physiological state rather than an abnormal state. It is thus important
to check it a few times at different states, to see if it is a significant problem.
An initial basic panel using conventional labs such as the following would be useful more useful to
help determine where problems are occurring to cause a loss of sex drive:
1. Free T3, Free T4, TSH
2. Cortisol AM, DHEA-s, Progesterone, Pregnenolone sulfate
3. Fasting insulin, Hemoglobin A1c
4. Total testosterone, SHBG, Estradiol, LH, FSH
5. Comprehensive metabolic panel (including fasting glucose, electrolytes, albumin)
6. Prolactin
7. CBC, Ferritin
8. Urinalysis
9. Lipid panel
10. Vitamin B12, Folate, Vitamin A
11. C-reactive protein, ESR.
When one is doing well, it would then be useful to get another snapshot with similar labs to help
determine what one's optimal state is.
Some practitioners advocate getting such a panel when one is young and without health
problems so that down the line, when one is older, one can compare one's status to one's healthy
baseline.
Re: Picture update, still not looking halfway acceptable
The picture appears to be of a slim male with wide shoulders and slim hips. The body is tall at 72
inches.
The body type is similar to that found in tennis players.
The body looks similar Ashton Kutcher's body. And lot (if not the majority) of women are certainly
attracted to Ashton. I think few women are attracted to an overly muscular man (e.g. as described
last year in a T-nation poll of women).
Body Mass Index is Normal.
Body Mass Index = (151 pounds/(72 inches * 72 inches) )*702 = 20 = NORMAL BMI (18.5-24.9).
It would be useful to see an immersion or skin caliper test for body fat.
A receding hairline does start in one's 20s. Most men have a significantly receding hairline by
their 10th high school reunion (around 28 years-old).
If one is unhappy with one's appearance, it starts with dedication to
1. Optimum and sound nutrition for the body build desired.
2. Optimum exercise appropriate to the muscularity desired, e.g. weight lifting for muscularity,
cardio for a slim body.
Much of one's ability to accomplish this depends on one's psychological status. A positive
mindset is highly important.
Depression, itself, can lead to an excess of inflammatory cytokine production which may be
counterproductive to one's goals. Bodybuilding while depressed many not accomplish much since
one cannot give each rep the best one can. In any sport, a depressed mood tends to lead to a
loss rather than a win.
Progressing toward a goal (e.g. I want to be more muscular) is a more positive point of view
compared to running away from a condition (e.g. I need to lose more fat).
Body dysmorphic disorder is an example of a serious psychological condition where one thinks
he or shee is good enough in appearance. People with this condition may develop depression,
eating disorders, run themselves to exhaustion in exercises, use drugs or countless medications
or develop more serious physical problems from their attempts at changing their appearance. If
one thinks they may have this problem, it would be highly useful to see a counselor or therapist.
Re: Chronic Insomnia and lack of energy all day?
Quote:
Originally Posted by DrmChld
Does anyone have any suggested for someone who has been experiencing chronic
insomnia for a few years? I really need to get more sleep.
I am not sure if I just have too much in my mind that I can't stay asleep (falling asleep is
easy)
With my lack of sleep it is causing problems with lack of energy and desire during the
day. Is there anything I can take to help boost up my energy during the day?
I currently take the following medications and suppliments:
60mg Citalpram
50mg Atenolol
(both for anxiety)
2 Multivitam(1 morning then in evening)
B-Complex
1,800mg Saw Palmetto (broken down to 3 times a day)
120mg Ginko Biloba
500mg Calcium
300mcg Biotin
For sleeping I will sometimes take a Xanax(1mg) or Temazepan(2x15mg) and this will
keep me out for 4 hours and then I have problems staying a sleep after that.
Besides drinking coffee or taking no-doze all day what can I do for pepping up more?
I work out 3-4 times a week, eat well(could eat more) take protien drinks etc.
Any ideas?
The question is why is there insomnia?
Rather than bandaging the condition with a nighttime stimulant or daytime stimulant, it is useful to
determine the cause in the first place. Addressing the cause in treatment can then improve a
person's condition while minimizing side effects or risks.
For example, insomnia and anxiety may occur with hypothyroidism or adrenal fatigue. In both
conditions, the brain compensates by making more norepineprhine - and/or glutamate.
The higher stimulant neurotransmitter levels wake a person up - counteracting the effects of
sedatives.
Thus if insomnia is due to hypothyroidism or adrenal fatigue, then addressing the condition
successfully can allow a person to more naturally fall asleep without having to use a sedative.
Atenolol is mildly soluble in fat - thus only a little gets in to the brain to block norepinephrine.
However, beta-blockers which are highly fat soluble and enter the brain well (such as
propranolol), more more highly likely to block Thyroid T4 to T3 conversion, resulting in
hypothyroidism.
High dose Saw Palmetto can be a concern because it can result in an increase in other hormones
(such as estrogens) rather than just reducing DHT. A 24-hour comprehensive hormone and
metabolite test would have to be done to determine this.
If estrogens are increased by Saw Palmetto, for example, then in some people, they would be
more anxious or develop insomnia or develop irritability and anger problems - if the estrogens
raise norepinephrine more than serotonin or dopamine in the brain.
B-complex is usetul to help improve energy. They participate in many energy producing
processes. They have to be taken as a group since taking an excess of one can cause a
deficiency in another.
The B-vitamins can have a short half-life (except for B12, which is store in the liver), because they
are water soluble and easily urinated out. Thus, it is helpful in some people to take them twice a
day.
The problem is that some of the B-vitamins can cause problems at too high a dose. For example,
Vitamin B6 can cause a neuropathy at doses over 500 mg a day.
Re: Chronic Insomnia and lack of energy all day?
Quote:
Originally Posted by DrmChld
I have had my T3/T4 checked recently and they were normal. I have not had anything
done regarding adrenal fatigue. Whenevr I mention this to my PCP they always blow me
off. I have another PCP since I have moved and will be going in Friday regarding this.
I have had the problem with lack of sleep and energy since I was a kid. All the doctors I
went to told me it was my weight (Highest was 350). I had gastric by-pass and am now
down to 185 and I am still having the same problems. ..
Hmmm. When I analyzed the lab ranges for thyroid, I found that the "normal" or average TSH is
actually a hypothyroid TSH. Yet it is smack in the middle of the range. Similarly with T3 and T4.
Why? Because up to 40% of people have hypothyroidism, and 15% have a more severe form with Hashimoto's Thyroiditis. This skews the probability curve that is used to determine the range
for thyroid hormone. Interestingly, children have a much higher high end for Free T3 than adults.
Perhaps fewer children are hypothyroid than adults.
For example, the average TSH is 3.5. If one just removes the 15% of people with Hashimoto's
Thyroiditis, then the average TSH becomes close to 1.2! If anything, 1.0 is a more realistic
"normal" TSH - assuming the brain is functioning optimally. As a psychiatrist, I realize that this is
not often the case - the brain is not often functioning well - particularly in mental illness. There are
many people I see who have a TSH near 1.0 yet their Free T3 and Free T4 are low. Their
pituitary glands just can't muster enough to make TSH or their hypothalamus can't measure Free
T3 correctly to determine the correct amount of TSH to produce.
Thus it would be educational for all of us to give us your "normal" T3, T4 levels to see for
ourselves what is happening. For thyroid hormone measurements, if gauging by lab tests only rather than by using the more important history and physical exam, to me, a person is most likely
hypothyroid if their Free T3 < 3.3 or Free T4 < 1.2 or TSH > 2.0.
With morbid obesity, I would strongly wonder if a person was hypothyroid and has adrenal fatigue
(adrenal fatigue drives the appetite for sweets). Having both hypothyroidism and adrenal fatigue
lowers metabolic rate and impairs the burning of fat for energy.
Again, hypothyroidism and/or adrenal fatigue forces the brain to make more norepinephrine. The
higher norepinephrine levels keeps a person awake. When a person has adrenal fatigue, often,
practically no sleep medication works. Melatonin often will not work because melatonin reduces
adrenal production - causing a person to produce even more norepinephrine to kick the adrenals
into working. Hypothyroidism and/or adrenal fatigue are the most common causes of a lack of
energy. Insomnia exacerbates adrenal fatigue.
Re: New Labs are In.
Quote:
Originally Posted by pmgamer18
The only thing I changed was to lower my does of DHEA from 25 mgs. 2x's a day to one.
My Armour was 2.5 grains on my last test this test I am doing 3 grains.
I told my Dr. I am not on 90 mgs. of Armour but doing 3 grains. He said OK but we need
to watch it in the next few months to be sure ft4 and ft3 don't go to high.
My tests are as follows doing 3 grains and I feel like I need to go higher on Armour.
FT4 = 0.88 the last time it was tested it was 0.86 range 0.71 to 2.23 ng/dl at this lab on
11-16-06 I was doing 2.5 grains of Armour.
FT3 = 3.17 up from 3.00 range 1.71 to 3.71 pg/ml.
T3 total = 1.26 up from 1.23 range 0.58 to 1.59 ng/ml.
T4 total = 7.04 up from 6.76 range 5.0 to 12.0 ug/dl
My DHEA = 326 down from 574H range 80 to 560 ug/dl.
Total Testosterone = 636 down from 1252H range 181 to 758 ng/dl.
Free Testosterone = 18.9 down from 31.8H range 7.2 to 23 pg/ml.
All we did was lower the HCG shots down from 400 IU's to 250 IU's.
I do a testosterone shot every 3 days and the HCG the 2 days each in between.
My SHBG come in low 22 range 23 to 38 nmol/L.
I am starting to feel better having more energy and starting to walk again on my tread
mill.
My lab posted a new range for men over 49 for total and Free T.
It is interesting how low your Free T3 and Free T4 are given the approximately 180 mg a day of
Armour Thyroid you are taking. I would wonder whether or not it is being absorbed well. I assume
you take it on an empty stomach at least 20 minutes before breakfast.
Labs have interesting reference range differences. Quest has a range of Free T3 between 2.2 to
4.2 pg/ml.
In any case, once a person gets to 180 mg a day of Armour Thyroid, it becomes much more
important to use physical signs and symptoms to gauge response than the lab test. Lab tests are
useful. But physical signs and symptoms are more important. Particularly when some patients
have thyroid resistance and the Free T3 can go to 5.0 and above in some yet they still are
clinically hypothyroid. In this case, a physician can still go higher in dose with precautions.
One should also avoid having palpitations (excessively strong heart beats), a morning resting
pulse over 90-100 beats a minute, and a morning axillary temperature greater than 98.6 degrees.
This would mean that the thyroid dose is intolerable and one can get into serious problems if it is
prolonged. Watching out for signs and symptoms of atrial fibrillation or congestive heart failure
becomes important.
As one goes to higher doses, it becomes more important to go slowly - to allow the rest of the
body to get use to the higher dose - e.g. the adrenal glands - which are stressed as the dose of
thyroid goes higher.
Adrenal support becomes much more important as the dose gets higher. Often the limiting
problem as adrenal fatigue - which sets in after long-term hypothyroidism. Both thyroid and
adrenal glands often need to be treated simultaneously in order to reach an adequate thyroid
dose to address hypothyroidism. The adrenal fatigue is the more difficult problem to solve. The
response to treatment can be difficult to obtain.
Re: Medical School and Hormones of intelligence.
Quote:
Originally Posted by Mmartin
Hey guys. This is a bit of an unusual question, but any ideas would help.
I'm in a unique position in that I'm still doing my undergraduate degree while attempting
to deal with hypogonadism. I don't like to make excuses, and so I can only say that my
hypogonadism - combined with a lack of motivation - has contributed to a relatively poor
GPA. Recently I've been considering something drastic, however: medical school. After
experiencing first hand a deficient endocrine system, coupled with the complete and utter
failure of the Canadian medical system, and hearing of the plight of everybody on these
boards, it planted the idea of pursuing a medical degree in my mind. I can't stand how I
feel, and can't stand that other men - and women - have to deal with these horrible
problems. With hard work I can pull my GPA up to 3.0-3.2 (Canadian), and I have 2
years left to flesh out my volunteer activities and complete the MCAT. With a 3.0-3.2
GPA I can apply to all Canadian medical schools, even if my chances are slim.
So I am asking for advice from anybody who has considered medical school, applied to
medical school, or been through medical school.
Is it possible to use hypogonadism as a benefit, turning it into a positive on a medical
school application? Or will I be discriminated against precisely because I am
hypogonadal?
Any ideas are helpful. Maybe I can finally find some direction, ironically enough through
a disease that sapped me of my energy for the past 4 years.
I would not personally mention hypogonadism. That may weaken a candidate in evaluator's eyes
- given the large emotional component that hypogonadism entails.
Finding a positive reason to be a physician is most important - not the negatives about whatever
health system one is in.
Medicine is a calling. It requires hard work. It requires love of the work. The best physicians are
craftsmen - always honing and improving their skills in whatever they do. Performing their work
because they love it. It isn't a job. It is a way of life.
Many physicians today would discourage others from entering medical school realizing the
sacrifices involved and the bureaucracy involved. One cannot cure a medical system's problems
by oneself. One can focus on being the best physician they can be.
----In regard to impaired concentration or intellectual performance, testosterone is not the most
important hormone.
Thyroid hormones and some of the adrenal hormones (cortisol, DHEA, pregnenolone,
progesterone) have more to do with clarity of thought than the other hormones.
Thyroid hormone can be thought of as the hormone of intelligence. It improves energy production
in every cell in the brain, it allows the production of dopamine, serotonin, GABA, etc. It has a far
greater effect on dopamine than testosterone itself.
Cortisol allows one to handle stress and provides the energy - glucose - to fuel the mind.
Pregnenolone is strongly involved with memory and concentration.
Progesterone maintains (via allepregnenolone) the myelin sheeting that insulates nerves and
speeds the transmission of signals.
Thus to improve intellectual functioning at least these four hormones need to be optimized. They
can all be measured in standard labs.
Thyroid treatment is tricky for a few patients, since there are people with thyroid resistance who
have perfectly normal or optimal lab thyroid levels but need actually more because they still show
signs of hypothyroidism. This is where an experienced physician becomes necessary to optimize
thyroid function - when lab tests become useless (and actually scary with subsequent treatment)
and the clinical exam and experience becomes paramount - particularly when the doses used
become scary high but yet are necessary for that particular individual. Nothing like crossing one's
fingers in a leap of faith while avoiding harming a patient.
Nutrition also is important.
For example, it is important to have B-vitamins to fuel thyroid hormone. Without adequate Bvitamin intake, Thyroid hormone would be spinning its wheels. B-12 for example has to be kept
above 400 (200-1100) to maintain also myelin sheeting/nerve insulation.
Thus if one wants to be the best student they can be - first think about thyroid and adrenal
function.
Think about it: Women have much less testosterone than men - yet they can just as equally
perform intellectually. Wny is that? Because testosterone does not play as large a role in
intellectual function as thyroid and the adrenal glands.
Pregnenolone.
Quote:
Originally Posted by JanSz
Progesterone--------------------------------------1.4 ng/dL (0.3-1.2)
Pregnenolone--------------------------------------23 ng/dL (10–200)
How to increase Pregnenolone?
I am taking a lot of supplements, possibly decreasing some would be beneficial.
Pregnenolone is an over-the-counter supplement like DHEA.
For men, the usual dose is between 50-100 mg a day to help improve memory and concentration.
It may have stimulant effects - though not a stimulant mechanism of action - and thus should not
be taken at night.
Because of the stimulant effects - combining it with Ritalin may cause cause agitation or anxiety.
It is not useful as an anabolic agent - in some cases, it may actually prevent a person from
gaining muscle mass when taken at higher doses.
In some men, it would be useful to do a 24-hour hormone metabolite test - before and after
treatment with Pregnenolone to determine if pregnenolone is being metabolized into other
hormones such as estrogens, particularly when side effects occur.
Pregnenolone is the grandmother of all the other cholesterol-based hormones. In many cases, it
is well-tolerated without metabolization to excessive amounts of other hormones which may then
cause side effects. But there are always the patients who do have side effects.
In regard to brain concentrations of neuroactive steroids, pregnenolone is the one in the highest
concentration, even compared to DHEA.
When the adrenals fatigue, the reduction in production of pregnenolone is one big reason adrenal
fatigue impairs memory and concentration - and even mood.
Re: Medical School
Quote:
Originally Posted by JustOne
Bureaucracy, thats the word I was looking for, perfectly describes the reason why most of
us here have problems with conventional medicine. Having a cousin who is a doctor I
know how bad this can be, its actually quiet shocking and from a patient point of view,
discouraging.
So does the 1st day of med school start with a brief that ends up with a handfull of people
walking out saying "screw this I'm gonna go study law!"?
The first day of medical school is actually very exciting and a blast.
It's like the first day of elementary school. One instantly has 120 friends.
Everyone is bright-eyed, bushy-tailed, filled with energy, optimism about changing the world for
the better.
No physician to be is going to say "screw this, I'm gonna go study law!".
Doctors and Lawyers have very different mindsets.
In general, doctors want to help people, to give of themselves, for the calling of medicine. It is
about caring for others - the good samaritan. These days, very few doctors become rich. It is far
better to go into business than to medicine because one gives up 11 or more years of their life
before they can earn a living in medicine. A brain surgeon, for example, after 4 years of college, 4
years of medical school, has to train another 12 years before he or she can practice
independently as a brain surgeon. A heart surgeon is in their mid 40s before they can practice on
their own.
Lawyers want to argue - day in, day out - argue, argue, argue. To be a great lawyer, one has to
have a well of deep seated anger. The anger allows one to take on causes and argue them. One
has to be an asshole, a shark, who would twist the truth to win. The only thing that counts is the
win. Another notch on one's gavel - the 99% kill-rate. It is not about justice or even the truth. No
one pays for justice or the truth. A lawyer gets paid to win. Period. I know many very successful
lawyers. They may look nice on the outside, but inside they seeth in anger. That is what makes
them successful.
Once in medical school, 99 percent graduate. Thus once one gets in, one has "made it". The only
reasons people drop out are for significant personal reasons such as illness - or drug abuse.
Usually one doesn't get cynical about medicine until one is about 2-3 years after graduating from
training (residency), and enters the real world. Otherwise, one is fairly shielded. Some doctors I
have known, continuously reenter new residencies and specialties - essentially entering one
specialty after another - to escape from the real world by staying in school. They are paid when in
residency (a relatively small amount but one can survive on it). And while in residency, they are
fairly low wage labor for the hospitals they work for. With the hours one puts in, it is ends up being
much less than minimum wage.
If anything, once in medical school, if one gets the inkling to want to become a lawyer, generally
one first finishes medical school then goes into law school. One then becomes eligible to practice
malpractice law or specialize in medical personal injury law, etc. These can be very lucrative
fields for a dual MD, JD.
Re: Medical School
Quote:
Originally Posted by adddoc
FYI - a low GPA is the biggest hurdle you will have getting into med school. Excuses
won't get you past the initial thinning of applications as that is purely a GPA based
exercise. You need to get the GPA up regardless of disease state before even considering
medical school or you will be spinning your wheels trying to explain why your gpa wasn't
up to muster. The problem isn't that people don't care about your performance difficulties
being other than intellectual, they simply have limited spots available and many
applicants. Solve yuor issues, get an adequate GPA and then apply.
adddoc
The GPA is the biggest hurdle. If one has a 3.0 GPA it is still possible to get into an American
Medical School, but one has to have high MCAT scores - at least in double figures. It also helps
to have a well-rounded personality with unique talents - so that one can write a good personal
statement that will allow one to get an interview. One can then impress the interviewer and have
a shot at getting in.
It is important to spend time studying specifically for the MCAT. The MCAT is actually like an I.Q.
test. Like an I.Q. test, it can be prepared for so that one can score highly. It would help to spend
time with companies that prepare you for the test such as the Kaplan MCAT preparation courses.
They have mock MCAT tests on which you can prepare your timing and practice until you can get
perfect scores. A very high MCAT score will perk up an application and stir interest in the
applicant.
As far as I know, compared to veterinary school, it is far easier to enter medical school than
veterinary school. When I applied, 1 out of 2 applicants got into medical school, whereas only 1
out of 40 got into veterinary school.
There are many options to traditional medical school if one wants to be able to prescribe
medications.
In the U.S., if one has a low GPA, it can be easier to get into an Osteopathic medical school.
D.O.s - doctors of osteopathy - learn traditional medicine and chiropracty. They can enter the
same residencies as M.D.s. They have the same prescribing priveleges as M.D.s. They have
their own medical board - which tends to be more protective of D.O.s than the Medical Board is of
M.D.s. I think the smart D.O.s actually do more chiropractic medicine than traditional medicine.
Doing manipulations can earn a good D.O. more on average than the average surgeon, with
much lower risks - e.g. malpractice lawsuits. As my D.O. friends say, D.O.s who do mostly
chiropractic work laugh their way to the bank.
Naturopathic medicine is another option. N.D.s can prescribe practically anything an M.D. or D.O.
can prescribe in many states such as California, and can work independently. With enough
knowledge, one can do a lot with an N.D. degree.
Re: Marianco --important adhd question please
Quote:
Originally Posted by taser
marianco,
is it common for those that suffer from adhd to perform poorly in social settings where
there are lots of people? for example,a large gathering,wedding,night club?
also,sometimes i feel weighed down and can't seem to muster up enough energy to talk or
engage in fun conversation///it feels as though i really have to push myself..other times i
perform greatly..any idea why this is?
thanks buddy.
There are different causes of ADHD.
ADHD due to adrenal fatigue can result in avoidance of social settings. The adrenal glands have
many functions - including improving concentration, handling stress (social settings are a stress),
promoting energy production, etc. When there is a cortisol deficiency, often a person cannot
tolerate being around others.
Re: Is it possible - hCG causing panic attacks?
Quote:
Originally Posted by DaVinci2
OK, my doctors aren't very helpful in this area. I mentioned that I was feeling very tired
after I get my shot. Both doctors I talked with said the same thing "I've never heard of
that happening so I don't know what to tell you." Then, I ask if it's possible (Over the las
3 weeks) that because of the hCG (Possible raise in E2) is causing panic attacks? Both
have no idea.
Any advice on these 2 issues?
I can't give you advice since you are not a patient.
However, I can give educational information about HCG (Chorionic Gonadotropin).
The issue of HCG and panic attacks is much more complex than what appears on the surface.
A partial account of the metabolic cascades involved is as follows:
HCG acts like LH (Luteinizing Hormone).
LH has several actions, such as:
1. It stimulates testosterone production from the testes
2. It stimulates the production of aromatase enzyme
3. It stimulates the production of Cytochrome P450sc enzyme
4. etc.
Testosterone has several actions, such as:
1. Increasing dopamine production in the brain.
2. Increasing OR Decreasing Thyroid hormone production.
3. Reducing ACTH production.
4. Directly reducing Adrenal hormone production.
5. Becomes Estradiol via Aromatase enzyme.
6. Becomes DHT (Dyhydrotestosterone) via 5-Alpha-Reductase enzyme
7. Promotes insulin sensitivity.
8. Has antiinflammatory signaling functions.
9. Excessive Testosterone can result in an increase in anxiety depending on the metabolic
cascades involved.
10. etc.
Aromatase Enzyme:
1. Turns Testosterone into Estradiol
2. etc.
Cytochrome P450sc enzyme:
1. Turns Cholesterol into Pregnenolone
2. etc.
Estradiol (and other estrogens) has multiple actions, including:
1. Acting as a Monoamine Oxidase Inhibitor in the brain
2. Reducing thyroid hormone activity by increasing production of Thyroid Binding Globulin from
the liver.
3. etc.
Monoamine Oxidase Inhibitors (such as Estradiol) to varying extents:
1. Increase Serotonin levels
2. Increase Norepinephrine levels
3. Increase Dopamine levels
4. etc.
Serotonin:
1. Reduces the perception of stress - thus has an antianxiety effect.
2. Reduces norepinephrine production from norepinephrine neurons - contributing to its
antianxiety effect.
3. Reduces dopamine production from dopamine neurons - if reduced excessively, this can
increase anxiety
4. Has antiinflammatory signaling functions
5. etc.
Norepinephrine:
1. Is the primary signal for stress
2. Excessive Norepinephrine can result in anxiety or irritability/anger.
3. Has inflammatory signaling functions.
4. Can increase energy by promoting adrenal hormone production - if the adrenal glands are not
fatigued excessively
5. etc.
Dopamine:
1. Promotes a sense of well-being, calmness
2. Deficiency in Dopamine production can cause agitation or anxiety, etc.
3. etc.
Thyroid hormone:
1. Promotes energy production, such as by increasing mitochondria production and
thermogenesis.
2. Promotes steroid hormone production - increasing testosterone production - thus lowering
thyroid hormone can reduce testosterone production.
3. Promotes IGF-1 production - which does most of the actions of growth hormone
4. Increases serotonine production
5. Promotes insulin sensitivity
6. Has antiinflammatory signaling functions
7. Deficiency in Thyroid hormone can result in anxiety or irritability/anger
8. etc.
Growth hormone/IGF-1 hormone:
1. Can promote a sense of calm and well-being - deficiency of which can result in a higher level of
anxiety.
2. Has antiinflammatory signaling functions.
3. etc.
Adrenal Hormone production, includes:
1. Cortisol
2. DHEA
3. Progesterone
4. Testosterone
5. Pregnenolone
6. Adrenal cortex hormone production - particularly Cortisol - promotes energy production
7. etc.
Cortisol:
1. Promotes energy - via gluconeogenesis, etc.
2. Feeds back to the brain to reduce Norepinephrine production - resulting in reduction in anxiety.
3. Deficiency in Cortisol production can result in anxiety
4. etc.
DHEA:
1. Increases Dopamine production in the brain
2. Promotes insulin sensitivity
4. Has antiinflammatory signaling functions
5. Deficiency of DHEA can result in anxiety.
6. etc.
Pregnenolone:
1. Has a stimulant effect.
2. Excessive Pregnenolone production can result in agitation, tension, or anxiety.
3. etc.
Progesterone:
1. Has a calming, mood-stabilizing effect.
2. Deficiency in Progesterone can result in agitation, tension, or anxiety.
3. Has antiinflammatory signaling functions.
4. etc.
Insulin:
1. Excess insulin can reduce testosterone production.
2. Has pro-inflammatory signaling functions.
3. etc. etc. etc.
Immune System:
1. Deficient antiinflammatory signaling may promote anxiety
2. etc. etc.
Nutrition:
1. Certain nutrients are necessary to promote function across the nervous system, endocrine
system, and immune system.
2. Deficiency of certain nutrients can promote anxiety in response to HCG as a result of
dysfunction in these systems.
Thus, when HCG causes anxiety, the story is actually more complex than just the resulting
increase in Estradiol.
1. If HCG increases Testosterone excessively, it can cause a cascade that results in anxiety - e.g.
by decreasing thyroid function, decreasing adrenal hormone production, etc - particularly if a
person is predisposed to anxiety such as by having hypothyroidism and adrenal fatigue.
2. If HCG increases Estradiol, it can cause a cascade that results in anxiety IF (a big if), Estradiol
increases norepinephrine more than serotonin and dopamine, or if it results in significant thyroid
hormone reduction (particularly if a person is hypothyroid and has adrenal fatigue).
3. etc. etc. etc.
The solution would involve examining all the involved systems and chemical messengers
(neurotransmitters, hormones, etc) rather than just knee-jerk blaming only estrogen and
attempting to reduce estrogen levels. The solution involves addressing the problems that are
actually present (e.g. hypothyroidism, adrenal fatigue, excessive insulin, etc.) to reduce the risk of
anxiety with HCG particularly when one wants to use HCG to preserve testicular size or to use
HCG as a replacement for testosterone replacement therapy.
Reducing estrogen levels blindly can increase the risk of multiple problems including anxiety itself
- such as when estradiol more strongly increases serotonin than norepinephrine in a person.
Lab tests and an exam would be necessary to help determine where the problem lies. Then
solving the problem would not involve so much trial-and-error and guesswork.
Yes, HCG can cause panic attacks in susceptible persons depending on the functioning of the
nervous system, endocrine system, and immune system - the sum of which I call 'the mind".
Re: Is it possible - hCG causing panic attacks?
Quote:
Originally Posted by role model
After reading that post, and all its combinations, would be like hitting the lottery if you
cure your problem any time soon.
Getting lab testing done to see where there would be problems would make obtaining a solution
easier.
Given that energy is a problem, besides panic attacks, then likely concurrent problems include
thyroid and adrenal problems since those two are the primary organs involved in energy
production in the body. If those were working well - a huge question since it can be difficult to
treat thyroid and adrenal problems well in some people - then any remaining problems many
involve the other systems.
Re: Is it possible - hCG causing panic attacks?
Quote:
Originally Posted by DaVinci2
I've had my thyroid and adrenals checked. They were checked in Dec. and Jan. Would it
be wise to have them both checked again now in Feb?
I will say that yesterday I noticed that my nipples were sensative while in the shower and
the water was hitting them. I don't know if this is the first sign to gyno, so that's
something else I'd like to consider.
The problem with being in Japan, concerning HRT, are not very knowledgeable. I have
been to 5 different doctors now. Had to get 5 different baseline blood work, all with the
same answers and was given 5 different choices for treatment. 1 doctor suggested a
herbal remedy. When I raised certain concerns or asked about whether I was primary or
secondary (Something NONE of them understood) I was told "Not to worry.". None of
them even really wanted to look into WHY I had low test.
Maybe you can share your lab results so that we can learn from them.
Interestingly, there are parts of Japan where many people live a long time - where there are
frequently many people who live past 100 years. In those areas, the average 50 y.o. Japanese
man has a higher testosterone level than the average 50 y.o. American Caucasian man.
Speculation (in reality the situation is even more complex and I continue to research the matter):
1. Testosterone can increase dopamine levels in the brain.
2. Increasing dopamine levels may reduce serotonin levels - since their production is inversely
related.
3. Serotonin help reduce perceived stress and helps reduce anxiety symptoms.
4. Reduction in serotonin level may increase the likelihood of perceived stress and anxiety.
5. Increased perceived stress and anxiety may cause the brain to increase Adrenocorticotropic
Hormone (ACTH) release.
6. The ACTH signal is received by the adrenal glands, which in turn starts the stress response
(including increasing cortisol, norepinephrine, epinephrine production, among the 50 hormones
produced by the adrenals).
7. Increased perceived stress may activate the sympathetic nervous system, which then
increases output of norepinephrine from the brain as part of the fight-or-flight reaction.
8. Increased testosterone may also lead to aromatization of testosterone to estradiol/estrone
(estrogens).
9. Estrogens have multiple effects including behavioral effects such as increasing anxiety,
irritability, hyperactivity and aggression.
10. Estrogen increases the expression of receptors and other associated proteins for
neurotransmitters including serotonin, norepinephrine, and dopamine.
11. Reduction in serotonin level from increased dopamine levels may affect thyroid hormone
conversion in the liver from T4 to T3 via the cytochrome P450 2D6 enzyme.
12. Reduction in active thyroid hormone may destabilize mood - perhaps contribute to anxiety,
hyperactivity
13. Estrogen itself may compete with thyroid hormone at the thyroid hormone receptor site creating a virtual hypothyroid state - perhaps also contributing to anxiety - despite normal thyroid
hormone levels.
14. Remeron's mechanism of action includes increasing serotonin release, increasing
norepinephrine release (at higher doses), and by blocking histamine receptors (accounting for
sleepiness and weight gain at lower doses).
15. Remeron, in my experience, does not work well to reduce anxiety.
16. Increased norepinephrine levels from Remeron makes a person more likely to have anxiety
when norepinephrine is further increased and serotonin decreased - from other causes - such as
those written above.
17. The higher the dose of Remeron, the higher the increase in norepinephrine, the higher the
likelihood of anxiety.
18. One of testosterone's functions is to reduce stress by reducing ACTH production from the
brain and by directly reducing adrenal gland hormone production (i.e. reducing cortisol
production).
19. Should the adrenal gland, from long term exposure to anabolic steriods, become tolerant to
the effects of testosterone, testosterone may not be able to reduce stress and anxiety.
20. Adrenal insufficiency may occur from long term anabolic steriod use - where the adrenals
cannot make adequate cortisol and other hormones as needed when stressed to handle stress.
21. Adrenal insufficiency/fatigue results in intolerance of stress, fatigue, chronic sleepiness,
irritability, anxiety.
22. Tolerance to testosterone's effects in the brain may occur with long term anabolic steriod use.
23. Testosterone usually has a calming effect. This may not occur if tolerance occurs to
testosterone.
24. With adrenal fatigue, progesterone levels are reduced.
25. Progesterone is being shunted to create more cortisol in adrenal fatigue.
26. Progesterone has a mood stabilizing, calming, antidepressant, sleep-promoting effects
through several mechanisms of action.
27. Progesterone increases seroronin, norepinephrine, GABA, dopamine activity in the brain.
Progesterone blocks NMDA Glutamate receptors. Progesterone promotes myelination of nerves
to improve signal transmission. Progesterone increases Estrogen receptor sensitivity.
Progesterone promotes thyroid hormone activity.
28. Low progesterone levels may lead to increased anxiety, insomnia, tension, and mood
instability.
29. Low testosterone levels and high cortisol levels (as a result), may lead to insulin resistance.
30. Insulin resistance not only predisposes one to diabetes, it impairs neuron signal transmission,
and directly reduces testosterone production.
31. Insulin resistance may increase the likelihood of mood instability, anxiety, depression.
32. A serotonin-reuptake inhibitor (a group of medications with many members) increases
serotonin more specifically than other effects.
33. Increasing serotonin has a calming effect.
33. Increasing serotonin excessively, however, causes a reduction in dopamine production.
34. Excessive serotonin, and subsequent reduction in dopamine causes a motor movement
disorder called akathisia.
35. Akathisia has symptoms including anxiety, panic attacks, insomnia, irritability, restlessness,
hyperactivity, agitation (to the point of suicide attempts by some people).
36. When attempting to balance or optimize the effects of one hormone/neurotransmitter, one
may have to balance or optmize the effects of others to obtain the desired state. Testosterone,
Estrogen, Progesterone, Cortisol, Insulin, Thyroid Hormone, Dihydrotestosterone, the metabolites
of progesterone, Norepinephrine, Epinephrine, Serotonin, Dopamine, GABA (gamma amino
butyric acid), Glutamate, Histamine, etc. are highly interlinked in their effects - with the endpoint
of allowing a person to maintain balance between health and the stress the person faces.
Quote:
Originally Posted by T Man
I read your fantasic reply about T and neurotransmitters. You mentioned that Remeron
was not good for anxiety. It seems that I can't tolerate SSRI's. They activate me and
aggravate my anxiety/panic. Especially prozac and celexa. Zoloft gave me anxiety attacks
after only a few days. Paxil made me get the shakes after a week. Also got the zaps when
I went off the very low dose of 5 mgs. Remeron @ 7.5mg is having some calming affects
on my GAD compared to before taking it. It has also helped my depression after crashing
from the anabolic cycle last year. I am very sensitive to all medications and usually need
to take low doses.
In your opinion what is a safe alternative route? For now The Univ Docs want me to stay
on the Remeron and try Buspar with it. They really want me to take .5 Klonopin daily.
But, I am fighting them on this because addictions run in my family and I am afraid of
possible long term side effects. Am I being foolish and misinformed about Klonopin? I
use .25mg of Klonopin 1 or 2 times a week sometimes less as needed.
They also mentioned Nardil which I really want to avoid. That seems like scary stuff with
all its restrictions and side effects.
The Docs at the Univ don't want to touch the Endocronology issues. They want to only
address the anxiety disorder and let my Endo treat the pituitary problem with HRT. My
Endo's listen but know much about HRT or anxiety issues.
Any thoughts would be greatly appreciated.
Its interesting to me, as I have become more adept at psychiatric neuroendocrinology - the
branch of psychiatry I am currently developing intensely, how much each specialty has
deliberately limited their knowledge and abilities - each specialty is an island - with the
consequence of promoting chronic illness and partial responses to treatment.
Off my soapbox,...
At a very low dose, the bulk of Remeron's effect is due to its ability to block histamine receptors
(an antihistamine effect) - which causes sedation, reduction in anxiety, and increase in appetite.
This becomes outweighed at higher doses by its ability to increase serotonin, then at even higher
doses, its ability to increase norepinephrine. Antihistamines (such as Vistaril) have been used as
mild anxiolytic medications. They are limited because at high doses they cause oversedation.
Many also have an anticholinergic effect - which can increase dopamine, but if dosed too high
can cause an agitated confused state, as well as a potentially fatal irregular heart beat - thus the
clinician has to be careful.
Serotonin Reuptake Inhibitors (SSRIs - such as Prozac, Paxil, Zoloft, Luvox, Celexa, and
Lexapro) simultaneously reduce dopamine levels while increasing serotonin levels. The reduced
dopamine levels (depending on the person's genetic predisposition), cause a mental/motor
movement disorder called Akathisia. Akathisia at the extreme causes severe agitation, a high
distress level that makes someone want to jump out of their skin. Some people end up
committing suicide as a result. At lower levels, akathisia can manifest as panic attacks, irritability,
anxiety, insomnia, physical discomfort that causes people to move frequently - e.g. to pace,
squirm in their seats, toss and turn in bed.
Besides increasing serotonin and blocking histamine, other psychiatric medication mechanisms of
action which may reduce anxiety include:
1. increasing GABA (e.g. benzodiazepines or some anticonvulsants),
2. blocking norepinephrine (e.g. beta-blockers such as propranolol or atenolol),
3. reducing norepinephrine output (e.g. alpha-2 adrenergic blockers such as clonidine or tenex).
4. increasing dopamine in the frontal cortex, reduction of dopamine in limbic system (e.g. low
dose antipsychotic medications - an old tactic, though with many side effects)
5. The anticonvulsants have numerous mechanisms of action - too numerous to list. They, in
general, are useful options for reducing anxiety. Except for Depakote, Gabapentin, and Zonegran,
the other anticonvulsants, however, speed up the liver and reduce levels of progesterone,
possibly the other steroid hormones, thus complicating birth control - and hormone replacement
therapy. This needs to be taken into account and appropriate adjustment made (e.g. raising
hormone dose) when the anticonvulsants and hormones are used together.
Additionally, depending on the person and the deficiency involved, restoring activity of
testosterone, progesterone, estrogen, and thyroid hormone (all of which affect neurotransmitter
activities through various mechanisms) can reduce anxiety.
Some supplements such as Valerian, theanine also affect GABA and other neurotransmitters in
reducing anxiety. Theanine (extracted from green tea) is particularly useful since it doesn't have a
sedative effect, though it appears to work at least by increasing GABA production in the brain thus promoting a calm wakefulness.
When a person is afraid of addiction, I usually explain the difference between "addiction" and
"dependence". Dependence happens with all substances when used for a long time. The body
develops a partial opposing force/activity to the substance which becomes uncovered when the
substance is abruptly stopped. Dependence even happens with aspirin - causing a withdrawal
migraine. In short, dependence is the presence of a potential withdrawal effect from the use of a
substance. When a medication is effective in improving a person's ability to function (such as the
medical use of a substance), I do not consider it addiction. Addiction is quite different. Addiction is
the non-medical use of a substance, which results in the development of impairment in function.
Impairment in function is the important concept.
Aside from hormone treatment, the most effective medications (for their indications) in psychiatry
are the stimulants and the benzodiazepines. Despite years of drug company ads touting the
effectiveness of serotonergic medications for anxiety and the stigma of their potential for addiction
and dependence, the benzodiazepines are still the most used subtances for the treatment of
anxiety. For good reason - they work more often than not. Long term use of benzodiazepines is
possible because full tolerance does not develop - there is still a residual effect which may be
enough for the patient to adequately reduce anxiety.
Klonopin is generally safe for long-term use. However, I generally check the liver (liver function
panel) twice a year to reduce the risk of developing liver inflammation - a fairly rare event. In more
than 16 years of experience with the use of benzodiazepines in the treatment of anxiety, I have
had to stop Klonopin twice and Ativan once due to the development of liver enzyme elevations.
The primary long-term problem with benzodiazepines, particularly the longer-acting ones is that
metabolism slows as we age. Thus, some benzodiazepines (such as Valium), end up lasting for
days, effectively saucing the brain, reducing cognitive functioning. This can be treated by
reducing the dose or shifting to a shorter acting medication (which is longer acting in a senior
citizen).
I rarely use MAOIs these days. They primarily act by increasing serotonin. But the Serotonin
reuptake inhibitors are safer - having much fewer interactions with foods and other rmedications. I
keep them as an option when other medications fail - particularly for depression.
Tricyclic antidepressants - which work by increasing serotonin and norepinephrine and by
blocking histamine - are useful for treating anxiety. They are limited by weight gain, oversedation,
anticholinergic side effects. I avoid them in potentially suicidal patients since they are the most
lethal medications I prescribe, when in overdose.
Re: Lithium's mechanism of action?
Quote:
Originally Posted by Sonny
marianco: How does lithium work to augment the effect of antidepressants? Over the
years, I have seen this strategy commonly used in treatment resistant cases.
Lithium has been useful to me as an anxiety medication. It does not "hit" with the same
intensity as a benzo...it's a lot more subtle, but very effective and it's long-term efficacy
has been excellent for me.
IMO, lithium is about as "natural" as you can go in terms of psychiatric medicine. It is an
element already found in your body. Throughout history, civilizations that consumed
trace amounts of lithium (usually in water) had far lower occurrences of mental distress.
Lithium and other mood stabilizing medications have extremely complex mechanisms of action.
One result is to increase serotonin levels - which may have an anxiolytic effect.
Mechanisms of action for Lithium include:
1. Stabilization of the inactive conformation of G-Protein
2. Inhibition of Adenylate Cyclase
3. Up-regulation of some Adenylate Cyclase subtypes
4. Uncompetitive inhibition of inositol-1-phosphatase - leading to a reduction in neuronal myoinositol levels.
5. Supressing the phophatidyl inositol pathway
6. Reduction of Protein Kinase C activity by down-regulating selective PKC isozymes
7. Reducing intracellular calcium levels via the intracellular signaling pathways - leading to the
regulation of synthesis and release of neurotransmitters, neuronal excitability, cytoskeletal
remodeling, and neuroplasticity
8. Reduction in the turnover rate of archidonic Acid (part of the omega-6 fatty acid pathway)
9. Down-regulation of arachidonic acid-specific phospholipase A12 protein
10. Inhibition of glycogen synthase kinase-3 by competing with magnesium for a binding site
11. Increase in the Extracellular Signal-Related Kinase signaling pathway activity (such as in the
frontal cortex and hippocampus).
12. etc., etc.
Which ones are most important for pharmacologic function is not clear - though the sum total is
probably the case - which each patient having individual differences in response.
Lithium is NOT a natural part of the body. Excessive doses, such as in the 1950s when
cardiologists thought it would make a good salt substitute, led to cardiac arrhythmias, confusional
states, and deaths.
Lithium has interactions with common medications such as Ibuprofen and other Non-steroidal
Antiinflammatory Agents - which block the excretion of lithium in the kidneys, leading to
sometimes excessive concentrations in the blood.
Lithium is unique medication in that the effective dose is extremely close to the toxic and lethal
dose. It is thus not a medication to play with. More is not necessarily better because it may also
be fatal. The physician has to be highly careful with its use.
Re: Doctors/anyone please... Testosterone and neurotranmitters
Quote:
Originally Posted by HeadDoc
thanks again for such a thorough response. Is there a directionality of neurotransmitters
to hormones? Do the neurotransmitters control the hormones?
It is a web of interactions.
Neurotransmitters can control hormones and immune system cytokines.
Hormones can control neurotransmitters and immune system cytokines.
Immune System Cytokines can control neurotransmitters and hormones.
From my point of view, there is actually no difference between a neurotransmitter, hormone, and
immune system cytokine. All are chemical messengers of the mind. And the mind is the sum
function of the nervous system, endocrine system, and immune system.
Re: Doctors/anyone please... Testosterone and neurotranmitters
Quote:
Originally Posted by JustOne
Is Akathisia more psychological like anxiety, or more physical like parkinsons?
I think I might of had it before, is loss of apetite and inability to keep food down one of
the symptoms?
Parkinson's disease is both a physical and mental illness. The mental symptoms of Parkinson's
Disease often start much earlier than the physical symptoms. They include depressed mood, lack
of motivation, impaired visuospatial thinking, impaired memory, anxiety, impaired concentration,
etc. On neuropsychological testing, the impaired visuospatial thinking is most prominent in
Parkinson's disease compared to other causes of dementia.
Similarly, akathisia is both a physical and mental condition. It is foremost considered a motor
movement disorder just as Parkinson's disease is.
Symptoms of akathisia generally do not include loss of appetite or nausea and vomiting
Doctor-Patient Confidentiality
Quote:
Originally Posted by Anonymous
Hi marianco,
I was wondering if the dr-patient confidentiality applies if I wanted something withheld
from one doctor to another.
Whenever my GP referes me to a specialist he will put in the letter that "I have a history
of anxiety problems" or "I am obsessed with the need for testosterone replacement" and it
is out of context with the rest of the letter and in some cases even irrelevant, and I find it
negatively influences the way I am treated by the specialists.
Is there anything I can do about this(not legally of course) like ask my GP to be
completly confidential about certain things or not include what may be personal opinions
in referal letters?
Thanks.
Yes.
One should be able to tell their doctor to withhold information if this would impair the assessment
of the consultant.
Particularly when it comes to psychological or mental health issues, it is important to leave much
of this out to prevent the consultant from becoming blinded or prejudiced by the information.
For example, when it comes to physical problems presenting with mental symptoms, up to 25% of
the time the diagnosis is missed if the physician focuses primarily on the possibility of a mental
illness. For example, when patients with chest pain and panic attacks come to the emergency
room, up to 25% of the time, they really have a heart attack.
As another example, often times, physicians get frustrated when patients come in with
"somatization disorder" - meaning that the physician can't find anything physically wrong with
them, so they say it is all in the patient's head. When such a physician comes to me asking what
they should do, I usually tell them to keep doing testing to make sure no stone has been unturned
to find out if there is a physical problem occurring. When I see such a patient, I many often find
something wrong with them that the physician missed and it is not just fabricated by the patient. It
was missed because the physician didn't have the skills or did the right tests to find out what was
happening. For example, I had a patient who was unable to work for years by severe fatigue and
depression. A string of doctors could not find out what is wrong. I found that her temperature was
mildly elevated and her pulse was high. I also did not think she had a psychological reason to be
severely depressed. I thought she had some soft of infection that was not yet found. A bone scan
reveased she had a dental infection that got into her nasal bones. After removal of the infected
bone and with antibiotic treatment, her depression and fatigue went away. Thus a string of
doctors could not find the cause of her problem and they attributed it to depression. If any one of
them could have kept going and not dismissed her problem as only depression, and do further
testing, he or she may have found the nasal bone infection that caused her problem. Luckily for
her, someone finally did.
If the doctor doesn't recognize or is open to the possibility of prejudice from the inclusion of
certain information and goes ahead and adds this information - causing prejudice to the patient in
the subsequent evaluation - I would change doctors.
The problem is that physicians can be all too human. And if they are not sensitive to a person's
mental health, they can be instead prejudiced by it in evaluating a patient. It is all too easy to
blame the patient for one's inability to find the cause of a person's problems.
Re: Dr. Marianco, decreased feelings/emotions
Quote:
Originally Posted by Legenden1999
Would you happen to know what hormones/neurotransmitters that are responsible for
decreased emotions. Like the inabillity to get relly happy about something, and feeling
love about someone.
Thanks in advance!
JH
All of them play a role.
The are a group which most people have problems with:
Dopamine
Serotonin
Norepinephrine
GABA
Glutamate
Thyroid
Cortisol
Aldosterone
Pregnenolone
Progesterone
Testosterone
Estrogens
DHEA
Insulin
Melatonin
Optimizing how these work together goes a long way toward feeling happier and being able to
relate better with others.
It's not just a matter of increasing one or the other. It is important to realize that these work as a
team. Thus, how they work together is a very important target of treatment. This is why what I do
feels a lot like a mechanic tuning up a car. One has to know how the entire car works as a whole
to do this well.
Optimization includes improving one's nutritional status. That involves a whole slew of things.
The above are the big ones - the primary targets of most treatment. There are many others, of
course. For example, some people, who have been neglected or abused in childhood also have
problems with Oxytocin - however manipulating this is very difficult. It can indirectly improve by
addressing the adrenal hormones including progesterone, and estrogen. Addressing the other
hormones, neurotransmitters, and cytokine problmes, would be part of fine tuning a person's
condition, once the big targets are improved. I would include growth hormone/IGF-1 in this group.
Hypogonadism from taking steroids
Quote:
Originally Posted by Anonymous
"If the guru himself prescribes me a type of recovery program should i go for it or
continue my natural route. Past 3 months I've grown more facial hair and quicker,
although theyre not strong i have had morning erections on probably half(or a little less
than half) the days in each month. Balls seem around 1.5 - 1.7 inches that might be a
little less than normal. Last test results total t= 315ng/dl LH = 2.1 (the first time in 3
years it's gone above 1.0) FSH= 1.7? . Doing anything naturally is always better than
doing something chemically, so I wonder is it possible I recover naturally on my own
despite being shut down for 3 years or should I give Dr. Shippens protocol for me a shot?
What I'm most worried about is having his program disrupt my natural recovery(if its
even possible). Just a reminder my case is secondary hypogonadal as a result of taking
steroids at age 17 (i'm now 20). Also what do you guys think he might recommend for
me?"
I'm not an expert in Anabolic Steroid Induced Hypogonadism (ASIH) and I have not yet treated
someone with such a problem, nor have I read extensive literature on it and it's treatment. John
Crisler, D.O., has much more experience in this regard, since he has treated so many patients
who have had ASIH.
As far as I know, it may take a long time for the hypothalamus and pituitary glands of the brain to
recover from being suppressed so long by elevated anabolic steroids. It would be like trying to
restart the adrenal glands after having used high dose prednisone for years - it can take many
years to get it toward recovery. The various treatments on the surface appear designed to
accelerate this process of recovery by causing the brain to think it has even less estrogens and/or
testosterone than it already has (e.g. using Tamoxifen).
I am not familiar with Dr. Shippen's protocol so cannot comment or speculate on it.
Re: Hypogonadism from taking steroids
Quote:
Originally Posted by BigAk
Dr. Marianco... I'm currently supplementing with 25mg of DHEA daily after my latest
bloodwork revealed levels a bit below normal range. I'm not on any form of TRT or
anything. In your opinion, do you think DHEA supplementation at this dose would cause
any negative impact or shut down of my HPTA?
As usual, we do appreciate your expertise and tremendous help to our community.
p.s. I'm 40 year old former ASIH patient currently on 10mg of Tamoxifen only.
I do not know how any individual person would respond to 25 mg of DHEA without an exam or
test to see where it is going.
DHEA at 25 mg a day could stay as is - which tends to occur with most patients who are low on
DHEA - i.e. have lower adrenal function/adrenal fatigue/aging, etc.
DHEA in some can turn into testosterone.
DHEA in some can turn into estrogens.
If DHEA does these two, then it could reduce LH/FSH production.
There are many directions for it go to.
If unwanted pathways are a concern, then one would have to be on the lookout for adverse
effects (e.g. gynecomastia from excess estrogen activity) or get lab testing. Currently, the best
way I have found is to do 24-hour urine tests for steroid hormones and their metabolites. It is
complicated to read but does help more than others in determining where a particular treatment is
going - particularly when one is concerned about adverse effects.
In general, for most people, I would stick with lab tests since insurance can pay for them, but in
some cases, the specialized testing is valuable.
Re: To Marianco--Gilbert's Syndrome
Quote:
Originally Posted by chip douglas
Hi Dr. Mariano,
Would you think having Gilbert's Syndrome may influence hormone metabolism and
neurotransmitters ?
I think it's now clear that I have Gilbert's Syndrome, as 3 out of 3 Bilirubin lab results
came in mildly elevated, and that's what my new doctor and PCP think it is. I know that
Gilbert's Syndrome is known to be a benign hepatic disease, in that there aren't many
symtoms associate with it.
I just remember that back then, I'd feel so much better when I used liver tonics. However,
liver tonics also affect other bodily systems, so it's a long shot as to whether they really
did me good by acting directly on the liver.
A retired endocrinologist from California that I've known but don't get to see very often,
has told me through emails, that this should be further investigated--he says that any
chronic liver enzyme(s) elevation is a disease and should be treated as such.
What I want to make sure, is know whether or not, GS can have any bearing on what I've
complained about for years.....I'm curious about it.
Many thanks,
Marc
As far as I know:
Gilbert's syndrome is caused by a genetic mutation causing approximately 30%-50% reduced
glucuronidation activity of the enzyme Uridine-diphosphate-glucuronosyltransferase isoform 1A1
(UGT1A1 or Bilirubin UGT), which occurs in about 3-7 percent of the population - a very common
condition. This results in an increase in unconjugated bilirubin - causing mild jaundice during
exacerbations. There may also be a genetically-caused increase in Alkaline phosphatase another liver enzyme. Many have a mild increase in destruction of their red-blood cells hemolysis. Some have reduced clearance of fatty acids. There are many causes of elevated
unconjugated bilirubin - thus the other potential causes may need to be evaluated.
Jaundice is also precipitated by dehydration, dieting (fasting), infections, menstruation, stress
(including overexercising, trauma).
The condition is generally considered benign - meaning it doesn't cause excessive problem in a
person's life or interactions with other health problems or medications. But then a person's
mileage may vary. Prognosis is generally exceilent with normal life expectancy.
However, it does have symptoms in some people. Symptoms may include fatigue, stomach
pcramps, anxiety - though often the symptoms are vague.
It does make a case for doing pre-treatment liver function tests since the elevated bilirubin levels
will complicate interpretation of adverse effects of treatment for many medications.
Steroid hormones also reduce activity of this enzyme. Thus elevating hormone levels may lead to
increased jaundice.
Bilirubin-UGT is one of several UGT enzyme isoforms responsible for the conjugation of a wide
array of substrates that include carcinogens, drugs, hormones, and neurotransmitters. Yes,
hormone and neurotransmitter metabolism may be slowed. Of course, this may imply an increase
in parent hormones and neurotransmitters since their elimination is impaired. Whether this is
relevant clinically is not known - though is probably not, given the generally benign course of the
condition.
Re: To Marianco--Gilbert's Syndrome
Quote:
Originally Posted by JustOne
If I stay up for really long like 24-40 hours straight, I go pale and abit yellow, and I slurr
my speech abit to the point where people think I am saying a diffrent word.
I have gilberts and the highest I have seen my billirubin is ~32 (0-20). Could the gilberts
be linked to the paleness and slurred speech, otherwise I dont think I have any symptoms
that I have noticed.
I suppose if hemolysis (with mild anemia) is a feature of Gilbert's Syndrome, then becoming pale
and then jaundiced is a possible effect.
Slurred speech has many causes - including not having slept for a prolonged peroid of time impairing one's coordination.
Re: To Marianco--Gilbert's Syndrome
Quote:
Originally Posted by jaydee
I wonder if Justone's problem could be to do with blood sugars? If your a little
hypoglycemic, you can get slurred speech and stuff.
Also Dr Marianco could gilberts syndrome have anything to do with the problems some
guys have with finasteride? I have got gilberts and also finasteride issues that are not
resolving. I often wonder if its somthing to do with how this drug is detoxed. Like maybe
its staying in our system for too long even though its got a short half life.
I know doctors who say that gilberts is straight out poor liver function and mean you
need to detox your liver. Since finasteride is metabolised in the liver, it makes me wonder
if there is a connection. I also noticed that my billirubin went through the roof while on
finasteride.
It is difficult to tell whether or not there is a relationship between Gilbert's Syndrome and
Finasteride problems.
A lot of people I have seen so far who have had problems with Finasteride have had other
hormonal problems instead, which were exposed by using Finasteride, which many not be simply
resolved by stopping Finasteride.
The interesting thing is that blocking alpha-reductase using Finasteride has far reaching effects
rather than simply reducing DHT.
For example, by reducing DHT, Finasteride favors testosterone going to estrogens. Doing so may
then reduce thyroid hormone activity, which then may cause insulin resistance, which then may
cause loss of magnesium and iodine from the body, which then may exacerbate and prolong
hypothyroidism, which may then not resolve from simply stopping Finasteride, which has to be
addressed as a separate issue in treatment. Insulin resistance, itself, is a self-perpetuating
problem since it can lead to abdominal obesity and testosterone deficiency - both of which can
further worsen insulin resistance.
These complex cascades can lead to situations which need to be discovered in testing before
they can be understood to exist and be targetted in treatment.
Re: To Marianco--Gilbert's Syndrome
Quote:
Originally Posted by jaydee
Thanks Dr Marianco. Do these guys usually recover with treatment or is there still a bit
of a mystery with finasteride? This finasteride is some scarey stuff.
If the actual problems caused by finasteride are addressed, then perhaps the person can recover.
Any treatment can be scary if given blindly.
Testosterone, itself, can cause significant and serious problems, if one doesn't consider the risks
involved and take measure to adjust for the problems as they occur. Yet, on this forum, not many
are afraid of it.
There are many people who are doing well with finasteride.
For those that want to continue finasteride to preserve their hair, yet are having problems with it
(such as a male model who was a patient of a colleague - who could not stop finasteride since his
career depended on it), then the goal would be to discover the causes of those problems and
address them so that one can continue on finasteride.
Re: Chronic Insomnia and lack of energy all day?
Quote:
Originally Posted by DrmChld
Does anyone have any suggested for someone who has been experiencing chronic
insomnia for a few years? I really need to get more sleep.
I am not sure if I just have too much in my mind that I can't stay asleep (falling asleep is
easy)
With my lack of sleep it is causing problems with lack of energy and desire during the
day. Is there anything I can take to help boost up my energy during the day?
I currently take the following medications and suppliments:
60mg Citalpram
50mg Atenolol
(both for anxiety)
2 Multivitam(1 morning then in evening)
B-Complex
1,800mg Saw Palmetto (broken down to 3 times a day)
120mg Ginko Biloba
500mg Calcium
300mcg Biotin
For sleeping I will sometimes take a Xanax(1mg) or Temazepan(2x15mg) and this will
keep me out for 4 hours and then I have problems staying a sleep after that.
Besides drinking coffee or taking no-doze all day what can I do for pepping up more?
I work out 3-4 times a week, eat well(could eat more) take protien drinks etc.
Any ideas?
The question is why is there insomnia?
Rather than bandaging the condition with a nighttime stimulant or daytime stimulant, it is useful to
determine the cause in the first place. Addressing the cause in treatment can then improve a
person's condition while minimizing side effects or risks.
For example, insomnia and anxiety may occur with hypothyroidism or adrenal fatigue. In both
conditions, the brain compensates by making more norepineprhine - and/or glutamate.
The higher stimulant neurotransmitter levels wake a person up - counteracting the effects of
sedatives.
Thus if insomnia is due to hypothyroidism or adrenal fatigue, then addressing the condition
successfully can allow a person to more naturally fall asleep without having to use a sedative.
Atenolol is mildly soluble in fat - thus only a little gets in to the brain to block norepinephrine.
However, beta-blockers which are highly fat soluble and enter the brain well (such as
propranolol), more more highly likely to block Thyroid T4 to T3 conversion, resulting in
hypothyroidism.
High dose Saw Palmetto can be a concern because it can result in an increase in other hormones
(such as estrogens) rather than just reducing DHT. A 24-hour comprehensive hormone and
metabolite test would have to be done to determine this.
If estrogens are increased by Saw Palmetto, for example, then in some people, they would be
more anxious or develop insomnia or develop irritability and anger problems - if the estrogens
raise norepinephrine more than serotonin or dopamine in the brain.
B-complex is usetul to help improve energy. They participate in many energy producing
processes. They have to be taken as a group since taking an excess of one can cause a
deficiency in another.
The B-vitamins can have a short half-life (except for B12, which is store in the liver), because they
are water soluble and easily urinated out. Thus, it is helpful in some people to take them twice a
day.
The problem is that some of the B-vitamins can cause problems at too high a dose. For example,
Vitamin B6 can cause a neuropathy at doses over 500 mg a day.
Re: Chronic Insomnia and lack of energy all day?
Quote:
Originally Posted by DrmChld
I have had my T3/T4 checked recently and they were normal. I have not had anything
done regarding adrenal fatigue. Whenevr I mention this to my PCP they always blow me
off. I have another PCP since I have moved and will be going in Friday regarding this.
I have had the problem with lack of sleep and energy since I was a kid. All the doctors I
went to told me it was my weight (Highest was 350). I had gastric by-pass and am now
down to 185 and I am still having the same problems. ..
Hmmm. When I analyzed the lab ranges for thyroid, I found that the "normal" or average TSH is
actually a hypothyroid TSH. Yet it is smack in the middle of the range. Similarly with T3 and T4.
Why? Because up to 40% of people have hypothyroidism, and 15% have a more severe form with Hashimoto's Thyroiditis. This skews the probability curve that is used to determine the range
for thyroid hormone. Interestingly, children have a much higher high end for Free T3 than adults.
Perhaps fewer children are hypothyroid than adults.
For example, the average TSH is 3.5. If one just removes the 15% of people with Hashimoto's
Thyroiditis, then the average TSH becomes close to 1.2! If anything, 1.0 is a more realistic
"normal" TSH - assuming the brain is functioning optimally. As a psychiatrist, I realize that this is
not often the case - the brain is not often functioning well - particularly in mental illness. There are
many people I see who have a TSH near 1.0 yet their Free T3 and Free T4 are low. Their
pituitary glands just can't muster enough to make TSH or their hypothalamus can't measure Free
T3 correctly to determine the correct amount of TSH to produce.
Thus it would be educational for all of us to give us your "normal" T3, T4 levels to see for
ourselves what is happening. For thyroid hormone measurements, if gauging by lab tests only rather than by using the more important history and physical exam, to me, a person is most likely
hypothyroid if their Free T3 < 3.3 or Free T4 < 1.2 or TSH > 2.0.
With morbid obesity, I would strongly wonder if a person was hypothyroid and has adrenal fatigue
(adrenal fatigue drives the appetite for sweets). Having both hypothyroidism and adrenal fatigue
lowers metabolic rate and impairs the burning of fat for energy.
Again, hypothyroidism and/or adrenal fatigue forces the brain to make more norepinephrine. The
higher norepinephrine levels keeps a person awake. When a person has adrenal fatigue, often,
practically no sleep medication works. Melatonin often will not work because melatonin reduces
adrenal production - causing a person to produce even more norepinephrine to kick the adrenals
into working. Hypothyroidism and/or adrenal fatigue are the most common causes of a lack of
energy. Insomnia exacerbates adrenal fatigue.
Re: Dr. Marianco, Urine more accurate then Blood?
Quote:
Originally Posted by TylerR
Hi Dr. Marianco,
Are you saying Urine Test is more accurate then Blood Test?
I'm confused, I have tried both, and from my results of the urine test I don't have any
problems, however my blood work shows something is definatly wrong?
My Blood Test show my T levels are are mid range, and E is high. It also shows I have
high DHT.
However my Urine Test shows that my T level is in the upper third of the range, and my
estrogens are normal, with low DHT numbers. So I'm really confused on which is
accurate.
I have had over 5 blood test with the same results, and I've only had one urine test so far.
I know have a lot of fat around my stomach and suffer from some ed, and absolutely no
libido.
I'm wondering could there have been an error in the urine sampling? Is it possible that
they measured an area of my urine that had more T and balanced hormones?
I'm just confused on which method is accurate.
Please let me know your thoughts.
Also has anyone else had blood test that differed from their urine tests?
How does one go about lowering Estrone levels?
Thank you!!!
Ty
It is not whether or not one is more "accurate" than the other. Both are "accurate" in what they do.
The question is what test will give one the information one seeks.
Interpreting urine tests of hormones and their metabolites is not as simple as looking at the lab
ranges and telling if the level is within that range.
It requires the physician reading the test to know the various steroid pathways in order to interpret
what is happening.
A blood test is a snapshot of one moment in time.
A urine test of hormones and metabolites tells one what is happening over an entire day.
Thus both have different purposes.
A blood test showing Testosterone in the mid-range, while the urine test shows it is in the upper
range may mean several things.
For example, if a person has a hyperexcretion syndrome, then perhaps testosterone is being
excreted too quickly.
Urine testosterone is free testosterone, by the way.
If testosterone in the urine is high, then perhaps it isn't being used - thus the metabolites of
testosterone can be low.
One has to look at all the interactions and the big picture to interpret a urine test. It is, however,
the only test which can give one an idea of what is happening to the hormones - e.g. what
pathways a particular hormone or medication is influencing.
For example, if one takes Finasteride to lower DHT, then some people on a 24-hour urine test will
show that not only is DHT being lowered, but Estrone is being increased. This is because
blocking 5-alpha-reductase with Finasteride forces testosterone down some other paths - some of
which may not be desired.
As another example, if one takes Pregnenolone - some people will end up with no change in their
hormones using 24-hour urine tests, some will end up with more DHEA, and some will end up
with more estrogens. The pathways an individual takes will vary. But which pathway an individual
takes is more clearly seen on a 24-hour urine test.
Unfortunately, this test is quite expensive - about $400 each time it is run. And it is not paid for by
insurance - thus one has to pay out of pocket - ouch.
Watching an expert - such as Jonathan Wright, MD - who has done this for over 20 years and his
staff - read a 24-hour urine test can be breathtaking by the amount of detail he can extract from
the test. Luckily, he and his staff help others are very happy to help other physicians interpret
their lab tests.
Re: Finasteride and muscle wastage?
Quote:
Originally Posted by rob123
I am new to this forum so I don't know if this issue has already been addresed. I use the
finasteride.jconserv.net forum and see jim1234 recommends this site.
I took finasteride 1mg from eary 2001 to early 2005 with a 6 months break in between 3.5 yrs in total.
For first 2 yrs all was OK, but in March 2003 I took what turned out to be a very stressful
office job and had some conflict at same time at home with neighours. From that moment
on I have experienced a tremendous amount of muscle wastage all over body, some loss
of concentration problems and chronic constipation.
However my libido is probably 3/4 what is was before, erections OK - although there is
some loos of sensitivity in penis and a slight curve to the left.
The office job ended in September 2004 (company relocated) and the neighbours moved
out around the same time, and, the stress basically ended there.
But the muscle wastage has continued to this day - I assume my DHT was too low to
combat the stress.
I have been weight training since age 18 (due to a back problem -scoliosis- imcompetent
doctors did not pick up on), I am now 38, but this has made no difference to wastage.
Infact I have felt no 'pump' for over 3 years, and I stopped training 5 months ago wastage continues at same rate.
May 2005 (2months after after stopping fin) my Test level was 14.
Dec 2006 I had results of LH 1.6 and FSH 2.2. but confusion on Test first told 4.8 then
14!
I have just seen andrologist Dr Minhas at UCHL London and am waiting on new test
results for Test and Estradiol.
My hair has been falling out again, but all I care about now is stopping the wastage.
I did try anastrozole for 2 weeks last summer and all I got was an unnecessary boost to
erections.
Any ideas would be much appreciated. Cheers.
When a person has unexpected problems with a treatment, it may be useful to do a
comprehensive 24-hour urine test covering all the steroid hormones and their metabolites, thyroid
hormones, growth hormone, etc. It is an expensive test.
Meridian Valley Lab in Renton, Washington State is probably the best at the job. It is run by
Jonathan Wright, M.D. (who has been doing hormone replacement therapy for about 30 years more experience than anyone I know) who convinced me in a meeting this past weekend of their
usefulness.
With the comprehensive 24-hour urine test, one can tell better how a treatment affects the various
hormone metabolic pathways. Given how variable these pathways are between individuals, this
lab test is useful to clarify how a person is responding to treatment - particularly when unexpected
or unusual things are happening.
For example, Finasteride in a few men can cause an increase in Estrone levels - which may not
be caught in when blood testing alone is done. Thus it is not only DHT that is affected - but the
levels of other steroid hormones also - in some cases, in unexpected ways. For example,
perhaps the increase in Estrone can affect overall anabolism..
__________________
Re: To Marianco > Serotonin deficiency > depression > andropause
Quote:
Originally Posted by chip douglas
Hi Marianco,
In his last book titled : ''Younger you'', Dr. Eric Braverman http://www.pathmed.com/
writes that Serotonin deficiency will often lead to depression and and as a result lead to
other health issues such as :
Accelerated calcification
Lower sex drive, triggering andropause and menopause
Lowering of Testosterone leading to andropause
Lower estrogen, progesterone
Weaken the immune system
Accelerate skin aging
This is one of several possible pathways. But it is too vague - the links are not clearly made. The
problem is that there is no explanation as to why this all occurs - for example, what pathways are
involved.
Looking at things from my point of view - that the mind is a fluid circuit involving multiple chemical
messengers and multiple possible metabolic cascades/pathways:
If one specifically kills off serotonin-producing neurons - for example, by using Ecstasy or
Fenfluramine (part of the FenPhen tablet that is now off the market) - then one can envison one
possible cascade (out of many):
1. A serotonin deficit leads to a reduction in thyroid hormone production (which depends on
serotonin, one of many cofactors).
2. A serotonin deficit also leads to loss of control over norepinephrine production (since serotonin
neurons help reduce norepinephrine production from norepinephrine neurons) - leading to an
increase in norepinephrine production.
3. The reduction in thyroid hormone production leads to a reduction in steroid hormone
production from the testes - particularly a reduction in testosterone production, then estrogen
production.
4. The increase in norepinephrine production leads to an increase in ACTH production, which
leads to an increase in adrenal cortex hormone production.
5. Over time the chronic increase in norepinephrine production leads to adrenal fatigue, and
reduced adrenal cortex hormone production.
6. Adrenal fatigue leads to a reduction in progesterone, DHEA, Cortisol, Pregnenolone,
Aldosterone, testosterone, estrogen production.
7. Adrenal fatigue, lower thyroid hormone levels, lower testosterone levels leads to even higher
norepinephrine production.
8. Lower thyroid and adrenal hormone production leads to an increase in inflammatory versus
anti-inflammatory signals on the immune system, leading to an increase in inflammatory
responses.
9. The increase in inflammatory responses leads to the development of atherosclerosis - and
calcification - of the arteries.
10. The increase in inflammatory responses versus antiinflammatory responses leads to
weakening of the immune system - inflammation, for example, in barrier cells such as the skin,
allows pathogenic bacteria and viruses an easier entry into the body. Inflammation precedes
infections and various diseases.
11. The reduction in thyroid, DHEA, testosterone and the general increase in inflammatory
signals leads to a reduction in IGF-1 production from growth hormone in the liver.
12. The reduced production of estrogens, IGF-1, and thyroid hormone leads to an increase aging
of the skin.
13. Lower thyroid hormone can lead to lower serotonin, lower dopamine, lower GABA production,
and a further increase in norepinephrine production.
14. Low thyroid, testosterone, GABA, dopamine, adrenal hormone production, and higher
norepinephrine production can lead to a reduction in sex drive.
I do not necessarily agree with the notion that lowering sex drive triggers andropause or
menopause, or that lowering testosterone leads to andropause. These are overgeneralizations.
Andropause is an age-related phenomenon - due to age-related decline in the pituitary’s ability to
make LH or due to age-related decline in the testes’ ability to produce testosterone.
Andropause is not necessarily related to a serotonin deficit - since a serotonin deficit can occur at
any age, be present due to genetics (thus one is born serotonin deficient), or be induced due to
drug abuse or medication adverse effects, etc. If Andropause is specifically due to a serotonin
deficit, this would lead to the nonsensical scenario of a male newborn with born with a serotonin
deficit being diagnosed with andropause.
Similarly, menopause is an age-related phenomenon, not necessarily related to a serotonin
deficit. Rather is is related to the end of the ovaries’ ability to produce eggs. Women are born with
a limited number of eggs. If the last egg is ovulated or the egg-shell surrounded the woman’s
eggs become so fibrous over time that the egg cannot get out, then menopause starts.
Also, the pathway delineated above is just one of several possible scenarios. Thus any given
person may take a different path with a different outcome.
For example, if a serotonin deficit occurs, then dopamine production is unleashed since serotonin
production leads to a reduction in dopamine production from dopamine producing cells. Serotonin
and Dopamine are joined at the hip in production.
The increase in dopamine may then lead to an increase in testosterone production, an increase in
sex drive, etc. An increase in testosterone production may then increase thyroid hormone
production (though it can also reduce it in some men). The end-point may then be very different
or is opposite to what was previously described.
Lower serotonin may lead to depressed mood, but then it can also lead to a non-depressed mood
depending on how high dopamine and it’s metabolic cascades go. Lower serotonin may then
alternatively lead to violent behavior in some people (e.g. in XYY chromasome disease, the men
have lower serotonin levels and tend to be more violent).
Given the possible pathways involved, it would then be up to the physician treating the patient to
try to see which pathways the patient may be going through. This allows the physician to then see
where the pathophysiology of illness is, then custom design a treatment to address that particular
patient’s situation. One has to dance with the patient's responses. To a physician, this is like
playing jazz. The ability to improvise is the mark of a good physician.
__________________
Re: To Marianco ; Vitamin C, DA> Norepi > anxiety> adrenal fatigue.
It is very difficult to do experimentation on oneself when the measures are anxiety and sex drive.
Just the realization that one is in an experiment and has expectations of the outcome causes
stress which can increase norepinephrine levels which can then increase anxiety and reduce sex
drive - irrespective of whether or not Vitamin C is there. This is why when subjects are in
experiments, a double-blind placebo controlled study is often best - where the subject doesn't
know what they are taking and the experimenter doesn't know what they are giving. The placebo
effect can be extremely potent as is the knowledge of being in an experiment. Just the increase in
thinking about the subject and self-observation - increases stress and anxiety.
Taking tryptophan - which has sedative properties - may have reduced one's anxiety during such
an experiment - thus undoing the increase in anxiety of the experiment itself. But then, this
introduces another variable into the experiment that complicates interpretation.
As a physician, I see large numbers of patients and can thus see patterns in response that one
may not see in an individual. This gives me a much more powerful vantage point to observe
responses to medications or other interventions to gain an understanding of the processes
involved, than one has if one experiments on oneself.
Norepinephrine is not always raised in adrenal fatigue. The other neurotransmitters - serotonin,
GABA, dopamine - may be reduced instead, thus causing a relative increase in norepinephrine,
not an absolute increase in norepinephrine. This also has to be correlated with brain function.
Glutamate may be increased rather than norepinephrine, etc.
Many times, adrenal fatigue does not exist without other comorbid conditions such as
hypogonadism or hypothyroidism or nutritional deficiencies. This complicates the picture greatly,
making it more difficult to do an adrenal treatment in isolation since the other comorbid conditions
may link together with adrenal fatigue and may have to be addressed simultaneously.
When taking a single nutrient - such as Vitamin C - one may be assuming that one's nutrition of
other nutrients is optimal. This may not be the case. Thus deficiencies in other nutrients may be
exposed when Vitamin C is taken, particularly at large doses.
When Vitamin C is taken alone, it can reduce copper, manganese, and zinc absorption - resulting
in a deficiency of these if one's levels were low to begin with - resulting in unwanted effects. Zinc
deficiency, for example, can cause reduced sex drive or libido.
A copper deficiency may then impair activity of dopamine-beta-hydroxylase - impairing
conversion of dopamine to norepinephrine - undoing Vitamin C's effects on dopamine-betahydroxylase.
Vitamin C as an antioxidant helps adrenal function. It is concentrated in the adrenal glands and
brain is up to 20 times more than the rest of the body.
In the brain, Vitamin C can reduce NMDA glutamate receptor responsiveness to glutamate, which
may then help increase dopamine activity, which may then reduce norepinephrine activity, etc.
Thus the story is complex and may depend on the individual's situation - the interactions among
the neurotransmitters, hormone, cytokines, nutrients, medications, stresses, health status, etc.
Which direction a person may go depends on the balance of the metabolic pathways activated by
an intervention. Some pathways (e.g. Vitamin C's effect on dopamine and norepinephrine or
Testosterone's effect on thyroid hormone) can go both ways (up or down).
One has to make some hypothesis and change treatment if unwanted effects occur. But it can be
made much more difficult by very complex interactions among the neurotransmitters, hormones,
cytokines, and nutrients.
And that's partially the rest of the story.
__________________
Tests for Adrenal Fatigue
Quote:
Originally Posted by coz
Saliva cortisol & DHEA-s tests are not available in the country I live in. I'm exhibiting
alot of the symptom's of adrenal fatigue (low sex drive, intermit ED, depression, fatigue,
poor concentration, anxiety, irritability, salt cravings, needing coffee, joint pain etc) and
want to know a list of blood tests or other tests I could run to help pinpoint this.
I've run cortisol blood tests many times in the past & they are always at the high end of
the range - although I think this is due to the stress of getting the blood tests done.
This is a list of tests I've come up with, any comments/additions appreciated;
- DHEA-s
- homocysteine
- progesterone
- potasium
- sodium
I've also always had low HDL cholesterol at the bottom of the range, could this also have
any effect ?
I've taken my temperature multiple times through the day over the last week. It fluctuates
alot through the day, although the avg for the day is almost the same (see attached)
Among the standard lab tests, what are useful for evaluating adrenal function include:
Cortisol AM (7-10 AM), Cortisol AM (3-6 PM)
Cortisol-Binding Globulin
DHEA-sulfate
Pregnenolone-sulfate
Progesterone
Aldosterone
ACTH
Sodium
Potassium
Chloride
Albumin
BUN (blood urea nitrogen)
Creatinine
Hemoglobin A1c
Fasting glucose
Fasting insulin
Lipid panel
Free T3
Free T4
TSH
Total Testosterone
Estradiol
Sex Hormone Binding Globulin
IGF-1
IGF-BP-3 (primary IGF binding protein)
Urinalysis
24-Hour urine Cortisol
ACTH Stimulation test (more sensitive if the dose of cortrosyn is about 10 times smaller)
The levels of these lab tests are linked in function. When adrenal fatigue is present, abnormalities
may be seen in many (if not most) of them. For example, good adrenal function is necessary to
have active diodinase enzymes that transform T4 to T3. Hypothyroidism, itself, can often result in
adrenal fatigue. When total testosterone is either too high or low, adrenal function may be
compromised. In postmenopausal women, all their testosterone and estradiol is generated via the
adrenal glands. To interpret the glucose level (which is lowered by cortisol deficiency of adrenal
fatigue), one has to know if insulin resistance is present. Insulin resistance increases glucose
levels. Thus if both adrenal fatigue and insulin resistance (e.g. from low thyroid or testosterone
deficiency) is present, then a person may have a "normal" blood glucose of 99 - but this is
actually an inflated blood glucose if insulin resistance was not present - and thus it is low for that
person. IGF-1 and Sex Hormone Binding Globulin production are controlled by multiple hormones
including DHEA, Progesterone, Testosterone from the adrenal glands. When aldosterone
production is decreased due to adrenal fatigue, then sodium, potassium, and chloride may be
reduced; and a person may exhibit signs of dehydration such as high albumin, high BUN, more
concentrated urine, etc. The 24-hour urine cortisol and ACTH stimulation tests may be useful
though not sensitive enough unless a person has very significant adrenal fatigue. Lowering the
dose of cortrosyn for the ACTH test improves its sensitivity - since the dose used is so high,
practically everyone responds (remember that this is a test for Addison's disease - where cortisol
production is in the lower 2.5% of the population that the lab sees).
__________________
Re: Suddenly, I am losing all my hard earned muscles!
Dieting usually causes a loss of both fat and muscle.
Just look at the professional and amateur bodybuilders. They try to retain as much of their muscle
mass as possible, but they do shrink A LOT. One middleweight bodybuilder I looked at, for
example, looked huge during the off-season, but is closer to wiry in appearance once he is
carved for the stage.
If a person is losing too much muscle mass in proportion to fat, then the diet itself may be a
problem. For example, one needs a certain proportion of carbohydrates - not just protein - to
prevent muscle loss.
Will Brink's websites may probably have information on what type of diet would best address
preservation of muscle during weight loss.
As one loses weight, thyroid hormone activity also may be reduced - to oppose the weight loss.
This would make losing fat that much harder. Monitoring thyroid hormone activity would thus be
useful.
__________________
Re: Marciano et AL; Please Direct.
Quote:
Originally Posted by Aidan
Hey all,
Thanks in advance for any advice! Its long but I wil truly appreciate input.
Im 22 and am on trt. testogel 5ged and hcg 250iu e3d and AIFM topical spray for
oestrogen.
I received some blood tests today and need some guidance.
1) First the trt.
Total T = 21 (8 - 33)
Androstenedione: 28 (2.8-10) ***********
Oestadiol 68 (0-130)
Ok so previously i was on 500 iu HCge3d and the gel and following advice on the board I
dropped to 250iu as oestradiol was way too high at 216 (o-130) Test was 31 (8-33)
One would think the drop in test can be expeced as the HCG dropped but what i can not
explain is the huge androstenedione reult which is much higher -nearly double- than
when I was on 500iu HCG. It is really confusing me.
Given the Test levels and the androstenedione I believe the hcg is having the effects and
that the gel is not getting through. I am therefore dropping this and changing to T
injections 100mg/wk. Ethanate is not licensed here but I am stil trying to get it. If not it
will be nebido 200mg/2wks.
Should the HCg be lowered in dose??
Other points why I am not satisfied with the gel is a weak libido. NEVER do I get a
morning errection and it takes a lot of stimulation to achieve one. Also DHt which was
not tested tough asked is prob high as I am thinning a smallbit on crown. Got prescribed
Nizoral for that may have to look into rogain -more money- not keen on alpha reductase
inhibitor at my age.
2) IGF-1 = 198
This is low as range is up to 400 and some labs show even up to 700 dep on age.
Previously I was on Trans D-tropin and this was successful and got it up to 380. This was
too dear though and tried an injectable gaba but obviously no good.
ant get HGH etc no insurance here as in America need a consultant.
Am now thinking of trying a product called symbiotropin (effervescent tablets)
I notice the difference from the lower levels, loss energy strength and poor sleep now.
3) Thyroid
TSH previously was between 4-7 taken many times. Was planning on going on Armour
but now TSH has dropped to 3.5 and Free T4 is 16.5 (11-21) so that is out.
I know over 3 still seems high but the doctor does not think i need to go on it.
I need to point the reason for this is the addition of I have a very fast metabolism and am
never cold compared to most so symptoms dont seem present though outer eyebrows do
thin.
No T3 given by labs though asked for.
(Dont get me started they left out cardiac kidney liver and electrolyte tests the idiots)
At the moment I am a small bit frustrated and confused on what to do so if anyone could
advise...
I think a consult with an anti-aging physician - i.e. a physician that specializes in optimizing
hormone functions - would be helpful when one has a complex condition. In Europe, the best
include Thierry Hertoghe in Belgium as well as his sister. Both come from four famous
generations of endocrinologists, but are much better versed.
Re: Lab results are back
A fasting insulin > 10 is suspect for insulin resistance or diabetes
A low SHBG is primarily caused by high insulin levels or insulin resistance. It may also be
contributed to by high testosterone, high DHEA, high growth hormone, low thyroid, low estrogen,
low progesterone.
A consequence of insulin resistance or diabetes is reduced production of testosterone.
In many people, low thyroid hormone can lead to insulin resistance or diabetes.
__________________
Re: Lab results are back
Quote:
Originally Posted by Dutch Buster
butt i am taking armour is this the way off up my shbg ?
and am i right that my shbg is low so that i have low energy ?
or do you see other things in the results ?
oww insuline before was 23 it is lowered,,
It would be useful to review my posts on adrenal fatigue and hypothyroidism to help understand
those conditions.
A problem with SHBG is an indirect indication that problems exist with the hormones. SHBG, by
itself, does little - as far as I know - to determine energy level.
Re: DHT is evil!!!
The answer is the usual psychiatric answer: "It depends..."
Excesses or deficiencies in anything can lead to problems.
A man with low testosterone levels is in generally going to die earlier than a man with high
reference range testosterone levels.
DHT may contribute to male pattern baldness - a problem with genetic and immune system
contributions.
However, having no DHT can be worse. DHT in the brain may be the active form of testosterone.
Thus zero DHT may impair testosterone's brain effects, impairing thinking, one's ability to relax, to
live a stress-fress, and enjoyable life.
Having no DHT may also cause a male to have a small penis as the mature, and no male
secondary characteristics - such as pubic hair or a beard.
What makes one look like a man (outside of muscle mass) is mostly DHT made from
testosterone.
If anything, a good word is "moderation". One wants moderation in whatever they may have.
Others want "optimal" - which may be better but can be difficult to achieve, though for some
people is a worthwhile goal.
When someone overreacts emotionally, perhaps there is a significant hormonal problem such as
adrenal fatigue, testosterone deficiency, thyroid hormone deficiency, etc.
Re: DHT is evil!!!
Quote:
Originally Posted by JanSz
I have enlarged prostate, no PC, checked via 6 biopsies.
My DHT=226(30-85)
when on daily Avodart DHT=29
Avodart have very long half-life.
How to adjust Avodart's dose so I would get aproximately DHT=75
Any other ways of controling DHT.
Today I switched from 7.5grams of Androgel to 0.75grams of Tcream 100mg/gram
in an atempt to reduce application area which supposedly induces DHT production.
When the half-life of a medication is long, then reducing its effective dose entails either 1)
reducing the daily dose or 2) taking the dose less frequently, e.g. once every other day.
Re: Optimizing HRT Routine (Gel + HCG)?
Quote:
Originally Posted by Megazoid
Well guy's i discovered i had a half a box of androgel left the other day in the cupboard
and decided to start using this stuff up so it doesn't goto waste. After going out drinking
last Saturday night the effects of low testosterone hit me really hard on the sunday while i
wasn't on any TRT (just natural). My joints ached, knee's hurt like crazy and my dick was
announced dead. My mood was pretty low too. I was fatigued and out of energy.
I am still waiting on the blood testing lab getting back to me to arrange dates but based
on previous tests i feel that Total T is low to low normal, DHT is low and E2 is low.
SHBG was 20 at last checkup. So i am guessing everything is pretty much the same.
I started on 50mg of androgel daily on Monday morning alongside ZMA and my usual
daily supplements. I felt a good improvement in mood and elevation of back pain by
Monday night (this had been bothering me for a few weeks). Joints were clicking less and
i felt pretty good all round. The last time i went on androgel i didn't shutdown even after
a month of usage. My LH went from 3.9 to 2.7 and FSH remained the same. My Total T
went up to 25.6nmol. Overall health was pretty decent but libido and erections were
unpredictable to say the least. E2 was bottom of the range.
By wednesday i had no elevation from the libido/erection problems so i decided to open
one of the boxes of Testim i had an apply this at the same time on the thursday morning
to see what the difference was like. Again i applied 50mg at 6.30am before work and felt
a world of difference by mid-day. Most of my symtoms were lifted and i even noticed my
skin was more greesy than normal which was a good sign as i have low E2 and dry skin.
Penis was hanging allot better and i got a spontanious erection for the first time in a
while and a few semi's but nothing to write home about. I felt a fair bit healthier, more so
than the androgel.
Still no great improvements in libido or erections and don't want to need viagra or
anything being so young. i can still achieve them with stimulation and they are a little
easier to get than before. Overall i am pretty happy so far. No noticable problems except
a little acne at application site.
I am going to see a urologist on Tuesday to check my testicles since the operation and see
how thing's are going with regards to the varicoceles. I might need another surgical
operation to repair blood flow but nothing is set in stone.
When i did 100mg of Testim the last time i got very emotional at the same time everyday
(about 3pm) for no known reason, i couldn't explain this, other than being maybe high
E2? I don't have any real body fat and i am young so i can't see how this is even possible.
Maybe i got into the super high range or something then E2/DHT went high.
I seem to respond better to Testim than androgel (which i think is common though?).
Until my testicles go back to normal size i can't see me recovering naturally and TRT is
lifting many of the symptoms i have so i am going to stay on it until my body is ready.
Naturally i don't want complete shutdown but i am thinking about experimenting a little
and trying one of the following for a few months:
Testim (50mg) daily + 250iu HCG 3 times a week
Testim (50mg) daily + 500 HCG 3 times a week
Testim (100mg) daily + 250iu HCG 3 times a week
I basically want to get the benefits of TRT but also help my nut's heal and grow back in
size, function and boast my T levels. I am hoping it improves libido and erection quality
too.
I think before all of this (the low t, etc) i had pretty high E2 (if that makes sense?)
because my skin was always thick and young looking. Good penis sensation too. This isn't
really reduced "that" much but not as good as before.
Any advice is good, i am going to start a journal on this forum when i get blood work
done.
When total testosterone is 650 ng/dl to 1000 ng/dl yet problems still occur - e.g. depressed mood,
libido problems, lack of energy, problems with erectin quality and consistency, the the problem
lies with the other hormones, neurotransmitters, or cytokines.
A low Estradiol can be improved with HCG since HCG stimulates aromatase production.
A low SHBG may indicate problems with insulin resistance or diabetes. It may also indicate
problems with low thyroid, low estradiol, high DHEA, low progesterone, and high testosterone.
Alcohol is toxic to almost every cell in the body. A single drink will waste that day's production or
dose of growth hormone since it will block the liver's production of IGF-1.
With testosterone replacement - no matter what the technique - a basic goal is to reach a total
testosterone of 650 ng/dl. If problems are still present, the problem lies with the other hormones.
In this way, testosterone replacement is actually a fairly simple procedure with many options e.g. HCG if one wants to maintain their testicular function, etc.
Yes, some men may benefit greatly from just using testosterone. However so many have a multihormone problem. For them, testosterone is just one component of their treatment. Frustration
can occur if they don't realize this and focus excessively on testosterone treatment itself. Even
DHT and Estradiol problems are not as frequent as problems with the other hormones in causing
problems to persist.
When one is frustrated or irritable or anxious - the adrenals are suspect.
When one is tired or has persistent energy problems - the adrenals and/or thyroid are suspect.
__________________
Re: Is low dose HGH and no Test a waste?
Quote:
Originally Posted by JohnTree
Posted on Steroid board with no response: Please give feedback.
I was a passenger in a serious auto accident 7 months ago with a variety of injuries
which may or may not heal without surgery. I read about baseball players using HGH
and testosterone to recover from injuries that might otherwise be career ending. It
seemed to make sense in my situation so I visited my local longevity doc who got me all
excited with words of HGH and T and the healing and re-building benefits thereof.
He gave me the Quest Diagnostics routine tests with these results:
Testosterone 423
T-4 8.2
TSH 1.76
IGF-1 132
My age: 46
Working out for 28 years, ex athlete, 6’5” 205 12.5% body fat.
Doctor prescribed HGH .75 units per day administered at bedtime via short insulin
needle.. Price is $150 per week paid to doctor for HGH. Doctor indicated that I do not
need Testosterone based on my 423 score.
My goals are: heal, build and regain muscle mass without using heavy weights that might
re-injure myself or interfere with my recovery. I’m up for lifting at 70% max. so I can go
pretty high intensity with medium/high reps at this point. Over the next 9-12 months I’d
like to add 10 pounds of real muscle that I permanently keep.
My concerns are:
1.) I am wasting my time and money paying a lot for too little dose HGH and not getting
the real muscle builder and tendon healer, testosterone.
2.) Without added testosterone I will not be able to build up without using very heavy
weights and extreme intensity workouts which will risk injury in my current condition.
3.) HGH ..75 at bedtime will be wasted because it might curtail my own natural
production at that time?
I went to a doctor in order do to this correctly (got the tests etc.) but I’m getting the sense
that I need a much better doctor advice because it seems like I am getting ripped off and
I’m not on a program that is nearly aggressive enough for my goals. Your comments are
appreciated. Thank you.
1. Why the impatience? Why not heal first then build muscle later? After all, a serious accident
with serious injury, happened a short time ago? Further, additional surgery may also be needed.
2. Building muscle mass is not a legitimate reason to prescribe testosterone. Rather, it would risk
the physician's medical license.
3. Similarly, faster healing is not a legitimate or lawful reason to prescribe growth hormone.
Growth hormone can only be legally (by U.S. Congressional law) prescribed for growth hormone
deficiency syndrome. There is no other legal indication for its use. There is no legal off-label use unlike any other medication.
4. With an IGF-1 of 132, a case can be made that one has adult growth hormone deficiency
syndrome, and thus can be prescribed growth hormone.
5. In the anti-aging conferences I've been to, I hardly see any bodybuilding types among the
practitioners participating. They are rare. A highly muscular morphology - from an anti-aging
perspective - could be viewed as an excess of testosterone, and is thus not healthy.
6. In prescribing growth hormone, the dose is started low then gradually increased if needed.
Thus 0.75 units may be just the starting dose. Given the possible side effects of growth hormone,
monitoring may be necessary (e.g. for the development of adrenal fatigue, thyroid hormone
deficiency), before escalating the dose.
7. Growth Hormone doesn't have feedback inhibition of production. Growth hormone only lasts in
the blood stream a few minutes (about 6 minutes) before it is destroyed. One of its effects is to
trigger IGF-1 production (which then lasts around 15-16 hours. Evening or nighttime use - it does
not matter much. However, if one wants to heal faster, the evening dose may be best since this
would augment the higher levels of growth hormone at night.
8. The higher the dose, the more enormously expensive growth hormone will be. One can get
much more bang for the buck as well as improved IGF-1 levels by optimizing the other hormones
- which would reduce the needed dose of growth hormone.
9. The effects of growth hormone are subtle - generally a vague but better sense of well-being. It
is not an in-your-face improvement in quality of life as with thyroid, adrenal and reproductive
hormones.
10. For general healing, perhaps more bang for the buck can occur from optimizing thyroid and
adrenal function.
11. A severe trauma can quickly deplete the adrenal glands ability to combate stress - causing
adrenal fatigue or even adrenal insufficiency - resulting in more inflammatory signals in the body resulting in impairment to the immune system, impaired healing.
12. Nutrition has a particularly large role in healing. Anti-oxidants become important in reducing
excessive inflammatory responses. A paleolithic diet may help one produce hormones and
preserve muscle mass.
__________________
Growth Hormone
Growth hormone is in a legally unique situation in the U.S.
Through a quirk in the legal process in the attempt to prevent cheating in athletics through the
use of anabolic substances, Growth hormone has a specific law of its own. It's law bans its use
for anything other than growth hormone deficiency.
Anti-aging doctors have been trying to fight this law to get it repealed. But as long as it is in place,
a physician cannot write growth hormone for anything other than growth hormone deficiency or
risk losing their license.
One can prescribe morphine or testosterone for most off-label use, however weird - e.g. for
gastritis. But one cannot prescribe growth hormone for off-label uses.
Controlled substance prescriptions are currently logged on a central government computer by
every pharmacy and monitored by the DEA in many states. Thus, the prescription of controlled
substances is done with caution in mind.
There is nothing like the DEA coming into your office and seizing your records and computers.
__________________
Re: Building up Serotonin to replenish Dopamine ?
Quote:
Originally Posted by chip douglas
In his book : The edge effect, Dr. Eric Braverman says that by building up Serotonin not
only will one get better sleep, but also Serotonin will help in replenishing Dopamine and
Acetylcholine.
Marianco, if you catch this post, would you be so kind as to let me know whether I'm
correct with the following assumption ?
Since Dr. Braverman doesn't provide any in-depth explanation of how Serotonin can help
in replenishing Dopamine and Acetylcholine (aside from the better sleeping patterns
part), I'll attempt from what I've learned from the many postings of Marianco to clear it
up.
First off, Marianco has recently posted and wrote many times in the past about SSRI's
being helpful in adrenal fatigue by decreasing percieved stress. Serotonin can decrease
the release of Norepinephrine from Norepinephrine neurons, in turn lowering the stress
response (CRH>Norepi.>ACTH> Cortisol). Key in achieving success here appears to be
in the dose--just the right dose, and the adrenals get proper rest, Norepinephrine output
is decreased, and Dopamine gets a chance to replenish. However too high a Serotonin
level, and it decreases Dopamine output from Dopamine releasing ( and IIRC production
of DA toned down as well) neurons.
In the above paragraph, I purposefully let Ach out of the picture, to concentrate on the
replenishment of DA alone.
Since I need to know how Serotonin can replenish Dopamine, I've attemtped to provide
an explanation for it, through my readings of Marianco's postings.
Marianco has made clear that dosage is key. This is often something that is not
mentioned on various web based information. We often read that Serotonin will kill one's
sex drive, but what I think is implied here, is that *excess* serotonin will kill it. Not much
is said about low or inadequate serotonin levels though, and the increased perception of
stress it brings about.
To reiterate, what I'd like to know is how Serotonin (presumably in individuals
vulnerable to stress) can replenish Dopamine. I think I'm pretty much correct with the
above explanation, but I'd like for others to either confirm it, or bring out flaws in my
attempted clearing up of it.
Thanks in advance.
The relationship between serotonin and dopamine is complex since other neurotransmitters,
hormones and cytokines are involved. Also, it depends on the circuitry in the brain involved. I will
discuss only some of the relationships.
In general - as a predictable effect - Increasing serotonin levels will reduce dopamine production
from dopamine-releasing neurons. This relationship is dose related. This may reduce attention
(which is helpful in OCD - which can be viewed as a condition of excessive attention on certain
subjects). The reduction in dopamine may also reduce libido, reduce motivation, impair memory.
As dopamine levels are further reduced, one can get more significant effects such as muscle
cramps, tremors, and akathisia (restlessness, agitation, fidgetiness, insomnia, anxiety, wanting to
jump out of one's skin, impulsive behaviors, etc.) . The lowered dopamine levels when excessive,
may significantly increase norepinephrine production from norepinephrine-releasing neurons.
This may then lead to adrenal fatigue.
Interestingly, as far as I know, there are some dopamine-releasing neurons, however, where
serotonin receptors are very close to dopamine-reuptake mechanisms. Serotonin may fit in the
dopamine-reuptake mechanism, block it partially, resulting in an increase in dopamine levels
locally. What this means is not yet clear - though is speculated to possibly help reduce
depression.
Increasing serotonin levels (as long as it is not excessive), can reduce norepinephrine production
from norepinephrine-releasing neurons. This helps reduce stress signals from the brain, allowing
the adrenal glands some respite, which allows them to recover from fatigue.
Reduction in adrenal fatigue, then allows improved cortisol, progesterone, pregnenolone, and
DHEA production. These have the effect of reducing norepinephrine production, which allows the
return of dopamine production, and improves memory and attention.
Where Acetylcholine fits in this circuit is not clear right now. Acetylecholine reduction can lead to
an increase in dopamine production from dopamine-releasing neurons. Excessive acetylcholine
can actually impair memory.
Since memory is sometimes only associated with acetylcholine - given how people with
Alzheimer's disease have a loss of acetylcholine-releasing neurons - perhaps the improvement in
memory associated with increasing serotonin levels (as long as it is not excessive), is associated
with an increase in acetylcholine.
However, the actual processes involving memory is much more complex - as shown by the above
involvement of adrenal hormones. Memory involves neurons which use complex interplay of
multiple chemical messengers including acetylcholine, serotonin, dopamine, estrogens,
testosterone, progesterone, pregnenolone, thyroid hormone, DHEA, nitric oxide, etc. as well as
various nutrients as cofactors.
__________________
DHT and Testosterone
Quote:
Originally Posted by drp90210
May I bother you with a question? The testosterone cream I am using gets my total and
free testosterone to middle levels (600-700 total test and 10-20 free test), but my DHT is
through the roof at 240 (normal is 17-66). Reducing the skin area of application has not
improved the DHT problem. I do not want lose any more hair, which is a big issue for
me. Do you know how I could get my DHT down? Would injectible testosterone
significanty reduce DHT versus creams? And would there be a problem with using
SMALL amounts of Propecia (like a 1/4 tablet a day) to simply get my DHT to the top of
the normal range? Any thoughts would be greatly appreciated. If you prefer, you can
email me directly or simply post to the group. Many thanks and best regards.
High DHT can occur with transdermal testosterone.
It is a concern in regard to hair loss, possible abdominal fat increases, and other negative effects
of DHT when it is at too high a level.
Possible ways to maintain control over DHT include:
1. High potency testosterone gels or creams allowing reduced skin area of application.
2. Alpha-reductase inhibitors like Finasteride or Saw Palmetto - to reduce DHT production. The
dose and potency have to be considered since alpha-reductase activity is important for brain
function. Saw Palmetto would probably be the safest of the alternatives. It is not as potent as
finasteride, and hasn't been shown to grow hair like finasteride. But it can reduce DHT levels.
Low dose Finasteride is a viable option - so long as one monitors for side effects.
3. Scalp application of an alpha-reductase inhibitor to avoid systemic alpha-reductase inhibition
(which can cause cognitive problems, sexual problems, etc.), while reducing hair loss at the scalp
itself. These included compounded lotions and shampoos containing products such as azelaic
acid or saw palmetto. ucprx.com (University Compounding Pharmacy) and minoxidil.com are
examples of compounding pharmacies that carry products like this.
4. If a man was progesterone deficient, rubbing a compounded progesterone cream into the scalp
is an option - progesterone being an alpha-reductase inhibitor.
5. Injection of a testosterone ester - e.g. depo-testosterone, testosterone enanthate, testosterone
cypionate, when done twice a week, help reduce DHT production. When injections are done once
every two weeks, DHT production can also be high, due to the higher peak levels of testosterone
obtained.
6. etc.
Re: DHT and Testosterone and Testocreme vs. injections.
Quote:
Originally Posted by drp90210
Many thanks. Would once-a-week injections of testosterone cause an unwanted DHT
spike? The thought of doing IM shots twice a week is not appealing.
Injections twice a week aren't so bad considering that the dose is half the size.
A smaller gauge needle can be used.
At around 25 gauge and smaller - plus the smaller dose - pain is much less or non-existant.
The ventrogluteal site is the least painful site - it has fewer nerves and blood vessels than the
dorsogluteal or lateral thigh (vastus lateralis muscle)
Realize that if one was on growth hormone, then one would be doing daily injections. If one was
on insulin for diabetes, one would be doing even more frequent injections - plus the needles
involved for monitoring blood sugar.
If one wants zero pain, then transdermal testosterone is the best.
Testocream is one version of a compounded PLO, oil-based testosterone cream which may
minimize DHT production compared to other creams and gels since it seems to have lower
storage in skin fat. Rather, the pharmacokinetics indicate most of the testosterone goes directly
into the intracellular space then into the blood stream. It also has an aromatase as a component.
One can Google to find it.
Re: Marianco: Igf1 and GHRH+arginine test results
Quote:
Originally Posted by Finn
I would appreciate very much any comments on the following test results:
igf1 9 (14-36)
GHRH+arginine test: max about 90 at 60min, -15min and -0min 0.1.
Because of of the high max value at 60min my endo says again that there should be no
problem with my GH production. My liver function has been tested ok and I am not
malnourished. Is there some other explanation I should consider ?
Some other tests:
ACTH Stim test
0min Cortisol AM 287 nmol/l DHEA-S 15.6 nmol/l (9-38) S-17HPROG 2.6 nmol/l (1.2-5)
30min Cortisol 447 nmol/l DHEA-S 25.8 nmol/l S-17HPROG 5.0
60min Cortisol 516 nmol/l (>550) DHEA-S 25.0 nmol/l S-17HPROG 4.3
Cortisol AM 108 nmol/l (150-550)
Plasma ACTH 18 (<46)
Sodium P-Na 135 nmol/l (137-145)
Potassium P-K 3.7 nmol/l (3.3-4.9)
Free serum Calcium Ion 1.17 (1.16-1.3)
Serum free testosterone 147 pmol/l (150-500)
Serum testosterone 23 nmol/l (10-38)
Prolactin 699 mU/l (50-300)
B12 vitamin: many tests results between 168 and 200 (180-660).
TSH 3.3 and 3.5 mU/l (0.4-4.5)
FT4 20 pmol/l (12-20)
Units are the ones used here in Europe. I don't feel like I have the energy to convert them.
I hope you don't mind. Fatigue is the major concern for me. Low libido comes and goes. I
have headaches all the time and so does my back. Aches get worse if I don't get enough
rest and I need a lot of it. It is not much I can do during one day without losing the nights
sleep and getting more pain. This fatigue and pain tend to depress me. I have had tried
more than ten antidepressants without relief. I get side effects quickly even on low doses.
I am a male in my 30s. I have not had any hormone therapy so far.
Thank you in advance for any thoughts.
IGF-1 is not growth hormone.
IGF-1 is too often thought to have a one-to-one relationship with growth hormone.
It does not.
Growth hormone triggers the production of IGF-1 in the liver.
Since Growth hormone lasts only minutes, it is IGF-1 that has the most of the major effects that
are associated with Growth hormone.
However, Growth hormone is only one of several factors that determines the production of IGF-1.
IGF-1 is determined not only by growth hormone, but also by testosterone, DHEA, thyroid
hormone, estrogen, adrenal function, nutritional status, body fat, insulin, etc. etc. Optimizing these
other factors can optimize the production of IGF-1.
This is why the addition of growth hormone to treatment is the last addition when optimizing
hormone status. It may not be needed in the end if IGF-1 is optimized through improving the other
hormones and one's nutrition first.
Suboptimal thyroid and adrenal function are common causes of fatigue.
The ACTH stimulation test is not sensitive enough to determine the presence of adrenal
fatigue/depletion. It is a test for Addison's Disease - a more severe form of adrenal dysfunction
where destruction of the adrenal glands is present. If the amount of Cortrosyn/ACTH used was
about 100 times less potent, then it may become sensitive enough to determine the presence of
adrenal fatigue.
A better test is a saliva test at least four times in a day for Cortisol, twice in a day for DHEA.
When B12 is below around 400 pg/ml (which is within the usual reference/"normal" range and
thus is not often realized), nerve demyelination starts to occur (i.e. nerves lose their insulation).
This can result in a variety of neurologic problems (memory problems, concentration problems,
depression, anxiety) as nerves essentially short circuit or slow down in signal transmission.
Fatigue can also occur as a consequence.
Elevated Prolactin may indicate a relative reduction dopamine levels. Reduction in dopamine
levels can result in lack of motivation, impaired memory, impaired concentration, lack of sex drive,
etc.
Antidepressants usually (except for Wellbutrin - which increases norepinephrine alone), work by
increasing serotonin levels plus or minus norepinephrine. Increasing serotonin too much results in
a significant reduction in dopamine. If a person is already low in dopamine, this leads to side
effects such as agitation, restlessness, anxiety, movement problems, muscle cramps, insomnia.
Increasing norepinephrine in a person with adrenal fatigue tends to worsen adrenal fatigue since
norepinephrine is the signal for stress - which leads to an elevation in ACTH production, which
then increases the workload of the adrenal glands. This would lead to side effects and intolerance
of the antidepressant.
Low sodium is often one sign of adrenal fatigue - resulting from the lack of cortisol or aldosterone
production. Other lab signs include lower potassium, lower progesterone, lower cortisol, lower
DHEA-s, etc.
A blood test with only one endpoint in the range, such as the ACTH range of < 46, is not really
sensitive enough to determine function.
__________________
Re: Marianco: Igf1 and GHRH+arginine test results
Quote:
Originally Posted by Finn
OK! Thank You for excellent information! Anyway, my IGF-1 seems to be very low. I
don't think I have seen anyone here have that low figures so far. Today I received a letter
from my endo, where she says that sometimes healthy people have below range IGF-1.
She does not think I need any more tests to explain low IGF-1. What do you think,
Marianco ?
I don't think my insurance does cover for a saliva test. Adrenal Fatigue is not recognized
here. Docs don't take it seriously. They like to see results from blood tests and don't trust
saliva tests.
We are working on this with my GP at the moment. I have been taking 1mg
Cyanocobalamin daily for 6 weeks. Three days ago I had my B12 tested. I hope it is
improving.
Another test came back normal. So, I should not be to worried about Prolactin ?
I hope I was living a little closer to you to be able to come to see you. This is far too
complicated for me.
I don't think it makes the test any less sensitive. Looks kind of odd though, like no figure
is low low enough to indicate central deficiency. I have been told that there was a change
in the method and the results are somewhat lower than before and that's why they have
now only one endpoint in the range. Do you think I could have central deficiency of some
of the hormones when my ACTH is 18 ?
Thank You very much again !
IGF-1 is like Free Testosterone. When either one is low, then there is a problem with the group of
hormones that determine their value. For IGF-1, this includes problems with testosterone, thyroid,
adrenal hormones, estrogens, growth hormone, insulin, etc. Tests are then needed to assess
these areas.
Blood tests for adrenal fatigue include:
1. Cortisol AM - done fasting. A Cortisol PM level can also be useful.
2. DHEA-s (not DHEA itself)
3. Progesterone
4. Pregnenolone sulfate (not Pregnenolone itself)
5. Fasting glucose
6. Hemoglobin A1c
7. Albumin
8. Sodium
9. Potassium
10. Total testosterone (in women)
11. etc.
Re: LAB Interpreation help needed
Total Estrogens is not a useful test of total estrogen activity since it includes much weaker
estrogens such as Estriol.
Estradiol is the preferred thest of total estrogen activity. It is not exactly a measure of estradiol
alone. Rather it measures the activity of estradiol plus the activities of the other estrogens
Re: Chroncally low DHEA - Ideas?
Quote:
Originally Posted by griffinannie
I have had chronically low DHEA-s even in the face of supplemenation. My lastest Lab
came back 150 range 90- 540. I supoplement 100 mg ( 50 am /50 pm) Ive change brands
a couple of times as my doc has increased doseages. Any ideas? I'm st\umped..
Occasionally, there are patients who have hyperexcretion syndromes of various hormones.
It would be useful to do 24-hour testing of hormones including DHEA and its metabolites to see if
this is the problem. Of course, one will have to know how to analyze the results - which can be
mind-numbingly complex. Even the best practitioner I know, who does 24-hour urine tests as a
standard in his practice - Jonathan Wright, M.D. (the inventor of Tri-Est) - doesn't remember all
the pathways and metabolites, having to refer to a chart each time he looks at them.
Having a high quality brand of DHEA will insure knowing what one is taking if one is having
problems with DHEA levels. Non-high quality brands may have only a fraction of what is
advertised
Re: Chroncally low DHEA - Ideas?
Quote:
Originally Posted by JanSz
Welcome back;
How to figure out brand quality?
I am using (massive?) 350mg DHEA and 100mg 7ketoDHEA daily in divided dose.
My last test show DHEAs=369ng/dL
Up from 119 in April2005
I am thinking of further rising my dose, trying to get up to 500 in my blood.
I am using Life Extension Foundation 300mg DHEA + (Complete DHEA.)
Thought it is quality product, comments.
I don't subscribe to any particular brand - particularly since many patients are cost-conscious.
Mental illness tends to drive people downward socioeconomically as well.
Some trial and error may need to be done to see which DHEA brand works best or more cost
effectively. Unfortunately, the amount of DHEA between brands may vary a lot from the
advertised amount. But costly brands can break the bank, whereas increasing the dose of a less
expensive brand may accomplish the same.
DHEA is made by the adrenal glands.
There really isn't much of a negative feedback loop when it comes to DHEA production
regulation. The brain primarily measures cortisol, blood sugar, stress level, to help determine the
production of cortisol - the production of which then triggers the parallel production of other
adrenal hormones.
During treatment of adrenal fatigue, adding DHEA is useful since treatment with cortisol or other
glutocorticoids will slow down adrenal function - resulting in a deficit of the other adrenal
hormones - which then can cause side effects - since their production is already lower when
adrenal fatigue is present. Thus adding DHEA is usetul to make up the difference in production,
until the adrenal glands are healthy enouth to make enough.
Low DHEA is one sign of adrenal fatigue. Addressing adrenal fatigue may improve production of
all the adrenal glands products - such as DHEA.
__________________
Re: To Marianco/long-chain omega 3 fatty acids
Quote:
Originally Posted by chip douglas
Is it known whether fish oils generally affect more serotonin over dopamine ? I know they
can increase both, and which one will be most enhanced may vary from one individual to
another, as with other supps. or drugs, but generally speaking, is what I'd like to know.
When i take fish oil, my well-being is enhanced significantly, I feel mellower, less in a
hurry, my sex drive picks up, I have better concentration, and smile more. No doubt fish
oil's good stuff.
Thanks
I haven't seen data one way or the other.
Fish Oil has numerous mechanisms of action. Directly increasing sertonin or dopamine is not one
of them. An increase in dopamine or serotonin may be final effect in the chain of responses to the
presence Fish Oil. However, I haven't seen measurements.
Fish Oil can help stabilize mood and reduce depression. Which of its numerous mechaisms of
action does this is nto known to me yet.
The dose is important since Omega-3-fatty acids are in a balance with Omega-6-fatty acids when
it comes to function. For example, Omega-3-fatty acids results in a reduction in inflammation,
while Omega-6-fatty acid results in an increase in inflammation. Both functions need to be in a
balance for wellness. Inflammation can be good or bad.
When treating bipolar disorder, for example, with fish oil, at a certain dose, it helps stabilize mood
and reduce depression. At higher doses, it may destabilize mood and worsen a person's
condition. Again, the watchword is balance.
Re: Neuro-Transmitter Tramadol Substitute?
Quote:
Originally Posted by JAF86
I took Tramadol for a couple of years to combat fatigue and lack of motivation. It worked
great and allowed me to workout without feeling a sense of total exhaustion afterwards.
The problem was that over the course of the two years I progressively built up a
tolerance and had to take larger doses to get the same effect. I'm not sure whether this
was due to the opiod-like mechanism of Tramadol or the neuro-transmitter profile. (I
believe it boosts both NE and Serotonin levels). I'd like to find a substance that has the
same neuro-transmitter profile without the opioid activity in the hopes that I won't
develop the tolerance second time around. Any ideas?
Tramadol has several effects and several ramifications of its effects.
Tramadol is a serotonin-reuptake inhibitor - increasing serotonin levels
Tramadol is a norepinephrine-reuptake inhibitor - increasing norepinephrine levels
Tramadol is a partial opiate-receptor agonist - acting partially like opiates (e.g. morphine,
Vicodin). It can possibly be addicting to heroin abusers.
Tramadol has possibly an antiinflammatory agent by reducing inflammatory cytokine production
(a common antidepressant mechanism of action - which is not commonly known).
--Increasing Serotonin helps block the perception of stress. It has a calming effect on mood.
Increasing Norepinephrine drives the adrenal glands harder so that one does not feel so
exhausted after the stress of working out. It has an uplifting effect on mood - so long as the
adrenal glands are not fatigued.
Activity at the opioid receptor reduces pain - though generally it doesn't have a euphoric
component like other opiate agonists. But reduction of pain may have helped give one a better
sensation of well-being by masking the damage done during a work-out. Opiate agonists can in
some people reduce adrenal function - which can worsen one's sense of well-being
The combination of Serotonin and Norepinephrine increases can increase one's tolerance of pain
- reducing the perception of pain.
Increasing Serotonin and Norepinephrine (with Norepinephrine doing its primary work through
driving adrenal function) may also reduce inflammatory cytokines which are released by the brain
in response to stress (such as of a workout or other stress). The inflammatory cytokines would
have slowed down recovery from a workout or illness - impairing one's immune system and
healing. Thus Tramadol may have an antiinflammatory effect.
Tramadol's effects can wear out over time because it is dependent on good adrenal function.
The increase in norepinephrine resulting from Tramadol works the adrenal glands harder.
Norepinephrine is the primary signal for stress in the brain.
Over time, the higher chronic levels of norepinephrine can cause adrenal fatigue.
Workouts are a stress to the neuroendocrine and immune systems of the body - of which the
adrenal glands are one of the most important organs.
The adrenal glands need to recover from a workout just as the muscles have to recover from a
workout.
Muscles may recover in 1 week. But the adrenal glands may take much longer to fully recover depending on the workload and stress they had to handle.
Progressively more intense workouts stress the adrenal glands out.
If one is masking oneself from the stress of a workout by taking Tramadol, then one may not
realize that one has not fully recovered their adrenal glands from the workout because of the
sense of well-being that Tramadol gives one.
As the adrenal glands fatigue, Tramadol becomes less effective a medication. The weakened
adrenal glands do not respond as well to the higher norepinephrine levels that the stress of
workouts and Tramadol create.
One then develops the return of fatigue and lack of motivation - as well as other problems
associated with adrenal fatigue if the depletion of adrenal function is severe enough.
There is no single substance that can substitute for Tramadol. It is a unique medication.
It is most like Effexor - if one removes the opiate-agonist property of Tramadol.
However, the limiting factor in both medications is the increase in norepinephrine level as one
mechanism of action.
Increasing norepinephrine - a stimulant effect - is a double-edged sword. It may keep one alert,
more focused, drive the adrenals to at least temporarily drive adrenal function to a higher level which then can improve mood and reduce stress levels.
Initially the adrenal glands may respond by increasing in size and productive capacity generating the good sense of well-being (if they become excessively large, one can become
psychotic or manic or agitated).
But over time, the adrenal glands can become depleted or fatigued when driven constantly to
high levels of activity - rather than being used intermittently, particularly when there is no
adequate period of rest for recovery.
In bodybuilding, one of the most important factors for growth is adequate rest to build muscle.
The recovery of adrenal glands are an important component of that rest period.
__________________
Re: Stopping HGH and IGF Levels
Quote:
Originally Posted by griffinannie
Doanyone know as to how long serum IGF levels will be elevated by hgh administration
after stopping therapy. Thanks
There is a lot of unclarity in the literature.
As far as I know:
Growth hormone lasts perhaps 3-6 minutes in the bloodstream.
During that time, it triggers the production of IGF-1 in the liver. IGF-1 is suppose to be a longer
lacting and the primary active version of growth hormone in the body (though growth hormone
itself has direct effects of its own).
However, Free IGF-1 has a half-life of about 4.5 minutes. Thus it is active for about 22 minutes.
IGF-1 becomes bound to various binding proteins. The primary binding protein is IGF-BP-3.
These binding proteins prolong the half-life of IGF-1 - just like SHBG prolongs the half-life of
Testosterone (Free Testosterone has a half-life of about 10-100 minutes).
Depending on the binding protein, the estimates of the half-life of bound IGF-1 varies between 620 hours with a common estimate of between 12-15 hours.
Assuming the half-life of bound IGF-1 is 15 hours, then IGF-1's activity is prolonged over baseline
by the addition of growth hormone approximately 75 hours.
Assuming the half-life of bound IGF-1 is 6 hours, then IGF-1's activity is prolonged over baseline
by the addition of growth hormone approximately 30 hours.
Re: Question for Marianco re: adrenal suppression
Quote:
Originally Posted by Ozzie
Regarding the use of hydrocortisone to facilitate the recovery of the adrenals, there
seems to be some confusion within the medical community regarding the issue of adrenal
suppression. While the works of Jeffries and others seem to indicate suppression not to be
an issue at physiologic doses (at the adrenals themselves despite ACTH blunting), other
works seem to indicate the contrary (i.e., atrophy of adrenals with deficient ACTH
stimulation and hypertrophy/hyperplasia of the adrenals in the presence of excess
ACTH). My recollection is that in one of your posts Marianco, you seemed to indicate
that this protocol is more of a passive nature which, when incorporated with lifestyle
changes, could actually work. I am wondering if you might be able to clarify the
confusion concerning the correlation between the degree of ACTH stimulation and
suppression of the adrenals (themselves).
I’ve also read the works of some physicians who buy into the notion of utilizing
glucocorticoids at physiologic levels, but will instead advocate the use of prednisolone in
many instances over hydrocortisone for reasons of compliance (i.e., one pill vice four
pills per day).
Is this an acceptable alternative in your opinion? Many thanks.
What commonly leads to adrenal fatigue/depletion is working the adrenal glands excessively until
they cannot recover despite attempts to rest. Usually sleeping overnight can recharge the adrenal
glands sufficiently for the next day.
Slowing down the adrenals - i.e. adrenal suppression without halting function - to allow them rest
even while they are being used is the idea used in the treatment of adrenal fatigue using
hydrocortisone. So long as the dose of hydrocortisone is below the physiologic production of
hydrocortisone (cortisol), then this may be accomplished with few side effects (usually
gastrointestinal since cortisol stimulates acid production). Taking a full physiologic or
supraphysiologic dose of hydrocortisone will stop the adrenal glands from working. When the
subphysiologic dose of hydrocortisone is tapered off, then the adrenal glands can function at a
higher level because they have more opportunity to recover from fatigue.
When the adrenal are slowed, it may be useful to add some of the hormones which are also
reduced in production - primarily DHEA.
The artificial versions of hydrocortisone - i.e. prednisone, methylprednisolone, prednisolone - are
viable alternatives. The practitioner needs to know how to use them in equivalent doses to
hydrocortisone. They have a much longer half-life and duration of action than hydrocortisone.
This can lead to more problems such as insomnia (since they can't as easily follow the
physiologic production of hydrocortisone). Methylprednisolone, for example, is devoid of
mineralocorticoid effects/aldosterone effects - which is usetul when one wants to avoid saltretention in a person who has significant hypertension or obesity. These artificial cortisols are
much more potent than hydrocortisone and thus have to be used with more caution. As such,
they always "freak out" conventional practitioners. When faced with diabetes, one has to be very
careful with hydrocortisone and its sisters in dosing since elevated blood sugars can result.
Re: A question to Marinaco regarding finasteride.
Currently, if the concentration of progesterone were raised enough, perhaps enough can be
converted to allopregnenolone. However, men can't tolerate this as easiliy as women.
__________________
The Labs I Run
Total Testosterone
Bioavailable Testosterone (sometimes called “Free and Loosely Bound”)
Free Testosterone (if Bio T is not available)
SHBG
DHT
Estradiol (specify by the “Extraction Method” or “Ultra-Sensitive”)
Total Estrogens
LH
FSH
Prolactin
Cortisol
Thyroid Panel (TSH, FT3, FT4)
CBC
Comprehensive Metabolic Panel
Lipid Panel
Homocysteine
PSA (if over 40)
IGF-1 (if HGH therapy is desired)
Fasting Insulin
At the one month point, I follow-up with these assays:
Total Testosterone
Bioavailable Testosterone
Free T and SHBG (if Bio T is not available)
Estradiol (specify by the “Extraction Method” or “Sensitive”)
DHT (if patient is using a transdermal delivery system)
SHBG
FSH (3rd gen "sensitive" assay)
CBC
Lipid Panel
Comprehensive Metabolic Panel
(if ALT/AST from above are elevated, then get a GGT)
...I hope this helps!
Bare Bones Testing
Quote:
Originally Posted by SWALE
Here is an absolute bare bones list:
Total testosterone
Estradiol ("sensitive" assay for males)
CBC
Comprehensive metabolic Panel
Lipid Profile
It is still better than what is being accepted by some docs out there.
You must understand, though, that it is not testing for the actual cause of yoour
hypogonadism, nor does it attempt to screen for a more serious cause such as a pituitary
tumor.
I must finish by saying the trick is in the interpreatation of the labs. That is why doctors
go to medical school.
Here's one bare bones list to help make decisions regarding hormone replacement:
Blood tests:
1. Free and Total Testosterone Panel (often gives SHBG and bioavailable testosterone - all for a
similar price to total testosterone alone)
2. Estradiol (ultrasensitive)
3. Free T4, TSH (Free T3 would be preferable but can be very expensive)
4. Fasting Comprehensive metabolic panel (usually very inexpensive)
5. Progesterone
6. Hemoglobin A1c
Saliva test:
7. Cortisol x 4 times a day
8. DHEA-s x 2 times a day
Note that from many labs that do Saliva tests, such as salivatest.com, it is possible to do
estradiol, progesterone, testosterone also for an inexpensive price, though I haven't found them
as reliable as a blood test when it comes to making decisions.
By "bare bones", as opposed to the full panel, many things are not checked as SWALE noted. It
does give an idea of reproductive, adrenal, thyroid, and pancreatic hormone function.
__________________
The Labs I Run
Quote:
Originally Posted by CaesarWilliam
I am down in Latin America. I have never had labs done before. I have located a Blood
lab in a town near hear. I want to go get my levels checked. My question is, what test do I
have them run? Do I ask for a Hormone test (Testosterone, Estrogen Ect?) Or is there a
specific named test? Down here you don't need a doctor for test referals and health care
is cheap and very good. I just don't know what to ask for.
Look up sticky called TRT: A Recipe for Success for SWALE/Dr. Crisler's protocol including the
initial labs.
The labs need to be customized to the individual. A comprehensive set of labs for my patiens
would cost close to $5,000 or more. Not everyone can afford this, even with insurance, nor may it
be necessary or practical in order to address the most important problems, so I customize the lab
tests for the person.
A fairly comprehensive general initial lab work-up using standard blood and urine tests may
include:
REPRODUCTIVE:
Free and Total Testosterone Panel (this includes Total Testosterone, Free Testosterone,
Bioavailable Testosterone, and Sex Hormone Binding Globulin), Estradiol, Progesterone,
Luteinizing Hormone, Follicle Stimulating Hormone, Prolactin, Prostate Specific Antigen (in men)
THYROID:
Free T4 (Free Thyroxine), Free T3 (Free Liothyronine), Thyroid Stimulating Hormone,
antithyroglobulin antibody, antithyroid peroxidase antibody, thyroid stimulating immunoglobulin.
ADRENAL:
Cortisol AM, Cortisol PM, Cortisol-Binding Globulin, Adrenocorticotropic Hormone (ACTH),
Dehydroepiandrosterone Sulfate (DHEA-s),
CARBOHYDRATE METABOLISM:
fasting glucose (included in comprehensive metabolic panel when fasting), Hemoglobin A1c,
fasting insulin, 3-Hour Glucose Tolerance Test (samples of blood for measuring glucose and
insulin are taken at 0, 60, 120, and 180 minutes after ingesting a 1.75 g/kg glucose solution).
GROWTH HORMONE:
IGF-1 (Insulin-like growth factor I / Somatomedin-C), Growth Hormone Stimulation Test using
GHRH (growth hormone releasing hormone) plus Arginine (samples of blood for measuring
growth hormone are taken at 0, 30, 60, 90, and 120 minutes).
GENERAL:
Comprehensive Metabolic Panel (glucose, urea nitrogen, creatinine, calcium, sodium, potassium,
CO2, cholride, total protein, albumin, globulin, total bilirubin, alkaline phosphatase, AST, ALT)
CBC (complete blood count)
Lipid Profile (including total cholesterol, triglycerides, HDL cholesterol, VLDL cholesterol,
calculated LDL cholesterol)
Urinalysis
Magnesium
Vitamin D, 1, 25-Dihydroxy
Vitamin B12
Folate
Heavy Metal Screen (blood)
The tests are done in the morning after fasting overnight (no food or drink after dinner except for
water). The patient should drink 0.5 liters of water before the test to avoid dehydration. The
patient should avoid strenuous activity the day before, avoid restaurant food and stimulants such
as coffee, eat their regular meals, and avoid stressful situations for at least 2 days before the test.
Cortisol-PM is done in the afternoon between 4-6 PM on the same day as the morning test.
The 3-hour glucose tolerance test and growth hormone stimulation tests should be done on
different days.
ADDITIONAL SPECIALIZED TESTS:
A comprehensive 24-hour urine hormone panel (including DHEA, Androsterone, Etiocholanolone,
Pregnanetriol, Cortisone, Cortisol, Tetrahydrocortisone, Tetrahydrocortisol, Allotetrahydrocortisol, Aldosterone, Tetrahydrocorticosterone, Allo-tetrahydrocorticosterone, Estrone,
Estradiol, Estriol, Pregnanediol, Testosterone, Androsterone, 2-hydroxyestrogens, 16ahydroxyestrone, 4-hydroxyestrone, 2-methoxyestrone, 2-methoxyestradiol, 5a-androstanediol,
5b-androstanediol, 11b-hydroxyandrosterone, 11b-hydroxyetiocholanolone, Free T3, Free T4,
Sodium, Potassium, Calcium, Phosphorus, Magnesium).
24-hour urine growth hormone
Saliva test for Cortisol (4 samples in a day), DHEA-s (2 samples in a day).
Urine test for neurotransmitters (including sertonin, norepinephrine, dopamine, GABA, glutamate,
epinephrine)
MRI of Brain
Chest X-Ray
EKG
The follow up tests include a subset of these tests as well as other tests depending on the
situation.
__________________
Re: The Labs I Run
Quote:
Originally Posted by JackBauer
I just had labs done yesterday, and drank plenty the night before, but none before my
blood work in the morning. (Fasting)
I chose not to drink because there seemed to be conflicting information online about it, I
did not see this thread until today.
How substantial of an impact could me not drinking the morning of the lab test, have on
results?
Thanks
Overnight, one can become dehydrated.
Dehydration will artificially raise levels on blood tests.
This will cause low test levels to artifically appear in the "normal" range when they may actually
be low. Thus, one risks not finding deficiencies by not drinking water before the lab test.
The amount to drink is about 0.5 to 1.0 liter.
The albumin level is one indication of the amount of dehydration that is occurring
Re: The Labs I Run
Here is an updated list of the labs I may run:
LAB TESTING IN PSYCHIATRY
Conventional Lab Tests
GENERAL:
Comprehensive Metabolic Panel (glucose, urea nitrogen, creatinine, calcium, sodium, potassium,
CO2, chloride, total protein, albumin, globulin, total bilirubin, alkaline phosphatase, AST, ALT)
CBC (complete blood count)
Lipid Profile (including total cholesterol, triglycerides, HDL cholesterol, VLDL cholesterol, LDL
cholesterol)
Urinalysis
Homocysteine
Uric Acid (if gout is a possibility)
Serum Myoglobin (if muscle aches are present)
TOXICITY:
Heavy Metal Screen (blood)
Urine Drug Screen
Specific Plasma or Serum Drug Level
REPRODUCTIVE:
Free and Total Testosterone, Sex Hormone Binding Globulin, Estradiol, Luteinizing Hormone,
Follicle Stimulating Hormone, Prolactin, Prostate Specific Antigen, Dihydrotestosterone,
Androstanediol glucucoronide
THYROID:
Free T4 (Free Thyroxine), Free T3 (Free Liothyronine), Thyroid Stimulating Hormone, Total T4,
Total T3, Thyroglobulin, Reverse T3, antithyroglobulin antibody, antithyroid peroxidase antibody,
thyroid stimulating immunoglobulin.
ADRENAL:
Cortisol AM, Cortisol PM, Cortisol-Binding Globulin, Adrenocorticotropic Hormone (ACTH),
Dehydroepiandrosterone Sulfate (DHEA-s), Progesterone , Pregnenolone-sulfate
CARBOHYDRATE METABOLISM:
fasting glucose (included in comprehensive metabolic panel when fasting), Hemoglobin A1c,
fasting insulin
3-Hour Glucose Tolerance Test (samples of blood for measuring glucose and insulin are taken at
0, 60, 120, and 180 minutes after ingesting a 1.75 g/kg glucose solution)
GROWTH HORMONE (if this was a consideration in treatment):
IGF-1 (Insulin-like growth factor I / Somatomedin-C), IGF-BP-3, 24-hour Urine Growth Hormone
Growth Hormone Stimulation Test using GHRH (growth hormone releasing hormone) plus
Arginine (samples of blood for measuring growth hormone are taken at 0, 30, 60, 90, and 120
minutes)
INFLAMMATION:
C-reactive Protein
Erythrocyte Sedimentation Rate
Rheumatoid Factor
NUTRITIONAL:
Magnesium
Vitamin D, 1, 25-Dihydroxy
Vitamin B12
Folate
24-hour urine iodine - or Random urine iodine if 24-hour urine iodine is not available
(best is iodine excretion test with 50 mg loading dose of iodine given orally then 24-hour urine
iodine done).
Vitamin A
Ferritin
Zinc
Copper
IMMUNE SYSTEM:
Interleukin-1 beta
Interleukin-2
Tumor Necrosis Factor-Alpha
Interleukin-6
Interleukin-10 (antiinflammatory cytokine)
The tests are done in the morning after fasting overnight (no food or drink after dinner except for
water). The patient should drink 0.5 liters of water before the test to avoid dehydration. The
patient should avoid strenuous activity the day before, avoid restaurant food and stimulants such
as coffee, eat their regular meals, and avoid stressful situations for at least 2 days before the test.
Cortisol-PM is done in the afternoon between 4-6 PM on the same day as the morning test.
The 3-hour glucose tolerance test and growth hormone stimulation tests should be done on
different days.
SPECIALTY LAB TESTS (Paid for by Patient Out-Of-Pocket):
NEUROTRANSMITTER PROFILE:
Spot-urine test which includes: Serotonin, Dopamine, GABA, Glutamate, Norepinephrine,
Epinephrine.
SALIVARY CORTISOL AND DHEA PROFILE:
Four saliva samples during the day for Cortisol and DHEA
Comprehensive 24-hour urine hormone panel
Which may include: DHEA, Androsterone, Etiocholanolone, Pregnanetriol, Cortisone, Cortisol,
Tetrahydrocortisone, Tetrahydrocortisol, Allo-tetrahydrocortisol, Aldosterone,
Tetrahydrocorticosterone, Allo-tetrahydrocorticosterone, Estrone, Estradiol, Estriol, Pregnanediol,
Testosterone, Androsterone, 2-hydroxyestrogens, 16a-hydroxyestrone, 4-hydroxyestrone, 2methoxyestrone, 2-methoxyestradiol, 5a-androstanediol, 5b-androstanediol, 11bhydroxyandrosterone, 11b-hydroxyetiocholanolone, Free T3, Free T4, Sodium, Potassium,
Calcium, Phosphorus, Magnesium
MRI of Brain
Chest X-Ray
EKG
Serum Myoglobin
Quote:
Originally Posted by Grimnuruk
Hi Marianco,
Could you expound on this a bit more: the testing for Serum Myoglobin (if muscle aches
are present).
I have major problems with myofascial pain all over my body and only get (temporary)
relief from: 1) extremely deep regular massage therapy (very expensive and difficult
finding /keeping a therapist who is willing and able (strong enough) to do it. 2)
constantly working trigger points against hard rubber ball and 3) TRT, initially it seemed
to almost all go away after starting and now it is creeping back. regular exercise and
stretching is a must or it hurts worse. It is obvious to me that my pain perception was
highly skewed due to low T and fatigued adrenals but my muscles actually knotting up
and needing an extreme amount of maintenance work to keep functional is what bothers
me.
Serum myoglobin is released from muscle cells when they experience injury or destruction.
It is commonly elevated in agitated mental states, seizures, high fevers, and other conditions
which cause muscle injury or destruction. Untreated, the elevated serum myoglobin is toxic to the
kidneys and may result in kidney failure.
It is frequently elevated when using anticholesterol medications such as Lipitor, Zocor, Crestor,
etc. when they cause weird muscle pains - and some other medications.
The condition of muscle destruction is called Rhabdomyolysis - a serious, potentially life
threatening condition. When it is obvious - such as when people have delirium and an agitated
state, then someone may think of getting the serum myoglobin done.
Unfortunately, in more subtle situations, very few physicians (if any at all) in my experience,
check this very basic test when they prescribe patients anticholesterol medications. They all test
for liver function as indicated by the prescribing information. But they don't think deeply enough to
do the serum myoglobin.
In some of my paitents, this resulted in unnecessary E.R. visits and hospitalizations due to
unusual pains such as unexplained facial pains until I myself checked their serum myoglobin.
__________________
Re: anything exist which prevents dht formation in the scalp alone
Quote:
Originally Posted by masterpp
guys, dht makes me feel good, and has improved my facial hair etc etc. but its also
destroying my hairline. is there anything which prevents the formation in the scalp alone.
i have propecia and saw palmetto, but i think prop is nasty stuff from what ive heard, and
i dont really think saw does much.
Im getting DIm shipped, which apparently is good stuff for dht and e2 (thanks phil), but i
was wondering if there was anything else anyone could recommend.
It is possible to have compounded lotions containing Azelaic acid, Saw Palmetto, or other
substances whicn can block the 5-alpha-reductase enzyme which transforms testosterone to
DHT in the scalp rather than going systemic.
For example, look up ucprx.com and minoxidil.com for their hair products.
__________________
Low SHBG
Quote:
Originally Posted by James23
I hear SWALE is asking all patients with SHBG problems to contact his office regarding
some "new" protocols. Does anyone have any information about what he is up to?
Low SHBG is most associated with high insulin levels due to insulin resistance or diabetes which is associated with Metabolic Syndrome.
SHBG is raised by thyroid, estrogen, and progesterone.
SHBG is lowered by insulin, testosterone, DHT, growth hormone, DHEA, and other androgens.
Supraphysiologic doses of testosterone or other androgens can drive SHBG lower.
I don't have any information on what Dr. Crisler is up to.
However, perhaps it may be related to the above information.
For example, if one has insulin resistance/diabetes, it may be treated with
substances/medications such as Actos or Avandia to improve insulin sensitivity. It may be
important to aggressively treat insulin resistance since leaving it untreated results in a much
higher risk of heart disease, hypogonadism, obesity, stroke, mood disorder, dementia, among
many other illnesses.
Low IGF-1
Quote:
Originally Posted by ili
Hello everyone,about a month ago I had a post about fertility and trt,well specialist
wants me to do two more tests,one in Jan,and one in Feb,while still of trt,to see where i'm
at before he messes with my hormones,in the meantime,I had two more tests I got
done,paid for it(provincial plan does not cover it)so I'm curious as to what it means,A
year ago I had low free test,but off shots now,I got dhea test done and igf-1 test,here are
the results:
Dihydrotestosteone......--3281--..............Age dependent: Range
9m-puberty 31------317
20---49y 217---1650 mine is pmol/L----3281
IGF-1(somatomedin-c) --93 ---- Range
112-296 ug/L mine is ----- 93So what does this mean?dhea is above norm,but IGf-1 is
low,off the trt shots I get tired quicker,and libido is very low,back muscles tire very
quickly,is my problem low test or is IGF the culprit,I see the specialist in Feb,but was
wondering if anybody has input.
Thanks for reading everyone
Dihydrotestosterone above the reference range may indicate a person has high total testosterone
levels or high alpha-reductase levels (the enzyme that converts testosterone to
Dihydrotestosterone). Free testosterone is not too useful. It would be better to have a total
testosterone level. High dihydrotestosterone may increase abdominal fat, contribute to insulin
resistance, and male-pattern baldness. The increase in abdominal fat and insulin-resistance have
their own consequences.
IGF-1 below the reference range may indicate a growth hormone deficiency syndrome. However
other hormones also affect the liver's production of IGF-1 including DHEA, Estrogens,
Testosterone, thyroid hormone, etc. Thyroid hormone deficiency is a very common cause of
impaired IGF-1 production.
Since IGF-1 is a multipli-determined hormone - not just determined by growth hormone - it is very
important to fix the other hormonal problems first before adding growth hormone to treatment.
Adding growth hormone prematurely can worsen the other underlying hormonal problems. For
example, adding growth hormone prior to optimizing thyroid hormone levels can worsen thyroid
problems, resulting in fatigue. Similarly with the adrenal hormones and adrenal fatigue.
It is usetul to also obtain the primary binding protein for IGF-1 (IGF-BP3) to help the interpretation
(e.g. to determine the amount of Free IGF-1 that is active).
Re: High Norepinepherine & Erectile Dysfunction
Quote:
Originally Posted by griffinannie
Can high nor-ep cause chronic ED ? If so , how? What can be done?
High norepinephrine levels (or relatively high norepinephrine levels compared to the other
neurotransmitters) can cause erectile dysfunction (chronic or otherwise).
Norepinephrine is the primary signal in the brain for stress. It is a excitatory neurotransmitter. It
keeps a person awake. It can help improve attention. It causes an increase in ACTH production,
which then drives adrenal hormone production. A spike of norepinephrine triggers
orgasm/ejaculation in men. Norepinephrine is the primary chemical messenger of the sympathetic
nervous system (the system that responds to fight-or-flight, stressful situations).
When a person has chronically high norepinephrine, it can cause anxiety or irritability. It can
eventually cause adrenal depletion, fatigue, or frank adrenal insufficiency. This can then lead to
erectile dysfunction, loss of libido, sexual dysfunction.
To keep norepinephrine levels high, the brain may have to lower the production of dopamine,
which can lead to loss of libido and erectile dysfunction. Lowered dopamine production, itself, can
reduce testosterone production (though high norepinephrine can raise it - causing a wash if the
balance is maintained). Lower testosterone can lead to erectile dysfunction. Lowered
testosterone production can lead to insulin resistance and further metabolic cascades that can
cause erectilve dysfunction and lack of libido.
Chronically high norepinephrine production in the absence of other neurotransmitter, hormone,
cytokine problems, can lead to premature ejaculation - since it doesn't take much to get a higher
norepinephrine spike to trigger ejaculation.
Chronically high norepinephrine can raise blood pressure. This leads to long-term consequences,
including renal dysfunction and erectile dysfunction.
What can be done is to either directly address the high norepinephrine production (e.g. with a
serotonergic, anxiolytic, mood stabilizing, beta-blocking medication or others), or treat the
consequences - such as adrenal fatigue (where the higher cortisol levels from treatment can help
reduce via a feedback loop in the brain to lower CRH production, to lower norepinephrine levels),
or treat the underlying cause of higher norepinephrine levels (which can include psychological
stress, trauma, mental illness, thyroid dysfunction, hypogonadism, insulin resistance, infection or
other chronic physical illness, etc.). In a way, a global treatment once assessment occurs, needs
to be done. I usually don't see a single substance (drug, hormone, or nutrient, or even herb)
working. There are many entrypoints to dysfunction when a single hormone/neurotransmitter is
out of whack in function. What I usually see are multiple hormone/neurotransmitter/cytokine
problems as a consequence.
__________________
Re: The Hormone Dance
It's nice to have another professional in this area.
I've been on vacation - to account for my recent absence.
I also work two full-time jobs (private practice and community mental health), have a continuous
heavy study load,. I am also starting to write what will be eventually two books (consumer and
professional) on Behavioral Neuroendocrinology, Immunology, and Nutritional Science - what I
would call Advanced Biopsychosocial Psychiatry - to give a palatable term to it for the
psychiatrists in the future I want to train, otherwise the former term applies.
Writing to professional book itself is a huge task, which will take at least 2 years. One of my
colleagues has taken more than two years writing a single-author book to be published this year
on diabetes, alone, working until 2 AM each day. Another friend took 5 years to complete his
book on cultural psychiatry.
Thus, my cup is overflowing when other aspects of life are added - limiting my ability for daily
participation in forums.
To me, medical school was an enormous lot of fun. It was like entering elementary school with
120 instant friends, willing to work together as a team. The study load was the equivalent of
taking 32 quarter units in a university - which can be done at 2 days a week by some students.
Today, I study a lot more.
One of the most important lessons to learn, if not the most important, from medical school, is the
ability to teach oneself. The reason is that most of one's learning occurs after one graduates from
medical school and residency. It occurs from one's own experiences and studies - not from a
class.
A good physician is like a jazz artist. To be good in jazz, one has to know the basics of music so
well that one can then improvise. If anything, improvisation is crucial in psychiatry since every
patient is different and there is nothing set in stone regarding protocols. Psychiatry is like
managing chaos. Psychiatry is not the field for physicians who are into cook-book medicine.
The subjects I have to study include knowledge in psychology, psychiatry, neurology,
endocrinology, immunology, nutrition, along with supportive material from sociology, internal
medicine, cardiology, gynecology, gastroenterology, sports medicine, computer science, physics,
chemistry, biology, philosophy, religion, photography, business, law, music and the other arts,
etc. You have to know a lot to be a good psychiatrist. It is not just neurotransmitters or even
hormones, as with anti-aging physicians
Re: borderline hypothyroid, still cold sweating.
Quote:
Originally Posted by chasingtime
the doc called and said im borderline hypothyroid but he doesnt think its why im cold
sweating. any experience would be appreciated. thanks, t
.
Hypothyroidism forces the brain to increase norepinephrine (and/or glutamate) production (at the
expense of serotonin, dopamine, GABA production), which overworks the adrenal glands to
generate energy. When the adrenal glands fatigue, the brain is forced to increase norepinephrine
production further. This leads to hot or cold sweats.
Re: Chroncally low DHEA - Ideas?
Quote:
Originally Posted by griffinannie
I have had chronically low DHEA-s even in the face of supplemenation. My lastest Lab
came back 150 range 90- 540. I supoplement 100 mg ( 50 am /50 pm) Ive change brands
a couple of times as my doc has increased doseages. Any ideas? I'm st\umped..
Occasionally, there are patients who have hyperexcretion syndromes of various hormones.
It would be useful to do 24-hour testing of hormones including DHEA and its metabolites to see if
this is the problem. Of course, one will have to know how to analyze the results - which can be
mind-numbingly complex. Even the best practitioner I know, who does 24-hour urine tests as a
standard in his practice - Jonathan Wright, M.D. (the inventor of Tri-Est) - doesn't remember all
the pathways and metabolites, having to refer to a chart each time he looks at them.
Having a high quality brand of DHEA will insure knowing what one is taking if one is having
problems with DHEA levels. Non-high quality brands may have only a fraction of what is
advertised.
__________________
Re: Chroncally low DHEA - Ideas?
Quote:
Originally Posted by JanSz
Welcome back;
How to figure out brand quality?
I am using (massive?) 350mg DHEA and 100mg 7ketoDHEA daily in divided dose.
My last test show DHEAs=369ng/dL
Up from 119 in April2005
I am thinking of further rising my dose, trying to get up to 500 in my blood.
I am using Life Extension Foundation 300mg DHEA + (Complete DHEA.)
Thought it is quality product, comments.
I don't subscribe to any particular brand - particularly since many patients are cost-conscious.
Mental illness tends to drive people downward socioeconomically as well.
Some trial and error may need to be done to see which DHEA brand works best or more cost
effectively. Unfortunately, the amount of DHEA between brands may vary a lot from the
advertised amount. But costly brands can break the bank, whereas increasing the dose of a less
expensive brand may accomplish the same.
DHEA is made by the adrenal glands.
There really isn't much of a negative feedback loop when it comes to DHEA production
regulation. The brain primarily measures cortisol, blood sugar, stress level, to help determine the
production of cortisol - the production of which then triggers the parallel production of other
adrenal hormones.
During treatment of adrenal fatigue, adding DHEA is useful since treatment with cortisol or other
glutocorticoids will slow down adrenal function - resulting in a deficit of the other adrenal
hormones - which then can cause side effects - since their production is already lower when
adrenal fatigue is present. Thus adding DHEA is usetul to make up the difference in production,
until the adrenal glands are healthy enouth to make enough.
Low DHEA is one sign of adrenal fatigue. Addressing adrenal fatigue may improve production of
all the adrenal glands products - such as DHEA.
Re: Alcohol + Hormones?
Quote:
Originally Posted by Megazoid
Last night i went to a DJ gig for the first time in a while, i didn't feel "too" bad for the
first part of the night or even on the way home. I am going to be getting fresh blood work
done this week so i can get a deeper insight into my hormonal problems but otherwise i
believe i suffer from low t, e and DHT. I believe my free T might be high as my SHBG is
at 19. Prolactin is also low and sometimes sexual function is bearable at least.
Thyroid/Adrenals are good on last check but i will re-evaluate on the next checkup.
I had a few too many beers last night but didn't feel too bad when i went back home to
bed. I woke up with mild morning wood.
By mid-afternoon i felt terrible though and not in a hang-over way either. But i noticed
everything had shrunk really bad down below (sack was ultra tight, penis hanging small,
muscles/bones hurting more, etc). By mid day i had complete ED (i was hoping to visit
my girl tonight). I searched on meso but couldn't find any threads related to this and
more the effects on someone going "natural" with low t.
What effect does Alcohol have on the hormone system? I am expecting it acts by lowering
T or creating lot's of estridol in exchange. Maybe someone like Marianco can have some
input on this one.
Alcohol has multiple negative effects on the endocrine system, such as:
1. Alcohol blocks the production of growth hormone and blocks the liver's production of IGF-1 in
response to growth hormone. If a person is on growth hormone replacement therapy, a single
glass of wine, can of beer, shot of liquor wastes that day's growth hormone dose. It is a waste of
time and money to give growth hormone to a person drinking alcohol daily.
2. Alcohol is a simple sugar. The brain senses this and thinks it has enough adrenal cortisol
production, then reduces arenal function for hours. Like eating a sugary candy or food or fruit
juice, one can worsen adrenal function for hours by drinking alcohol. This causes fatigue that
lasts long after the drink of alcohol.
3. Alcohol withdrawal can occur from non-abusive doses of alcohol. This can interrupt melatonin
production and sleep.
4. Alcohol can suppress testosterone production.
Alcohol is toxic to practically every cell in the body. If one chooses to drink alcohol, it should be
intermittently - as a treat so to say - rather than being regularly used.
__________________
Re: Alcohol + Hormones?
Quote:
Originally Posted by Megazoid
Thanks for the reply Marianco. As always, the man with the answers.
Does it cause an increase in E2?
In women, it increases estradiol levels.
Alcohol's effect on Estradiol level in men is actually more complex.
For example, in men, it depends on whether or not there is adequate folate in the diet.
If there is adequate folate, then alcohol use leads to increased estradiol.
If there is low folate, alcohol can also lead to a lowering of estradiol level.
Chronic alcohol use can lead to nutritional deficiencies including low folate.
Re: Hcg As Sole Terapy??
Quote:
Originally Posted by techytech1
Im 42, average semi-athletic build..and recently got some bloodwork done. Total
test=384. Free test =15. My IGF-1 = 285. Estradiol =33. All other results from my blood
work are good...lipids, etc. etc. I have spoken with approx 7 online clinics, all telling me I
need to go on 200mg cyp weekly for 10 weeks, the HCG for 4 weeks, with some Arimidex
also. Then on and off repeating same..etc. I saw a local MD who specializes in HRT and
tells me I need HCG solely for my treatment, with possibly some Arimidex in case I need
it. Says I will get in the 700-900 total test range and 150-180 on "free test". What u guys
think. Im new here...I respect what you guys know and have been through . Thanks.
HCG is a valid form of treatment for testosterone deficiency/hypogonadism - an alternative to
testosterone injections or transdermal testosterone.
It works best when one is young. As a man reaches 65 years-old, many don't respond as well to
HCG due to the aging of their testes.
Not everyone has problems with Estradiol on HCG. If it exists, then it can be adjusted for.
Testosterone injections themselves can result in supraphysiologic estradiol production and its
problems.
A limitation of HCG therapy is that HCG is not stable. It has to be kept cool. Once it is exposed to
water, it lasts 30 days or less. When one is traveling, one has to keep it in an cooler, like insulin
is. This may be problematic with the limitations in liquids on planes. I prefer giving a prescription
for two a month since HCG can go bad. I don't, however, see much of a difference between
Novarel and generic HCG. Some patients use generic and achieve testosterone levels of 700+.
Supplies of generic HCG are much more plentiful.
__________________
Re: Sudden Weight Gain starting TRT??????
Quote:
Originally Posted by bigjimcalhoun
Hi
I just started TRT and have had two injections of Test (100 mg each) in the past 12 days
with a third week starting later this week. I have had no noticable change in labido,
mood, etc. I have however gained 7 lbs in 12 days. I have jumped from a morning weight
of 186.5 to 193.
I have not had sugared soda in a month
The only junk food I have had in the past month is one cookie on thanksgiving. No pie, no
stuffing my face, no other junk food, nothing else. I have cut down my food consumption
from before the testosterone and I have gained weight. I walk a fast 2 miles every day
at lunch. I have cut caffeine due to some concerns about blood pressure, but aside from
that, I am confused. Some people doing cycles do not gain this much weight. I have been
lifting but not to the extent that most people here do.
I have a Christmas party at work Saturday and I can't fit into my suit anymore.
For many men, improving testosterone levels from hypogonadal levels can improve energy and
reduce weight.
However, other men can have problems such as weight gain. It may depend on the dose and the
effects of testosterone on other hormones.
For example, rather than increase thyroid hormone production, some men on testosterone
replacement have a reduction in thyroid hormone. This can cause weight gain by reduction one's
metabolic rate.
Excessive amounts of testosterone may also do the opposite of what is expected. For example, it
may excessively slow down adrenal function or result in insulin resistance. This may result in
weight gain. Testosterone acts like a governor of adrenal function. When stress raises adrenal
production, testosterone reduces it back to normal like a stretched rubber band contracting back
to normal size. This limits the stress response to a transient rather than permanent response.
However, too much testosterone makes it hard to have an appropriate stress response, and
suboptimal adrenal function may result. This can cause transient suboptimal blood sugars in
response to stress or suboptimal rises in metabolism in response to stress. High testosterone
doses can result in high DHT levels, which can increase abdominal fat and insulin resistance which promotes weight gain.
__________________
HCG IM versus SQ injections.
I think both IM and SQ injections are both valid routes.
For fertility protocols, both are equivalent, for example.
IM injections will give you a faster response since muscle has many more blood vessels than
subcutaneous fat. The higher peak levels of HCG can then stimulate a higher peak testosterone
and estradiol production which in some people gives them a better sense of well-being - however
transient that may be depending on the half-life of testosterone and estradiol in that particular
person, and the other hormone influences of testosterone and estradiol.
A SQ injection will give you a smaller peak of HCG in the blood but a longer duration of action.
This may be useful then when one wants to reduce testicular atrophy by using intermittent HCG
injections, rather than daily HCG injections.
It may be worthwhile to try both routes to see what one prefers
Re: HCG IM versus SQ injections.
Quote:
Originally Posted by kincaiddave
Welcome back Dr. Marianco!!! We've missed you!
Thank you for the kind words.
I've been on vacation.
I work two full-time jobs.
I have continuous massive amounts of study to do, since what I do combines knowledge in
psychology, psychiatry, neurology, endocrinology, immunology, nutritional science, and other
fields.
I am writing a book on "Advanced Biopsychosocial Psychiatry" - which is a title palatable to other
psychiatrists - for what I do (behavioral neuroendocrinology, immunology, and nutrition). This
itself is a massive effort, which will come out in a professional and consumer form, which will take
at least 2 years to do.
Thus my cup is full professionally, among the things I do. I'll be on this board when I can.
Re: Test Results - E2 question
Quote:
Originally Posted by tzutzu
Free testosterone was 40.8 (8.7-25.1 is the suggested range)
sensitive estradiol was 37 (3-70)
Dihydrotestosterone was 59 (30-85)
Free T4 was 1.18 Free T3 was 3.0 (2.3-4.2)
CBC and iron studies were normal
DHEA-S was 38 (120-520)
==============================================
So right off, cutting down the test supplement by about 30% and adding DHEA at 50mg
per day.
My question is in regards to the E2.
My "total" test has been stable at 750's for several months. With my free test so far above
the normal range, would this suggest I have low SHBG? If this is the case, then my E2 is
probably too high at 37.
My libido is still pretty pitiful but I am physically feeling a lot better than I was with 150
total test.
Total Testosterone = 750. This is in the upper range of normal. If there are any problems with
libido, energy, mood, etc., then the problems most likely will be in the other neurotransmitters,
hormones, and immune system cytokines.
Estradiol = 30-40. This is an expectable level of Estradiol for the corresponding Total
Testosterone. Unless a person has too low an Estradiol (e.g. < 20) (which can cause libido
problems, high cholesterol, etc). or too high a level (e.g. 80+) with symptoms of excess Estradiol
(such as gynecomastia), then adjusting estradiol is usually not necessary. Estradiol levels can
also vary depanding on whether or not one is having sex. In some men, after sex, estradiol levels
rise. Since estrogens are important in functioning, lowering estrogen level by adding an
aromatase inhibitor may itself cause more problems than it solves.
SHBG. Low SHBG correlates mostly with high insulin levels - which is a sign of insulin resistance
or diabetes type 2, unless one has supraphysiologic levels of testosterone. A low SHBG can also
mean there are problems with the other hormones such as having low thyroid hormone, low
estradiol (!), high DHEA, high testosterone, high growth hormone, high DHT, etc.
Free T3, Free T4, TSH: I would suspect hypothyroidism in a person who has a Free T3 < 3.3, OR
Free T4 < 1.1, OR TSH > 2.0 depending on their history and the findings on physical exam.
DHEA-s. DHEA-s is just one of the measures of adrenal function. A low level indicates the
possible presence of adrenal fatigue or insufficiency, depending on the person. DHEA production
also drops with age. Other measures using conventional lab test which give information of
adrenal function include: Cortisol AM (and PM), Progesterone, Pregnenolone sulfate, glucose
(fasting), sodium, potassium, albumin, ACTH, hemoglobin A1c, (total testosterone, estradiol - in
women), aldosterone, etc.
Of the adrenal neurotransmitters and hormones, the most important is Cortisol production.
Cortisol production is controlled by ACTH production by the brain. The other hormones (except
aldosterone) are stimulated in production once Cortisol production is stimulated. If there is
adrenal fatigue or depletion, the production of these other hormones is reduced in favor of
producing the much more important Cortisol. Without Cortisol production, one cannot generate
glucose in the liver from protein and fat. Without Cortisol, one cannot reduce inflammation.
Without Cortisol, one cannot respond to stress.
__________________
Re: Once per week GH closer to market
I would look forward to this version of Growth Hormone.
However since it is in Phase II trials, unless it is on a fast track, it won't be available for several
years. There are Phase III and IV trials to go.
__________________
Re: My T results, could you help interpret?
Quote:
Originally Posted by canes1
I am 29.
My Total T was 349ng/dl, normal values are 250-1100.
% Free T was 1.88%, normal values are 1.1-2.8%
Free T was 65.5 pg/ml, normal values b/w 35.0-155.0.
I have been having symptoms of low T such as decreased libido, trouble recovering from
workouts and bit of sluggishness. The decreased libido is the biggest factor which has
negatively affected my relationship.
So when I got the results my Doc said good news there all in the normal ranges, but after
further research the mean total T for my age group is around 669 ng/dl. 552 is the mean
for ages 55-59!! I'm 29!
What is the interpretation b/w Free T and % Free.
Thanks
Total Testosterone is the best measure of testosterone activity.
Free Testosterone and % Free are unreliable measures.
To obtain Free Testosterone, one often gets the value for SHBG (Sex Hormone Binding
Globulin).
Free Testosterone is determined by SHBG. SHBG is determined by multiple hormones including
testosterone, DHEA, DHT, Estradiol, Thyroid hormone, growth hormone, Insulin, etc. A normal
free testosterone or SHBG won't tell you if any of these other hormones are off and causing
problems since their effects may cancel out when determining Free Testosterone. Thus it is best
then to obtain levels of the other hormones to determine where problems may lie.
If other hormones are in optimal working activity, then one can have normal libido even with low
levels of testosterone, sometimes even as low as 200 ng/dl.
The common end-point of neurotransmitter, hormonal, or immune system cytokine problems
which cause lack of energy is impairment of thyroid or adrenal function.
Recovering from workouts includes muscle recovery - which generally is about a week, when one
has good sleep - and neuroendocrine recovery - importantly, recovery of the adrenal glands in
function - which takes a more prolonged course when they are depleted or fatigued.
__________________
Add
Quote:
Originally Posted by Anonymous
Quote:
Originally Posted by marianco
Quote:
Originally Posted by Anonymous
I have Inattentive type ADD and will be seeing my GP for this soon. I have tried
Adderall and do not like the wired feeling and clammy hands and feet. I am
interested in seeing what you think about Concerta and/or Wellbutrin for the ADD
and a mild lift from winter blues. I do not metabolise stimulants very well unless
taken early in the day.
My hormones have been optimized.
Thoughts or suggestions?
Methylphenidate (as in Concerta) increases norepinephrine less than amphetamines
(such as Adderall). Both increase dopamine - which helps improve mood and attention.
Norepinephrine improves attention and alertness but also can burn out the adrenal
glands - thus the clammy hands and feet as possible side effects. Wellbutrin increases
only norepinephrine. It is a problem when a person has impaired adrenal function.
When a person has side effects from a stimulant, then a lower dose may be useful.
Thyroid and adrenal function are both stressed by winter - particularly with colder
weather. This is a highly important factor when one has ADD, thyroid or adrenal
problems since a stronger treatment may be needed.
Thanks Marianco,
I have been taking 18 and 36 mg of Concerta with the only side effect being headache at
36mg. My mood, motivation, and energies are good, but attention is only slightly
improved.
In short, I like the Concertas mild positive effects except I cannot feel my prefrontal
cortex being activated like I do from Adderall. Perhaps the Adderall XL version is what I
need. I wonder if running Concerta concurrent with Wellbutrin or with Adderal XL might
be the answer. Do you do this with some patients?
Knowing I suffer from Adrenal Insufficiency, can I use Adderall or Wellbutrin as long as
I supplement with 20mg of Hydrocortisone?
I had a urinary neurotransmitter test done and it revealed the following:
Low in: NorEpinephrine, Serotonin, Glycine (suboptimal)
Elevated in: Dopamine, Histamine, GABA, Glutamate
Normal: PEA, Taurine
The panel was done by NeuroScience Labs, with explainations at Neurorelief.com. An
amino acid product called ExcitoPlus has been recommended along with a product
called AdrenoCor which over timeis supposed to elevated my deficient NeuroHormones.
If one has adrenal insufficiency, the hormones are not optimized.
I wonder what other hormone problems are present - e.g. hypothyroidism, etc.
What other substances are being taken, besides Methylphenidate that can contribute to the
neurotransmitter profile described.
And why are there mood problems - the condition is then much more complex than Attention
Deficit/Hyperactivity Disorder alone.
A seasonal affective disorder is actually not really related to light levels. I think it is related to the
higher demands made on the thyroid and adrenal glands to maintain energy levels. One finding in
seasonal affective disorder is the presence of photophobia. This happens to be also a symptom
of adrenal fatigue.
Treatment of ADHD is often done using medications such as the stimulants, which increase
dopamine and norepinephrine. Wellbutrin only increases norepinephrine significantly in humans.
Strattera primarily increases norepinephrine - though has mild increases in serotonin and
dopamine.
A problem of increasing norepinephrine is that it can cause - and often not realized by
conventional psychiatrists - adrenal fatigue. This leads to the mood problems found in ADHD thought to be a feature of the illness or a side effect of treatment. Unfortunately, often this is
treated with an antipsychotic such as Risperdal, to knock down the mood symptom, at the
expense of risking serious side effects such as diabetes or cholesterol problems or neurological
problems.
To keep treatment going, it is then important to institute a treatment for adrenal fatigue to
maintain adrenal function. This may include hydrocortisone and other treatments, including
nutritional treatments.
When it comes to neurotransmitter profiles, the most reliable sign of a pure attention deficit
disorder is a increased amount of dopamine. This is a genetic form of attention
deficit/hyperactivity disorder, where there is dopamine resistance and the brain compensates by
producing more dopamine to get the same effect.
In other neurotransmitter profiles, where serotonin and other neurotransmitters are affected, I
would also look for other underlying problems which may be the actual cause of attentional
problems - for example, depression, anxiety disorders, hypothyroidism, adrenal fatigue, bipolar
disorder, etc. A stimulant may be used in treatment, but more caution may be necessary to avoid
worsening the underlying problem. For example, in bipolar disorder, a stimulant may worsen the
person's condition.
It is possible to use a stimulant along with Wellbutrin to try and improve attention by increasing
primarily norepinephrine. The usual warning about worsening adrenal fatigue applies.
It is possible to mix stimulants. However, In more than 14 years of practice, I have not found a
need to do so, nor have a seen another psychiatrist do so. Other concurrent conditions may be in
play to reduce the effectiveness of a stimulant. For example, once adrenal fatigue sets in, all
stimulants stop working, since the lack of adequate cortisol production will impair concentration
itself and worsen mood, motivation, etc.
__________________
Re: hydrocortisone is not a miracle
Quote:
Originally Posted by DAVID
When I've speaking with some people who have addison's disease about your energy
level. Some have less energy than before disease.
Myself have "adrenal fatigue", may be because I've taking synthroid since 20 year's. Now
I take synthroid with armour ans hydrocortisone 20 mg morning and 10 mg in the
afternoon.
This strategy help me, but when I have a stress day, or if I train more than half hours I
feel exhausted depiste hydrocortisone at 30 mg. I'm not sure that more hydro is better.
My question is to understand if there are a catecholamine deficiency with adrenal fatigue
from(medullo, nervous system). ?
In fact, when you read old study who can read "nervous exhaustion". It's look like " I lose
my nerve". The belly have a big distension depiste low body fat, you muscle lose power,
your brain feel depress...
Thank
My body fat is low but my stomach have a distension ( a symptom of adrenal depletion)
too
Hypothyroidism can lead to adrenal fatigue since the brain is forced to use the adrenal glands
more often to compensate for the loss of energy due to hypothyroidism.
Using Synthroid in many people does not adequately treat hypothyroidism, resulting in a higher
likelihood of developing adrenal fatigue.
In more severe cases of adrenal fatigue, the medulla of the adrenal gland (which makes
norepinephrine and epininephrine) can also be depleted, not just the cortex (which makes
cortisol, DHEA, progesterone, testosterone, aldosterone, and other steroid hormones).
Hydrocortisone is a miracle in the treatment of adrenal fatigue. However it is a passive treatment.
By "passive", I mean that it does not force the adrenal glands to be better. It only allows the
adrenal glands to slow down so that they don't have to work too hard to produce cortisol and
other steroid hormones.
Despite treatment with hydrocortisone, if one's stress level is still high or if hypothyroidism is still
undertreated, then the adrenal glands can still be overwhelmed by stress.
To maximize the opportunity to recover full adrenal function, one may have to do many things
including some of the following:
1. Work on changing one's lifestyle and psychological health to reduce stress levels
2. Take a serotonin-increasing medication to block external stress signals to the adrenal glands.
3. Adequately improve thyroid activity to improve the brain's source of energy - thus reducing
reliance on the adrenal glands for energy.
4. Take other supportive substances for the adrenal glands including Vitamin C, Magnesium, etc.
such as those listed in James Wilson's book on Adrenal Fatigue.
5. Give the adrenal treatment time to work. For example, it may take 2 or more years for the
adrenal glands to recover.
6. Avoid stimulants - which increase norepinephrine - which worsens the stress to the adrenal
glands.
__________________
Re: Body production of T
Quote:
Originally Posted by SinginHawk
I mean when you go on T and your LH and FSH shut down, what causes that to happen.
Is it the amount of Total T in the blood or Free T or DHT?
LH and FSH production are reduced by bioavailable testosterone (testosterone loosely bound to
albumin plus free testosterone), in conjunction with progesterone; by dihydrotestosterone (free
and loosely bound); and from the estradiol and other estrogens produced from testosterone.
__________________
Re: Buspar
Quote:
Originally Posted by Recless
I was wondering if anyone has experience using this drug. It's supposed to be a mild antianxiety med. My Dr. wants to put me on this short term until my test levels have fully
recovered and return to hormonal homeostastis. I have a case of ASIH that I am
currently treating with another round of nolvadex. I am nervous though that Buspar will
have negative impact on test levels. In terms of libido my Dr. said that it has not been
shown to have negative effects, in fact has helped some patients in that department. Any
thoughts? My anxiety is becoming dehibilitating to an extent, but I know that once my T
levels come up I feel much better mentally.
Buspar is a relatively mild antianxiety agent. However, it does not work in many people. Those for
whom it works are the lucky few. Generally, it will have no effect on testosterone or other
hormone level. There are a few who have significant side effects, but for most, it almost does
nothing - acting like a placebo - which is why it is not often used by psychiatrists.
For short-term use, a low dose of a benzodiazepine such as Diazepam (Valium), Clonazepam
(Klonopin), Alprazolam (Xanax), or Lorazepam (Ativan) is much more useful, reliable in
antianxiety effect.
AACE guidelines for HCG?
Quote:
Originally Posted by dano79
What are everyone's opinion of the AACE guidelines for HCG use of 1,000 iu's every
three days? Is this a good protocol? Anyone use it and see results?
HCG is an option to testosterone replacement.
There is a risk of testicular desensitization to HCG and LH with prolonged use at higher doses meaning one won't recover pituitary-testicular axis function if this occurs (though I usually don't
count on this happening anyway with hypogonadal patients who haven't abused steroids).
However, I also have patients who do well with HCG 1000 IU three times a week, who have done
so for years, with testosterone levels around 600-800 ng/dl.
Thus one's mileage may vary. And one has to determine if the risk of desensitization is worth the
use of HCG.
HCG subcutaneosly is probably the best way to use it since it prolongs the effects of HCG and
avoids high peak levels of HCG, reducing the risk of desensitization to HCG/LH.
HCG injections are remarkably less painful than testosterone depot injections since the needle is
very small, the liquid is not as thick as with testosterone cypionate or enanthate, and a
subcutaneous rather than intramuscular injection can be used.
__________________
Re: Why is Armour thyroid sometimes intolerable?
Quote:
Originally Posted by raw1973
I had issues tolerating Armour ( a couple times)and had to come off. I'm waiting to get
tested for adrenal issues, but in the meantime I'm wondering why many people have
problems.
I assumed it was the T3, but one grain of Armour only has 9mcg T3 along with 38mcg T4
along with unmeasured T2,T1, and soforth. You see guys ramping up T3 cycles starting
at 25mcg and going up to over 100 with no adrenal issues. I've also in the past taken
many stimulants in excess such as ECA, Clen, NYC, with no problem. Any comments?-Rob
The human body has a ratio of about 10% T3, 90% T4.
Armour Thyroid is about 20% T3, 80 % T4. This can cause problems with some people, who
cannot tolerate well the activity of the much more potent T3 than T4.
Often, what makes Armour Thyroid intolerable is the presence of Adrenal Fatigue/Depletion.
Thyroid hormone makes more demands on adrenal function. If the adrenals cannot tolerate the
extra workload, then they worsen in fatigue/depletion. This leads to a surge in norepinephrine or
other stimulant neurotransmitter production, which leads to anxiety, irritability, hypertension,
tachycardia, sweating, and other effects in addition to symptoms of adrenal fatigue.
Armour Thyroid also contains an unspecified amount of Calcitonin - which lowers blood calcium
level. Lowering blood calcium excessively in patients can cause multiple problems including
irritability, confusion, muscle spasms, congestive heart failure, breathing problems, etc.
Armour Thyroid also contains T1 and T2, which have additional thyroid activities - thus a larger
overall activity than just from T3 and T4 - the only hormone specified in Armour Thryoid.
Thus one has to be careful and have ideally, physician monitoring, to help determine what is
happening when one has adverse effects from Armour Thyroid. Armour Thyroid is a much more
complex compound that just T3 and T4.
Not everyone can tolerate Armour Thyroid, no matter how small the dose. For some patients, I
would use Synthroid (T4) and try to optimize thyroid function via other means if they cannot
tolerate Armour Thyroid.
__________________
Re: Is exogenous testosterone...
Quote:
Originally Posted by Rangeball
always suppressive?
Or in certain circumstances can low dose T supplement what your body produces
naturally? If it can, what are these circumstances?
Exogenous testosterone is usually but not always suppressive of pituitary LH production (which
determines endogenous testosterone production).
What determines LH production is estrogen activity and the combination of testosterone and
progesterone activity, and dihydrotestosterone activity (which is about 7 times more potent than
testosterone itself). Progesterone is necessary to improve the brains sensitivity to the presence of
testosterone.
Thus there is one example scenario: if one has low aromatase activity and does not produce
much estradiol from testosterone; low 5-alph-reductase activity resulting in less
dihydrotestosterone (which is more potant than testosterone in being sensed by the brain); and
one has adrenal fatigue/depletion leading to low progesterone production, then less than the
expected rise in estradiol can occur from adding testosterone, less dihydrotestosterone will be
sensed, and the added testosterone will less likely be sensed by the brain since progesterone
level will be low. Thus there is a chance that adding additional testosterone won't lower LH. There
are a lot of "ifs" in this scenario. Proof of the pudding would be to measure LH before and after
the intervention.
Re: what are these labs saying?
Quote:
Originally Posted by brobinson
I got my thyroid labs back today when I went to see my doctor. I wanted to convert these
for the Americans (I'm Canadian) but it doesn't say what they are measured in or what
the acceptable range is. Here's what it says;
SPECIAL CHEMISTRY
TSH-5.58 #H
Free T4-14.4 C H
LH- 1.8
FSH- 2.0
PSA- 0.6 C
SPECIMEN DISPATCH
Bio Test.- --> <C>
free T3- 5.6
free testoster->
Testosterone- 27.15
I don't understand that last part at all. My doctor is sending me for more blood work and
an ultrasound next week. He gave me antidepressants for now. He says there's likely
thyroid problems but the TSH and free T4 contradict each other. What do the experts
here think?
Brad
Generally, the ISO and American Conventional Units for TSH are the same - mIU/L, with a range
for one major lab being 0.4-5.50 mIU/L.
The units for Free T4 in American Conventional Units is ng/dL.
Free T4 can be high if one does not convert T4 to T3. T3 is the most active version of thyroid
hormone. T3 is also the version of thyroid hormone which is measure by the brain to determine
how much TSH to produced to stimulate thyroid hormone production. Thus if T3 (Free T3) is low,
then TSH is going to be high.
Assuming the brain is correct, then a high TSH means a person has hypothyroidism.
As one ages or if one has a mental illness or brain injury, the TSH production may be wrong.
Often it may be too low for the amount of Free T3 available. This may result in hypothyroidism,
despite a seemingly normal TSH. Thus, it is wrong to only assume that the brain is correct and
that the TSH is the right indicator for the presence of hypothyroidism.
__________________
Bio-identical versus synthetic testosterone
Quote:
Originally Posted by drp90210
I just read that Andrgogel uses "bio-identical" testosterone. I think that means that it was
naturally derived from yams, as opposed to manufactured synthetically, but I'm not sure.
In any event, I was wondering if anyone knew whether bio-identical testosterone was
easier on the body or provided any other benefits over synthetic testosterone. I just
switched from Androgel (which uses bio-identical testosterone) to a cream (which uses
testosterone of an unknown type) and I feel noticeably lousier and sometimes flushed. My
estrogen and test levels just came back and are fine (to my surprise), so perhaps my
symptoms have nothing to do with TRT.
Bio-identical testosterone means that the chemical structure of the testosterone is identical to the
testosterone produced by the human body. Thus, a person cannot become allergic to it. And it
functions identically to the testosterone produced by the human body. Bio-identical testosterone
are often produced from progesterone derived from the wild-mexican yam, via chemical
processes.
Bio-identical testosterones are used in Androgel and generally other testosterone gels and
creams. The term "USP Testosterone" insures that the testosterone is bioidentical.
Testosterone enanthate and testosterone cypionate end up being bio-identical because the
enanthate and cypionate esters are cleaved off by enzymes in the body once they are injected,
resulting in pure active testosterone. The esters allow the testosterone to be slowly released to
the body.
Synthetic testosterones are not identical to the testosterone our body produces. They undergo
different paths for metabolism and do not have the same activity (they may be more potent for
example), nor the same safety as the testosterone our body produces.
Examples of synthetic testosterones include methyltestosterone, Anavar, Nandrolone, and other
androgenic steroids.
__________________
Re: Adrenal Fatigue and Wilson's Glandular Extracts
Quote:
Originally Posted by Normandy
Anyone here with Adrenal Fatigue tried any sources of adrenal glandular extracts out
there?
Anyone have thoughts on the pros and cons? I'll be honest, it seems like a alot of bull to
me and somehow can't get past the notion that Dr.Wilson's site is all about making
money. But deep inside, im hoping there's something to his research after all.
Any of u guys have any success with it?
-- Normandy
The best adrenal glandular extract is IsoCort. It has the best standardized (albeit not published)
level of hydrocortisone. It is milder than the same mg of Hydrocortisone.
It is useful for treatment of Adrenal Fatigue/Adrenal Depletion (my new term for it, since most
doctors cannot understand the term "fatigue" as it applies to the adrenal glands. I sometimes use
the term "stress-induced adrenal insufficiency" though the term "adrenal insufficiency" has been
monopolized to mean only Addison's disease.).
The other adrenal extracts, I've found, tend to be too mild. They are useful for some people particularly those with milder versions of adrenal fatigue.
I don't like the Licorice that is often added to adrenal extract combination products because it
often leads to sharp drops in cortisol levels, leading to a person crashing with hypoglycemia and
dizziness when Licorice's effect wears off. Licorice also often causes nausea.
__________________
Re: Best way to raise DHEA-S?
Quote:
Originally Posted by Rangeball
Was wondering what the best way to increase DHEA-S is? As I understand it, if it's low it
can cause low Testosterone. However supplement straight DHEA seems to preferentially
convert to estrogens in males. 7-keto doesn't, but apparantly it can't convert to
Testosterone either, so what's the point taking it?
What about transdermal? Would that avoid the liver's conversion into estradial?
Taking DHEA does not necessarily increase estradiol in males. The other estrogens are much
weaker than estradiol. One can easily measure estradiol level to determine if adding DHEA will
increase estrogens. But then, estradiol can be controlled using an aromatase inhibitor.
The fear of conversion of DHEA to estradiol is unfounded. It is the increase in testosterone which
leads to the increase in estradiol. Does one avoid testosterone replacement then, if one fears an
increase in estradiol?
Taking testosterone will lead to an increase in estradiol since it is made directly from
testosterone.
DHEA-s is the way to measure DHEA since free DHEA itself varies too much to be useful as a
measure of DHEA. DHEA-s is the storage form of DHEA.
Taking DHEA is the best way to increase DHEA, hence DHEA-s.
DHEA has many important functions (other than converting to testosterone then to estradiol). This
includes maintaining sensitivity to insulin (i.e. reducing the risk of diabetes), reducing blood
pressure, improving mood, improving concentration, improving immune system function, reducing
abdominal fat, promote sex drive, increasing IGF-1 (the active portion for the most part of growth
hormone), etc. DHEA levels decline significantly as we age. Such a decline may itself promote
the changes due to aging due to the lost of DHEA's functions.
__________________
Re: Chronically High DHEA-S, is this bad?
Quote:
Originally Posted by wildfox
My DHEA-S numbers have always been at or just over the top of normal for the past year
and a half. Whether I take Testim, HCG+Arimidex, TCyp, Androgel or T Gel+HCG......it
doesn't seem to change the DHEA-S.
I do not take a DHEA supplement. I had a CT scan of the adrenals done and was told
they were fine.
None of the 5 doctors I've asked about this are concerned. They just ask of I take DHEA,
then say "hm" and move on.
One did say that he could order an ACTH stim test if I wanted, but what would that be
for? He also mentioned I could be lacking an enzyme, 3?-Hydroxysteroid dehydrogenase.
That doctor wouldn't explain this to me in any more detail.
Anyone familiar with this?
High DHEA is often a sign of stress. This includes exercise, physical illness, emotional, and
environmental stress.
ACTH stimulates the production of the adrenal steroid hormones including DHEA. If ACTH is high
(such as with a rare pituitary ACTH-secreting tumor), then all of the hormones would be
increased, not just DHEA. Such a tumor would cause darkening of the skin throughout the body
since melanin (skin pigment) is secreted when ACTH is made.
__________________
Re: Excessive Norepinephrine
Quote:
Originally Posted by mkl13
What is the best way to decrease high levels of norepinephrine? I've read some research
with dilantin, but was wondering if anything else has been shown effective. Thanks as
always..
Outside of a pheochromocytoma - a norepinephrine secreting tumor - which can be lifethreatening, there are numerous medications used to reduce norepinephrine activity. Which one
to choose depends on the condition being treated.
Norepinephrine is a neurotransmitter that signals the presence of stress. It also keeps a person
awake, alert. It helps improve focus. It triggers the male orgasm/ejactulation. It clears up the
lungs so one can breath more easily. It increases heart-rate and the pumping of blood by the
heart to improve the response for stress. It causes anxiety, fear or anger as a response to a
stress. It increases blood pressure so one can change positions and not faint. It opens one's
pupils so more light can come in. These, to name a few, are all appropriate functions when not in
excess.
When one has anxiety, medications to increase sensitivity to GABA (such as benzodiazepines
and antiseizure medications) can reduce norepinephrine production to reduce anxiety.
Medications that increase sertonine (such as Paxil, Prozac, Citalopram, etc.) also help reduce
norepinephrine production and reduce anxiety. Substances which can increase dopamine (such
as testosterone) may help reduce norepinephrine production.
When one has bipolar disorder (where high norepinephrine levels are associated with mania),
then Lithium may help reduce norepinephrine. Antiseizure medications may also help by
increasing sensitivity to GABA, blocking calcium channels or sodium channels, or through
numerous other mechanisms of action.
When one has hypertension, medications such as beta-blockers and alpha-blockers block
norepinephrine receptors, preventing norepinephrine from acting. Medications such as Clonidine
or Tenex act on pre-synaptic norepinephrine receptors, which results in a reduction in
norepinephrine production.
When one has insomnia, sedatives which increase sentisitity to certain GABA (such as Sonata)
help reduce norepineprhine.
When one has premature-ejactulation, often serotonin-increasing medications such as the SSRIs
(Paxil, Prozac, etc.) are used to reduce serotonin levels and prevent ejaculation.
Re: Excessive Norepinephrine
Quote:
Originally Posted by JanSz
I have a problem getting 3rd ejaculation over span of one week. The pines is hard and
functional but it lack sensitivity. I see from your comment that it may be about
Norepinephrine.
Any sugestions?
Being able to obtain an erection, but having difficulty in achieving orgasm is a condition which
may involve multiple neurotransmitters and hormones.
To achieve an orgasm, a rush of norepinephrine has to be produced by the brain to trigger
ejaculation. Multiple neurotransmitters and hormones, however, can inhibit the increase in
norepinephrine, preventing an orgasm.
Excessive serotonin, for example, can prevent orgasms and reduce sensitivity. This occurs, for
example, with serotonin reuptake inhibitors, such as Lexapro or Paxil.
Having too much testosterone can increase dopamine too much in the brain, inhibiting the
norepinephrine surge for orgasm. Maybe this is why male porn stars have to masturbate
themselves to orgasm.
Achieving an orgasm also requires having enough energy. When a person has adrenal fatigue or
hypothyroidism which is partly treated, then they may have energy enough to get an erection but
not enough to fully achieve orgasm.
__________________
Re: Excessive Norepinephrine
Quote:
Originally Posted by griffinannie
How does norepinepherine level or the ratio of noepinepherine to epinepherine play into
erectile dysfunction?
From my observations and inferences - not necessarily backed yet by literature:
Persistently high norepinephrine levels (which signal stress and lead to an increase in adrenal
hormone production) can eventually lead to adrenal fatigue/depletion which can cause sexual
dysfunction, including erectile dysfunction.
To increase norepinephrine production, the brain reduces dopamine production in addition to
other reductions in neurotransmitters (my observation). The reduction in dopamine leads to
sexual dysfunction.
Unverified, but another observation from a colleague, is that a high norepinephrine to epinephrine
ratio is associated with insulin resistance. This leads to a reduction in testosterone production,
which can contribute to sexual dysfunction (aside from diabetes type 2).
Re: serotonin resistance- it's real
Quote:
Originally Posted by DAVID
Many physicians said that low serotonin is the culprit with aging and insomnia. For sure
aging people have low sex hormone and serotonin resistance
My hypothesis is that aging people have more serotonin in the blood but have problem
with serotonin resistance... High carbs diet, low sex hormone and stress disturb serotonin
pathway
The whole country – meaning Baby Boomers – are being prescribed AmbienSR®,
Lunesta®, Sonata®, Prozac®, Zoloft®, Paxil®, Seraquel®, , Sarafem®, Effexor®,
Celexa®, Cipramil®, Seroxat®, Aropax®, Lexapro®, Cipralex®, Luvox®, Faverin®,
Cymbalta®, Wellbutrin®, Zyban®, Elavil® and Ativan®, Xanax® and Valium®. All of
these drugs have soporific side-effects and some of them are just garden variety sleeping
pills.
Mid-life means broken sleep and broken sleep means high serotonin levels that never had
the chance to convert to melatonin in the dark and drop while you slept, because you
didn’t.
Serotonin that can’t convert in normal daily rhythms up and down will enact a fear
response – like paranoia, panic or that feeling of trying to wade through peanut butter. In
nature, serotonin goes up in response to “fight or flight” scenarios because serotonin is
needed to metabolize stress hormones like cortisol.The drugs mentioned above are
predominantly SSRIs, some with a little nor-epinephrine effector added as a “chaser”.
SSRIs are medications that evolve their effects at the serotonin transporter. They increase
the level of serotonin by inhibiting its reuptake into the presynaptic void.Why would we
need drugs to increase our serotonin, when we never sleep and it can’t drop? Because
the range serotonin is in matters more than if it’s high or low. Low serotonin means no
impulse control, high serotonin means numb or no effect.
The more carbohydrate you eat the higher your serotonin goes. Self-medicating with cake
or pasta is just as effective as Paxil.
1. I would dispute the assertion that low serotonin is the primary cause of age-related insomnia.
Serotonin, other neurotransmitters, hormones, and immune-system cytokines are highly linked in
their production. The nervous system, endocrine system, and immune system form one system,
which I call the mind, which is organized like a computer chip circuit - where in place of electrons
traveling through wires, chemical messengers travel through a fluid to transport information.
There are thousands if not millions of these chemical messengers, which can work in
combinations.
This makes the mind much more extremely complex than the best computers (which only use
one messenger - the electron, which can transmit only one message (either on or off). There are
1.1 trillion cells in the brain which is the most important organ of the nervous, endocrine, and
immune systems. This combined with the billions of other nervous, endocrine, immune system
cells makes for an extremely complex information processing system.
The neurons which release serotonin, the neurons which release dopamine, and the neurons
which release norepinephrine, etc. exist as separate groups of neurons, which regulate large
groups of other neurons. These regulatory neurons are organized as circuits, which can in turn
control one another. For example, there are circuits of dopamine-releasing and serotoninreleasing neurons which reduce the release of norepinephrine from the norepinephrine-releasing
neurons. Some acetylcholine-releasing neuron circuits can control dopamine-releasing neurons.
Etc.
When serotonin is low, there may be other problems contributing to it which may be the more
direct factor in causing insomnia.
For example, when thyroid hormone is low (which occurs in up to 40-50 percent of people
depending on the country), serotonin production is lowered because thyroid hormone acting on
presynaptic serotonin receptors, determines serotonin production. Hypothyroidism can cause
insomnia.
When adrenal fatigue is present, norepinephrine production and release is increased to force
more output from the adrenal glands. To increase norepinephrine, the brain reduces serotonin
production. It is the high norepinephrine levels which keeps the person awake. Further, in adrenal
fatigue, the lower production of cortisol prevents cortisol from reducing Corticotropin Releasing
Hormone production. Reducing CRH causes a reduction in norepinephrine production.
2. Self-medication with carbohydrates is not the same as taking Paxil.
Paxil is a complex medication which has multiple mechanisms of action. For example, it
increases serotonin levels by blocking reuptake. It can block acetylcholine receptors. It can block
histamine receptors - which can cause sedation. It can block norepinephrine receptors. It can
increase norepinephrine level by blocking reuptake. it can increase dopamine level by blocking
reuptake or by increasing serotonin levels near some dopamine neurons, which have a dopamine
reuptake transporter which can be blocked by serotonin, etc. It can block Cytochrome P450 2D6.
etc.
Why do some people self-medicate with carbohydrates. The answer is that it serves a purpose.
What is that purpose? The answer is that the person has difficulty in producing their own
carbohydrates (i.e. glucose) from fat or protein because of impaired gluconeogenesis, which can
occur with cortisol deficiency, i.e. adrenal fatigue or insufficiency. The presence of cortisol
deficiency results in a rise in norepinephrine production and release, which then keeps the person
awake.
3. Melatonin deficiency can occur as one ages - as a consequence of the aging brain and
difficulty in producing melatonin - not serotonin.
Melatonin is made from serotonin. But the production of serotonin in serotonin-releasing neurons
is independent of the production of melatonin in the pineal gland. Melatonin production is
determined by the cycle of light and dark as sensed by our eyes, and by our internal body clock the suprachiasmatic nucleus of the hypothalamus. There are other timing circuits in the brain,
which may also contribute.
Remember that neurons are arrranged as circuits where the neurons produce their specific
neurotransmitter independently of other neurons (in general - there are exceptions such as nitric
oxide - which is a retrograde neurotransmitter). Norepinephrine-releasing neurons make
dopamine, then make norepinephrine from the dopamine. However, the dopamine is never
released. Only the norepinephrine is released. The dopamine production from norepinephrinereleasing neurons is independent of the dopamine production in dopamine-releasing neurons though the circuits can be arranged to control one another.
The majority (90 percent) of serotonin which can be measured in blood or urine is made in the
enteric nervous system (the gastrointestinal nervous system) - which is almost totally
independent of our central nervous system. The two can correlate many time. But there are
circumstances where they do not correlate, complicating the interpretation of the lab tests,
necessitating additional thought or problem solving or correlation with other data to determine
what is happening. If one is measuring blood or urine neurotransmitters, is the level reflecting
brain levels or is it primarily a enteric nervous system level? It is up to the skill of the practitioner
to determine this.
4. The ability to sleep will depend not only on the presence of melatonin (which is a timing signal
for sleep, but is not sedative itself), but the balance of inhibitory and excitatory neurotransmitters which in turn can be influenced by the activities of the hormones and cytokines. And in the big
picture, stress - whicn in a simplistic definition is anything that forces a person to get out of bed influences the production of neurotransmitters, hormones, and cytokines.
For example, if there is a predominance of norepinephrine (a signal from the sympathetic nervous
system indicating stress or a fight-or-fight condition, which also determines wakefulness and
alertness), or histamine (which helps determine wakefulness), or glutamate (which is involved in
synaptic plasticity and learning, which is also the main excitatory neurotransmitter, which can
cause cell death in excess), then a person is forced to stay awake as a side effect of the actions
of these excitatory neurotransmitters.
Why are these increased? Stress. Hypothyroidism. Adrenal fatigue. Testosterone deficiency.
Progesterone deficiency. Estrogen deficiency. Serotonin defiency (as in panic disorder or some
depressions). Dopamine deficiency. Excess pro-inflammatory cytokines. Etc.
There are many conditions which may lead to a higher level of excitatory to inhibitory
neurotransmitters - which then leads to insomnia. Serotonin is not the only chemical messenger
involved.
It is up to the person and their physician to determine what problems are occurring in concert that
can lead to the problem. Many times, it is more than a single neurotransmitter, hormone or
cytokine. Addressing only one will often lead to no improvement. All of the problems have to be
found and solved.
__________________
Re: serotonin resistance- it's real
Quote:
Originally Posted by Andromeda
I'm so glad that you bring in all this useful information because I often find with all the
points you raise in answering someone elses post you also answer a lot of other peoples
problems. Tell me if I've got the following right....
A couple years ago I was discussing neurochemistry with a lay person who knew next to
nothing about the neurotransmitters etc. yet he made one comment which in hindsight
seems to be the most insightful point of the whole conversation ie: "Adrenaline and
Dopamine are all related "
In my particular case I have been trying to find out the reason for my poor energy and
lack of sex drive for years now and while I know theres probably a lot more to it than
neurochemistry, I am fairly sure I am low on dopamine. Adrenal fatigue has been
suggested as the source of my problem, and now it makes sense in light of your point I
have quoted above.. Tell me if this explanation is valid....
Low cortisol leading to hypothalamic over emphasis on CRH production leading to high
norepinephrine at the expense of Dopamine production. Lower dopamine then leading to
lower testosterone and therefore even less adrenaline effectiveness, and a tendency to
estrogen dominance exhibited in the form of gynecomastia
Also I recall another post you made recently saying that sexual activity is only something
that can take place properly in a 'relaxed' mode of bodily function. Is it possible that
excessive NE levels through adrenal fatigue keep my body in a 'non relaxed' state and are
thus the source of my poor erections due to vasoconstriction etc.?
I'd love to hear your critique of my above theory - It could be a milestone in figuring out
whats going on... and if anyone feels like I'm hijacking a thread please let me know and
I'll do this as a private msg with Marianco...
Cheers in advance,
You are close.
Norepinephrine = Noradrenaline
Epinephrine = Adrenaline.
Norepinephrine (Noradrenaline) and Dopamine are linked. Epinephrine (Adrenaline) is a minor
neurotransmitter in the brain.
Norepinephrine is the primary neurotransmitter to signal the occurrence of stress.
Norepinephrine is the primary neurotransmitter of the fight-or-fight part of the nervous system,
called the sympathetic nervous system.
In order to increase norepinephrine production and release from the norepinephrine-releasing
neurons, the neurotransmitters, which inhibit norepinephrine production, need to be reduced from
their respective neurons. These neurotransmitters include serotonin, dopamine, and GABA.
Norepinephrine increases adrenal hormone production by stimulating the release of Corticotropin
Releasing Hormone (CRH) from the hypothalamus. CRH then increases Adrenocorticotropic
hormone (ACTH) release from the pituitary. ACTH then travels to the adrenal glands to stimulate
steroid hormone production - the primary one being Cortisol.
Norepinephrine also triggers a signal that goes through the sympathetic nervous system nerves
which travel parallel to the spine. These nerves then trigger the production of Norepinephrine and
Epinephrine from the center of the Adrenal Gland. The adrenal gland, itself, is an enlarged
ganglion of the sympathetic nervous system.
What is interesting about CRH is that it travels not only to the pituitary to stimulate ACTH
production, but it also travels to the rest of the brain, where it stimulates Norepinephrine release.
CRH thus participates in a positive feedback loop - where increased Norepinephrine results in
increased CRH - which then increases Norepinephrine release. If this positive feedback loop is
not stopped, the stress signal is magnified repeatedly. If not curtailed, this stress signal snowballs
and causes panic attacks. If it is stopped, then the stress signal is stopped.
What stops this positive feedback loop is Cortisol. Cortisol produced from the Adrenal glands
goes to the hypothalamus and reduces CRH production - a negative feedback loop. The
reduction in CRH reduces ACTH and reduces adrenal hormone production. The reduction in CRH
also results in a reduction in Norepinephrine release.
In adrenal fatigue, the adrenal glands do not adequately produce Cortisol in response to stress.
The lower Cortisol production then fails to stop the CRH-Norepinephrine positive feedback loop,
causing a person to be susceptible to any stress, large or small. This results in an almost
constant high level of stress. Stress can't be stopped.
The brain responds to the lack of Cortisol from adrenal fatigue - which causes a deficit in glucose
production - by increasing norepinephrine production. This ends up further increasing stress
levels. It forces the adrenals to work harder, but it also pushes the adrenals further into fatigue.
High norepinephrine levels signal that the person is in a flight-or-fight condition. Sexual function is
inhibited. For example, I doubt that any soldier in combat exhibits an erection.
If there is some sexual function, since norepinephrine triggers ejaculation, the already high
norepinephrine level makes ejactulation much easier to occur. This causes premature
ejactulation.
Since dopamine production is reduced to allow higher norepinephrine production, sex drive can
be further reduced by lower dopamine levels.
The lower dopamine levels may also reduce testosterone production.
Testosterone, itself, increases dopamine production in the brain. The reduction in testosterone
production also results in a further reduction of dopamine production in the brain, further reducing
sex drive.
If the dopamine production is low enough and involves dopamine neurons in the hypothalamus,
then prolactin production can increase. Prolactin can then reduce testosterone production, and
possibly contribute to gynecomastia - if the prolactin elevation is high enough - which it may not
be.
Gynecomastia may occur alternatively when there is a high level of estradiol or when the potency
of estradiol is increased by progesterone.
In the scenario of adrenal fatigue, there is lower testosterone production from the adrenal glands
themselves. The adrenal glands provide about 5% of total testosterone in men.
The reduction in testosterone results in less estradiol production from testosterone. This and the
lowered progesterone production during adrenal fatigue makes it less likely that gynecomastia
occurs - in general. This will depend on multiple factors such as the amount of aromatase
enzyme a person has - with those using HCG or those with high abdominal fat having a larger
amount of aromatase enzyme.
The ability to have an erection depends on numerous neurotransmitters and hormones, not just
norepinephrine. Vasoconstriction of the outlet blood vessels from the penis is what allows the
filling of blood which causes the erection - the penis being similar to a balloon.
__________________
Re: serotonin resistance- it's real
Quote:
Originally Posted by Andromeda
Oooer a wealth of useful information once again.... I might actually get somewhere with
this soon!
In my research into adrenal fatigue I started with the basics of adrenal function, and I
learnt that ACTH activates both the adrenal medulla (part of adrenals that produce
epinephrine and NE) and the cortex (Cortisol and DHEA)
From your response above it seems to be that most ppl with adrenal fatigue suffer
primarily fatigue of the cortex while the medulla continues putting out normal NE levels?
Is this the case? I thought both would fatigue at a similar rate (generally) ? If not, why...
Additionally, if a person exhibited low salivary cortisol plotted throughout the day, yet
they had high progesterone, and DHEA levels, then must they have some sort of
enzymatic problem in the creation of cortisol, rather than primary adrenal fatigue?
Cheers
Norepinephrine secretion from the locus ceruleus of the brain, result in two signals to the adrenal
glands.
First, the norepinephrine signal results in an increase in ACTH secretion from the pituitary gland,
which travels to the adrenal glands and stimulates adrenal cortex hormone production - the
steroid hormones such as Cortisol, DHEA, Progesterone, Testosterone, Aldosterone.
Second, the norepinephrine signal travels down the sympathetic nerves parallel to the spine to
the adrenal medulla, where it triggers the production of norepinephrine and epinephrine.
Both parts of the adrenal glands do not fatigue at the same rate. Most people have fatigue of the
cortex - which is the part that fatigues first - before the medulla fatigues.
A synonym for adrenal fatigue is "adrenal depletion".
Re: serotonin resistance- it's real
Quote:
Originally Posted by Andromeda
Wow, talk about misconceptions - I thought that all adrenal output was exclusively the
result of the Pituitary ---> Adrenal pathway by ACTH! So the locus coreleus is a source
itself ....
As to why most people suffer fatigue of the cortex first is there a reason?- Is it because
most people are parasympathetic dominant, and therefore the cortex ends up being taxed
more frequently out of the two adrenal regions?
By all means tell me if this theory is mistaken too, as I've encountered apparent
contradictions. For example, in my research into the ANS I learnt that the
parasympathetic nervous system innervates the adrenal cortex (Cort), where as the
sympathetic system innervates the medulla (NE) Yet at the same time I read that higher
parasympathetic activity means lower cortisol. The only way I can reconcile this is that
sympathetic dominance means more NE and therefore more CRH output with the net
result being higher Cort. Whereas in parasympathetic dominance the NE is low to begin
with because it is only linked to the adrenals by the cortex which means less NE and its
subsequent cortisol inducing loop.?
OR, is it the case that in parasympathetic dominance the body usually has more cortisol
to start with (before encountering a stressful situation), and therefore the whole locus
coreleus activity and emphasis on NE production is usually less?
Keen to hear your thoughts.. I think the implications could be huge given our ability to
manipulate the ANS with techniques such as unilateral nostril breathing and diet etc...
Andromeda.
As far as I know, there is both sympathetic and parasympathetic innervation to the adrenal
medulla and adrenal cortex. Note that the adrenal gland itself can be considered an enlarged
ganglion of the sympathetic nervous system.
I do not use the terms "parasympathetic dominance" or "sympathetic dominance". This is too
extreme an oversimplification of what is occurring. It leads to confused conclusions as a result.
The sympathetic and parasympathetic nervous systems may act antagonistically in many
circumstances, but they can also act toward the same goals.
For example, the ability to have sex is both a sympathetic and a parasympathetic nervous system
activity. The parasympathetic nervous system plays a role in maintaining an erection. The
sympathetic nervous system triggers the ejactulation. Both are necessary.
Digestion is another example. Digestion is also a parasympathetic nervous system activity. But
eating food also stimulates the sympathetic nervous system, thus helps keep a person awake.
Digestion requires production of cortisol from the adrenal glands to help reduce inflammation that
occurs from the digestion of food.
The adrenal cortex may be the first to be depleted or fatigued because it has a larger job to do
than that of the adrenal medulla. The cortex has to modify cholesterol - a larger molecule than an
amino acid - into about 150 different forms. The cortex has also a larger and more diverse role to
play than the medulla - e.g. maintaining salt and fluid balance and blood pressure, maintaining
activity of the immune system and help fighting infections, reducing inflammation and helping
digestion, maintaining blood sugar and energy, burning fat, maintaining mood stability,
responding to stress, maintaining brain function such as the myelin sheating of neurons,
controlling memory and attention, maintaining sex drive, helping activate thyroid hormone, etc.
After menopause, for women, the adrenal glands become crucial for producing all of a woman's
steroid hormones - testosterone, estradiol, progesterone, aldosterone, cortisol, DHEA, etc.
__________________
Re: Looking for some input ahead of my doc appointment
Quote:
Originally Posted by Rangeball
Hello all.
I posted here quite a while back for awhile, and still lurk. I'm a 42 year old male, and I
was diagnosed hypothyroid over a year ago, and have been slowly working my way up
the armour doseage scale. My doc is a general surgeon and GP, and a family friend. He
was out of his comfort zone on the armour and bigger doses I kept requesting since my
TSH all but dissapeared but my FT3 and 4 levels were still in the tank. I have a 2.5 grain
script for armour from him, and am using thyroid-s to supplement and increasing on my
own with help from others who've gone before me. I focused on Thyroid as swale said it
can mimic hypogonadism and should be treated first. I found I needed to start isocort as I
wasn't tolerating the armour at higher doses, and have been using it for a few weeks now
with good results.
In denying my last request for an armour bump, my doc said other things could cause the
symptoms I am experiencing, primarily low libido, weaker erections, brain fog, poor
memory, low energy and down mood. So I asked to run a bunch of tests, and he agreed.
Results were as followsVitamin D Panel*
Vit D, 1,25-Dihydroxy- 47 15-60 range
Vit D, 25-OH, total- 24 20-100 range
Vit D, 25-OH, D3 24
Vit D, 25-OH, D2 <4
*Measurement of 25-OHD2 is an indicator of compliance with supplements. Levels >4
suggest compliance. 25-OHD3 indicates endogenous production. Therapy should be
based on measurement of Total 25-OHD, with levels <20 suggesting Vitamin D
deficiency and levels between 20 and 30 suggesting a possible need for supplementation.
I am supplementing Vitamin D3 at 4000 IU daily.
Vitamin B-12 469 200-1100 range
From what I've read, while in range it's still low. I supplement sublingual B12 tabs daily.
Estradiol (ultra sensitive) 20 10-50 range. This one suprised me. I was sure it would be
eleveated. According to Swale I'm right in the sweet spot, iirc.
Cortisol- 7 5-21 range for males sample taken 8-10 am.
While in range, still low, just like I suspected. I plan to continue the isocort to allow my
adrenals to heal since they've obviously been picking up the thyroid's slack.
SHBG- 44 8-46 range. No wonder.
Total Testosterone- 436 250-1100 Much lower than it should be. I'm 42
Free Testosterone- 47.7 35-155 Hmmmm...
% Free Testosterone- 1.09 L 1.1-2.8 range. Not good.
DHEA-S- 257 43-345 range. From what I've read this should be higher. I supplement it
now daily with 50 mg DHEA, will switch to 7-keto to avoid estrogen conversion soon.
FSH- 5.6 1.6-8 range
LH- 4.8 1.5-9.3 range Looks like the boys are getting called on, they're just not up to it?
Prolactin- 6.1 2.0-18 range. I've read where this is high for males with prostate cancer,
but can't find much for normal males.
Sorry for the long post, but I meet with my doc next thursday to discuss TRT. I've emailed
him my thoughts and Swale's protocol. I have drug insurance that would cover androgel,
and if transdermal work will eventually compound my own to lower my cost. Pellet
therapy sounds interesting, but I don't think my doc does it.
Ahead of my appointment I'm trying to brush up to be prepared. With my results, do I
have Primary, secondary or central hypogonadism? I've printed out charts that show the
symptoms of low T, I have most of them. I wanted to print out the graph that shows
average T levels by age, but that red line that says "recommended treatment level" is
lower than my total T, so I'm not sure that I should. My super low Free T bothers me, and
is probably the root of my remaining symptoms.
Any help you guys can pass my way would sure be appreciated.
Thanks for taking the time to read this long ass post...
Low free testosterone means there is relatively high SHBG, which means there is a problem
involving one or a combination of thyroid hormone, progesterone, testosterone, DHEA, insulin, or
growth hormone, and other androgens.
SHBG is raised by high thyroid, high estradiol, high progesterone, low testosterone, low DHEA,
low insulin, or low growth hormone, or a combination.
__________________
Re: Looking for some input ahead of my doc appointment
Quote:
Originally Posted by Rangeball
Thanks.
I did plan to test DHT and I guess now progesterone before I started TRT if that is the
way my doc is headed.
Marianco, if a patient presented to you with the listed symptoms and labs, what would be
your approach or recommendation? If there is a fixable cause that would prevent me
from being tied to TRT, I'm all ears, and trying to be informed ahead of my visit this
week.
The top dose for Armour Thyroid is 300 mg a day (about 5 grain). If a person is still having
problems at this dose, then it is highly important to evaluate for other causes of his/her
symptoms. For example, are there other contributing factors such as an inability to activate T4 to
T3 due to problems with the deiodinase enzymes? Is adrenal fatigue significant so that it
interferes with the activation of thyroid hormone? It is important to get follow up evaluations and
have good parameters to measure because a person should avoid hyperthyroidism since it risks
atrial fibrillation and congestive heart failure, among other effects.
IsoCort may be too mild for many people with adrenal fatigue - and costly when very high doses
are used. Appropriate doses of Hydrocortisone, Medrol, Prednisolone, or even Prednisone may
be necessary to use instead.
Ideally (though the world is not ideal), treatment of hypothyroidism and adrenal fatigue is done
before testosterone replacement (particularly in a person with testosterone over 400 ng/dl). When
thyroid hormone and adrenal hormone activities are optimized, sex drive, fatigue, depression, and
other problems can improve significantly even with low testosterone levels. What a physician
does will, of course, depend on a person's condition and situation. The treatment has to be
customized to the person.
__________________
Re: Looking for some input ahead of my doc appointment
Quote:
Originally Posted by Rangeball
I've been self monitoring for hyper-thyroid, and whenever I feel it is a possibility I back
down on my armour. Since starting armour (at 1 grain with a re-test every 6 weeks and a
.5 grain bump up to 3 grains then back down to 2.5 because my TSH bottomed out) I've
had brief moments where my symptoms resolved, but each time returned as endogenous
production slowed in response to the armour. So you feel I should see if I can get up to 5
grains if needed and not pursue TRT until I've done so if symptoms are not resolved?
I've been trying to locate hydrocortisone. I can't convince my doc to go any higher with
the armour (I'm doing so myself and am up to 4 grains) so I'm doubtful he'll give me a
script fo the hydrocortisone. I've been upping isocort, but it's not really helping and I'm
concerned doing so because of the company's reluctance to disclose it's ingredients and
amounts (I understand it's not standardized).
If the brain is unable to measure Free T3 correctly and thus produces too little TSH when Free T3
is low (e.g. due to aging, brain injury, etc.), then TSH becomes a less important measure. Rather,
it is more important to measure Free T3 and Free T4 to determine the course of treatment, in
addition to the person's signs and symptoms.
IsoCort is standardized. However, if the company advertises that it contains hydrocortisone, then
it would get into trouble with the FDA - which would then benefit no one.
Re: Looking for some input ahead of my doc appointment
Quote:
Originally Posted by Rangeball
Marianco, as I stated I am trying to find hydrocortisone to replace the isocort. This may
prove to be a long, drawn out process.
In the interim, what are your thoughts on using nettle root, dim or saw palmetto to bind
up some SHBG and possibly free up some testosterone?
If not these, would you recommend anything else?
Most physicians are more familiar with Prednisone, which is approximately 4 times more potent
than Hydrocortisone.
Free Testosterone does not reflect testosterone's activity. Total testosterone is the best measure,
in my opinion. Bioavailable testosterone is the second best measure. Free Testosterone primarily
serves as an indicator that there is something wrong with one or more hormones including:
insulin, thyroid, estrogen, progesterone, testosterone, DHEA, growth hormone.
SHBG serves a purpose. When bound to testosterone or estrogen, it can bind to SHBG receptor
and transmit signals to cells. SHBG prolongs the life of testosterone - helping maintain a higher
total testosterone level.
Re: Looking for some input ahead of my doc appointment
Quote:
Originally Posted by Rangeball
One more question then I promise to wait until you respond
What are your thoughts on my prolactin levels? I've had some tell me they are elevated
and should be closer to 2, but the only info I can find to back that up is in men with
prostate cancer history.
Based in the current knowledge I have, when Prolactin is within the reference range for men, then
the level is fine.
Prolactin is elevated under certain circumstances including:
1. When dopamine levels are low - such as after an orgasm
2. When there is a prolactin-secreting pituitary tumor
3. When taking a medication (such as an antipsychotic) which blocks dopamine
Re: Best test for Dopamine?
Quote:
Originally Posted by kimura
My prolactin has tested high. The following two comments are from marianco:
8. When prolactin level is high, dopamine production may be low. It is important to
determine if there is a pituitary tumor via MRI which is affecting prolactin production.
9. When dopamine production is low, it is important to determine if there are
neurological problems, such as Parkinson's Disease, which affect dopamine levels.
I'm not sure if my prolactin is high enough (14ng/mL 3-13) to warrent the MRI or
dopamine test but I'll ask for them when I see my primary care doc tomorrow.
So- what is the best test for dopamine? blood, 24hr urine, other? LabCorp has a few
different tests listed on their website. Are there any other related tests I should ask for
while I'm there?
Thanks
A conventional lab test for dopamine, norepinephrine and epinephrine would be the 24-hour
fractionated urinary catecholamine test and tests for their metabolites. This is a test for a
catecholamine secreting tumor such as a pheochromocytoma. The problem of this test is that it is
not sensitive enough for lower levels of dopamine, norepinephrine and epinephrine for conditions
other than cancer.
A spot urine neurotransmitter test can be obtained from labs such as sanesco.net or
NeuroScience, inc. This correlates pretty well with functional problems such as depression,
anxiety, sexual problems, impaired cognition, etc. However the test is not a recognized standard,
the practitioner has to register with the lab to order it, and the test is paid out-of-pocket (not
covered by health insurance generally). It is often relegated by conventional physicians to the
"alternative medicine" bin.
__________________
Re: how after many days who can check free and total testosterone
Quote:
Originally Posted by DAVID
When you take a new HRT like androgel, how after many days who can check free and
total testosterone with estradiol ?
Changes in total testosterone and estradiol are fairly rapid. They can be checked in a week to two
weeks if one uses a gel. They can be checked in days after an injection - the number of days
after an injection depends on the purpose of the test (e.g. checking for peak or trough values,
etc.).
However, changes in free testosterone depends on changes in the activity or production of
multiple hormones - thyroid, estrogens, progesterone, testosterone, growth hormone, DHEA,
insulin, etc.
Changes in these hormones may take months. Free testosterone would thus be a moving target.
If testing for free testosterone, the earliest would be about a month out from starting. But in
reality, it may be best to check it three months to 6 months later, once the effects of testosterone
replacement are more stable.
For example, if one has significant abdominal fat resulting in insulin resistance (and high insulin
levels), then it will take a while for the abdominal fat to disappear with testosterone replacement.
It may be prudent then to check free testosterone after 3-6 months.
Nonetheless, the cost of total testosterone alone is about the same as a free and total
testosterone panel (which includes SHBG and albumin). Thus, free testosterone can come along
as an almost freebie.
__________________
Re: trt and infertility
Quote:
Originally Posted by ili
One more question,am I primary or secondary? intilal lab work was:
sTSH- 1.80---------norm is0.35 -- 5.00 mu /l
LH---- 1. ---------norm 1------10 iu/l
DHEAS 4.0 -------norm 2.6--- 7.7 umol/l
FSH 1. ----------norm 1---- 14 iu/l
Prolactin 12. ------norm <18 ug/l
estadiol 88 ---------norm 50---218 pmol/l
My free test was 29.6 norm--37--81
What do you think?
Thanks
Testosterone replacement can reduce fertility by decreasing LH and FSH production.
HCG is an option when one wants to maintain fertility. Clomid is another - at least temporariliy - to
increase sperm production.
TSH < 2.0 does not rule out hypothyroidism. Free T3 and Free T4 need to be done to determine if
hypothyroidism type 1 is present. A history and physical exam is needed to determine if
hypothyroidism is present, not matter what the type (e.g. type 2, etc.). Hypothyroidism reduces
testosterone production.
Primary hypogonadism is when there is testicular failure to produce testosterone. When primary,
there is no other choice but to do testosterone replacement (since HCG or Tamoxifen or Clomid
wll no longer work well to stimulate testosterone production)
Secondary hypogonadism is when the testes can produce enough testosterone but due to other
reasons (e.g. pituitary problems, other hormone problems, etc.), the signals to promote
testosterone production are not adequate.
Stress does reduce sex drive. Sex is a rest-relaxation activity. Vacations are times people relax
and rest. The neurotransmitters are in different levels of activity in rest-mode and fight-or-fight
mode.
__________________
Re: trt and infertility
Quote:
Originally Posted by marianco
Testosterone replacement can reduce fertility by decreasing LH and FSH production.
HCG is an option when one wants to maintain fertility. Clomid is another - at least
temporariliy - to increase sperm production.
Additionally, sometimes HCG (which emulates LH) and the testosterone increase that results are
not enough to stimulate sperm production. In that case Pergonal (which has LH and FSH) can be
used to help stimulate sperm production.
__________________
Re: trt and infertility
Quote:
Originally Posted by ili
Very interesting,so first a trial with hcg,get tested for fertility,if no luck,add the hmg?how
long with the hcg first,1 month 2 or 3?
Thanks
The best person to answer that question is a reproductive endocrinologist who treats male
infertility.
How long to take HCG would depend highly on the results of the lab evaluation of sperm to see if
improvement has occurred with HCG.
__________________
Re: Low Free Test
Quote:
Originally Posted by eeso
I'm off HRT, here are my most recent labs. 23, in shape, weight trainer. Was on HRT for
2 years, came off a few months ago. I've done some searching of the forums and found
some similiar senarios but no answers, so I thought I'd do my own thread.
Cortisol 800 nmol/L (220 - 660) High
TSH 4.5 pmol/L (0.40 - 4.00) High
free Thyroxine (ft4) 16 pmol/L (10-20)
free T3 5.4 pmol/L (2.8-6.8)
LH 9 U/L (3-20)
FSH 5 U/L (3-20)
Estradiol 134 pmol/L (40-250) High - should be 36-110
Progesterone 2 nmol/L ( < 3)
Testosterone 21 nmol/L (10.0 - 33.0)
Free Test 61 pmol/L (60-130) Low
SHBG 15 nmol/L (13-71)
I also had DHEA done and it was midrange I think, I don't have the copy.
Anyway, my free test sucks and I feel lousy. I get pretty lethargic the day after big
workouts. I generally feel "ok" but I have ZERO sex drive, and when I do get it up I seem
to have premature ejac??? I've never had this before. When I was on HRT, it was a bit of
guess work getting my levels right, but when I did I could go for aaages. Now I can't even
get it up hardly and when I do I'm done!! Not good.
I've tried using arimidex to lower my E2 to try and boost my Free Test but I don't seem to
be feeling any different.
The doc wants me to get some more blood tests in a few weeks to see if my TSH is still
high. Should I get an insulin sensitivity test? Or anything else?
It's wierd because when I was on TRT my free test was really good. Like, my total test
would be high 20's the day after a shot, and free test would also be right up there. But
now I'm natural and total test is ok, yet free test sucks!
All comments most welcome.
Thanks
It would be best to convert the units into conventional units rather than leave it as ISO units, so
that more of us can understand what is occurring.
Cortisol = 800 nmol/L = 29.0 mcg/dl
TSH = 4.5 pmol/L
Free T4 = 16 pmol/L = 1.24 ng/dl
Free T3 = 5.4 pmol/L = 350 pg/dl
LH 9 U/L (3-20)
FSH 5 U/L (3-20)
Estradiol = 134 pmol/L = 36.5 pg/ml
Progesterone = 2 nmol/L = 0.63 ng/dl
Testosterone = 21 nmol/L = 605 ng/dl
Free Testosterone = 61 pmol/L = 16.6 pg/ml
SHBG = 15 nmol/L (13-71)
CORTISOL, PROGESTERONE: high cortisol indicates that a person is under stress. Low DHEA,
low Progesterone (< 1.0), low to low normal glucose (e.g. < 93 mg/dl) are clues that adrenal
fatigue may be occurring even with a high cortisol. A saliva cortisol measurement with at least
four samples in a day may indicate the presence of adrenal fatigue.
TSH, Free T3, Free T4: TSH > 2.0 or Free T3 < 3.3 or Free T4 < 1.1 is suspicious for
hypothyroidism. This can be verified by history and physical exam. Many people have normal
thyroid hormone levels. However they are still clinically hypothyroid (by history and physical).
These people may have hypothyroidism type 2 - thyroid hormone resistance due to defective
mitochondrial DNA. Despite normal thyroid hormone levels, they actually need more. There is no
test for hypothyroidism type 2. The best test is a trial on thyroid hormone (e.g. Armour Thyroid).
TESTOSTERONE: A total testosterone over 600 ng/dl generally would not indicate the need for
testosterone replacement. If there are problems such as lack of energy, low sex drive, premature
ejactulation - then there are problems with the other hormones or neurotransmitters - not with
testosterone. Testosterone treatment may indirectly improve these other hormones - such as by
improving thyroid hormone production - resulting in improved functioning. But it would be best to
address the other hormone problems directly.
ESTRADIOL: Depending on the person, estradiol can be too high or too low. Some men, for
example, benefit from maintaining estradiol below 30, some need a level closer to 40, some like it
between 20-30, some like a ratio of testosterone to estradiol of about 20:1, some do better at
40:1. It all depends on the individual. High estradiol - such as from having significant abdominal
fat - can increase thyroid binding globulin. This can cause a relative decrease in thyroid
hormones, causing hypothyroidism. Estradiol also can compete with thyroid hormone for the
thyroid hormone receptor, reducing thyroid hormone's effects.
FREE TESTOSTERONE, SHBG: Free testosterone does not indicate testosterone's activity.
Total testosterone is the best measure of testosterone's activity. Bioavailable testosterone is a
close second. Free testosterone is related to SHBG and Albumin. Since Albumin is usually
steadily produced unless one has severe dehydration or some life threatening disease, Free
testosterone is most closely linked to SHBG. Free testosterone when high or low tells us there is
a problem with one of several hormones. A Free testosterone can be normal when two opposing
hormonal problems cancel each other's effect on SHBG. SHBG is increased by thyroid, estradiol,
progesterone. SHBG is lowered by testosterone, DHEA, insulin, growth hormone, and other
androgens. Conditions where SHBG can be low include: hypothyroidism, low estradiol (low
aromatase), low progesterone (such as in adrenal fatigue), high insulin (as in diabetes or insulin
resistance), high testosterone or DHEA.
__________________
Re: Low Free Test
Quote:
Originally Posted by 1cc
Your DHT is probably whats causing your problem because of the finasteride use. Have
DHT checked.
When lack of energy is a symptom, generally the thyroid glands or adrenal glands or both are
affected by whatever underlying problems there are.
Hypothyroidism and Adrenal Fatigue/Adrenal Depletion can result in low sex drive.
For example,
if a person has too much estradiol, the estradiol can increase thyroid binding globulin to the point
of reducing available thyroid hormone excessively.
If a person has low testosterone production, then less thyroid hormone production may result,
depending on the person.
If a person has high stress levels, then the adrenal glands may become depleted, resulting in
fatigue.
If the pituitary ages and is not capable of producing enough TSH, then low thyroid hormone
production may result.
If a person has mania of bipolar disorder, the high norepinephrine levels can lead to adrenal
depletion and fatigue.
etc. etc.
Re: Low Free Test
Quote:
Originally Posted by 1cc
You are correct Marianco and have addressed his problem comprehensively. I forgot to
qualify my post in that it was in reference to his ED problem, which he mentioned in a
different thread. I know someone however you did "crash" with extreme fatigue after
taking finasteride for one week.
The question would be why would finasteride cause extreme fatigue. It is unclear why it would do
this.
Finasteride works by blocking 5-alpha-reductase. There are three types. Finasteride blocks one
of them, but may also block the others to a lesser extent but that may depend on the person.
5-alpha-reductase transforms testosterone into dihydrotestosterone. Blocking the enzyme
reduces DHT, resulting in hair-growth for some men.
5-alphe-reductase also happens to have other important functions. In the brain, it transforms
progesterone into allopregnenolone. Allopregnenolone is the signal for brain glia cells to wrap
neuron axons with the insulating material called myelin, so that nerve signals can travel faster. If
this function is impaired, then nerves may lose their insulation, resulting in havoc in the brain.
Nerve signals can be short-circuited, for example by traveling to neighbor neurons which were not
suppose to receive the signal. Such a situation may take possibly a long time to correct,
producing the problems from Finasteride which some people experience. Note that the large
majority of men who use Finasteride do not get these side effects, as far as we know, and as far
as the FDA knows. But some men are susceptible to it.
If the metabolism of progesterone and potentially other hormones which depend on 5-alphareductase function is disturbed, perhaps since progesterone is also made by the adrenal glands,
then impairment of cortisol production may occur, resulting in a condition like adrenal fatigue. The
reduction in cortisol production may also lead to an impairment in deiodinase enzyme activity,
resulting in lower thyroid hormone. These and other metabolic cascades may be contributing
factors to why some people with Finasteride have problems.
This is speculation on my part, though some articles note problems when 5-alpha-reductase
blockade occurs.
__________________
Free Testosterone
Quote:
Originally Posted by Gator8
My primary doc who is treating me for diabetes, fatigue, fibromyalgia, pain and a whole
host of other issues ran a free-t test which came back at 2.8 on a normal lab range of 6.528. He prescribed Androgel packets and tested after two weeks. The result with two
weeks treatment was 15 for a normal lab range of 7-24. The second test was run by a
different lab.
After a month of Androgel, my prescription plan formulary declined Androgel, saying
Testim was required instead. I had trouble with itching and some other issues and I had
questions about supplementing t vs stimulating the pituitary with hgc. So I consulted an
endo I had never visited before.
The endo explained that primary vs secondary should be examined first. That makes
sense to me and more tests were run after a few weeks without any t. LH, FSH and free-t
were checked a few weeks off-t supplementation. He calls to say all tests are normal and
t-gel is not needed and not warranted, not advised. I'm thinking he said 14 but I didn't
really hear the numbers.
I don't understand how free-t can be this low before treatment and then be "normal" later
without treatment. I am waiting for the lab to mail me my test results for my own eyes to
see. My suspicions are aroused after reading here and elsewhere. It would almost be
remarkable for my free-t to be "normal" considering 30 years of diabetes for this obese
55 yo and varicocel on each testicle.
Comments?
Free Testosterone is not the best way to determine whether or not one has a deficiency of
testosterone.
Free Testosterone is not a reliable lab test, for one. It measures a tiny fraction of the total amount
of testosterone.
Free Testosterone is not an independent measure. It is highly dependent on the amount of Sex
Hormone Binding Globulin and less so on albumin (which tends to be a stable value unless there
are large changes in protein intake or loss or dehydration or overhydration)
Sex Hormone Binding Globulin is in turn highly dependent on numerous other hormones. SHBG
is raised by thyroid hormone, estrogens, progesterone. SHBG is lowered by testosterone, DHEA,
DHT, Growth Hormone and Insulin (e.g. high insulin levels from insulin resistance or diabetes
type 2).
Free Testosterone is not representative of testosterone activity. Rather it represents the sum of
testosterone, DHT, DHEA, growth hormone, insulin, thyroid hormone, estrogens, progesterone,
and other androgens. It is a mess of a measure.
The only use of Free Testosterone is to indicate whether or not there is a problem with these
hormones. Since some raise and some lower Free Testosterone, they can also cancel each other
out, therefore telling nothing about hormone function.
The best indicator for testosterone activity is total testosterone. Second is bioavailable
testosterone. Bioavailable testosterone is actually a calculated value - not a measured one which is obtained by formula from the total testosterone, albumin and SHBG values.
I think a person should have the right to find out what their lab findings are. This way they can see
for themselves what is up.
In an obese person with diabetes, Free testosterone can conceivably be normal. This is because
the high insulin levels in diabetes type 2 can be negated by low testosterone from diabetes, and
higher estrogen production from abdominal obesity. Abdominal obesity can also cause a relative
hypothyroid state via higher estrogen production causing an increased production of thyroid
binding globulin. The low thyroid acvity can then reduce SHBG and lower testosterone
production, throwing another complicating factor into the mix. Free Testosterone is a useless
measure in this circumstance.
By the time men are about 50 years-old, many will have some age-related secondary
hypogonadism from the aging pituitary being unable to produce enough LH, and some agerelated primary hypogonadimsm from aging testes which are not responding to Luteinizing
hormone as when younger. This and other complicating factors (such as hypothyroidism and
diabetes) is why about half of men 50 years old are hypogonadal and reaching for Viagra.
__________________
Deiodinase
Quote:
Originally Posted by Gator8
I see your points. It's not clear to me why "free testosterone" is the only test first run.
Perhaps cost and insurance was a consideration. Is "free testosterone" so non-specific
that a measurement of 2.8 for a lab norm of 6.5-28 is useless for making a yes or no
decision?
I've had thyroid tests numerous times, always normal except for "reverse T3". What is the
significance of high reverse throid other than it's inactive?
Free Testosterone is run under the assumption that it indicates the testosterone that is actually
"active" - meaning the testosterone that is not loosely bound to albumin or tightly bound to SHBG.
This is a wrong assumption. Testosterone that is loosely bound to albumin is also active.
Testosterone bound to SHBG also has signaling function at SHBG receptors.
The physicians who use Free testosterone also don't realize that many hormones determine free
testosterone. Further Free testosterone can be normal while total testosterone can be very low
(e.g. 170 ng/dl). The physician who relies on labs rather than history and physical exam will think
the person is not hypogonadal, but that person is more commonly hypogonadal. This is a
physician who treats the lab rather than treats the person.
The cost of doing Free Testosterone is often higher than doing total testosterone. It is much more
difficult to measure free testosterone since it is a smaller value than total testosterone. This is
also one reason the measure is unreliable - it is a very small value.
High reverse-T3 indicates that type-3 deiodinase activity is high in comparison to type-2
deiodinase activity. Type-2 deiodinase is the main enzyme that activates T4 to T3. Type-3
deiodinase inactivates T4 by converting it to reverse-T3. Type-1 deiodinase can activate T4 or
deactive T4.
Increasing type-2 deiodinase activity or production (to better activate T4 to T3) requires adequate
T3 levels, insulin, norepinephrine, and growth hormone/IGF-1. IGF-1 is not only determine by
growth hormone but DHEA and other hormones.
The need for T3 to activate type-2 deiodinase is one reason Armour Thyroid (T3, T4 + T2, T1)
has an advantage over Levothyroxine (T4) in thyroid replacement therapy.
When a person has adrenal fatigue, the prolonged low glucose levels can lead to prolonged low
insulin production. This can then lead to less activation/conversion of T4 to T3 and a hypothyroid
state. This is opposed though by the high norepineprine levels that can occur with adrenal fatigue
- which increases the activation/conversion of T4 to T3. Which pathway wins depends on the
person.
__________________
Re: Enigma
Quote:
Originally Posted by Gator8
My primary doc who is treating me for diabetes, fatigue, fibromyalgia, pain and a whole
host of other issues ran a free-t test which came back at 2.8 on a normal lab range of 6.528. He prescribed Androgel packets and tested after two weeks. The result with two
weeks treatment was 15 for a normal lab range of 7-24. The second test was run by a
different lab.
I obtained my test results. These tests followed pre-treatment the prior night with
dexamethasone to evaluate for Cushings. It follws two weeks wash-out time for androgel.
I gather the low cortisol is the desired result from dexamethasone.
testosterone, serum 455 (ref 241-827)
LH 2.6 (ref 1.5-9.3)
FSH 3.2 (ref 1.4-18.1)
Prolactin 2.4 (ref 2.1-17.7)
TSH 0.813 (ref 0.350-5.50)
T4 free, (direct), 1.1 (ref 0.61-1.76)
Cortisol 1.3 (ref 3.1-22.4)
The doctor who prescribed androgel treats by careful interview concering symptoms, but
he prescribed the free-t test, seemingly missing the mark. The doctor who did the above
work-up goes by numbers, not symptoms.
With these test results, would I benefit from TRT?
It would be difficult to say that a man with a testosterone over 400 ng/dl is hypogonadal. Sexual
dysfunction would more commonly have other hormonal causes such as adrenal fatigue,
hypothyroidism, diabetes, excess estradiol, etc.
Testosterone optimization (e.g. raising blood levels over 650 ng/dl, while trying to avoid
supraphysiologic levels), may be helpful in some cases to reduce diabetes or insulin resistance,
to improve a person's tolerance to pain, to improve energy (e.g. via improving thyroid hormone
production - though in some men, thyroid hormone production is reduced and fatigue worsens
instead). Testosterone, in general, is also an anti-inflammatory hormone (reducing the levels of
inflammatory cytokines - immune system chemical messengers). It can help reduce hypertension
(though in some men it can increase blood pressure - if not enough of the other hormones are
made - such as DHEA, Estradiol, Progesterone, Thyroid hormone). Testosterone may also help
reduce abdominal fat (though excess DHT may increase abdominal fat), help reduce the damage
from stroke or heart attack, etc.
The primary problem is in getting a physician to prescribe TRT for these indications. An anti-aging
physician may - but it varies. Many of the big-name anti-aging doctors will target around 550-650
ng/dl, others may go higher. It depends on the physician's philosophy on the matter.
__________________
Re: pituitary tumours?
Quote:
Originally Posted by DaVinci2
If the entire pituitary must be removed, what treatment would be necessary afterwards?
Would it be best to just leave the tumour there and go on HRT? Just curious...I'm going
in for my MRI tomorrow.
Essentially, many of a person's hormones have to be placed on manual control.
THYROID HORMONES:
T4
T3
SEX HORMONES:
Testosterone - Testosterone or HCG or a combination
Estradiol
ADRENAL HORMONES:
Cortisol
Aldosterone - usually Fludicortisone. But Aldosterone itself is available as a compounded
medication.
Progesterone
DHEA
OTHERS:
Antidiuretic Hormone - DDAVP
Growth Hormone
Ideally, the levels are optimized so that a person has as close to ideal functioning as possible. But
I most often get patients where this is not done. For example, a fixed dose of Cortisol does not
make sense since a person still has to be able to respond to stresses. Yet most often, a fixed
dose of Cortisol is given.
Re: why dont uros/endos use hCG?
Quote:
Originally Posted by JustOne
Over at the testicular cancer website the guys who are on HRT from there endos and
urologists are only on Androgel and thats it, no hCG.
One guy had atrophy in his remaining testicle and his urologist said its from the androgel
and didnt mention hCG.
It seems the use of hCG in HRT is rare.
Past the age of 40, many do not believe that the testes will respond to HCG.
__________________
Re: New Lab work, bad endo? can't make sense of it
Quote:
Originally Posted by Scottyo
Ok. I havent posted here in quite some time, and very little on this account as it is. So a
little background. I am 23 and have been battling libido and low test symptoms since I
was 18 (did a very intense crash diet after senior football season and went from a solid
linebacker's 190 to 160 lbs in less than 5 months.)
Anyways, despite wishing I could fix that, I am now 23 and still have problems, although
they have had ups and downs and I have beeen able to pack on muscle with a couple of
androgen cycles. With that said, i have not been ON in almost a year, and since August
have had very test results.
Here are my last 3 (also had test checked about 2-3 yrs. ago and was similar to the
august test)
Here are the two oldert tests, plus my latest bloodwork from about a week ago. The latest
bloodwork is after about 12-13 days of androgel at 50mg a day (1 packet).
8/26
LH: 1.6 (1.5-9.3)
FSH .5L (1.4-18.1)
Total Test 164 (241-827)
Free Test 5.2L (9.3-26.5)
Prolactin 9.7 (2.1-17.7)
Fasting Cortisol: 29.3 (4.3-22.3)
oct 16 (unsure of ref ranges)
LH 1.93
FSH 1.10
free T4 1.37
TSH 2.45
T3 78.
Total Test 268
Estradiol-17b <20
Cortisol (non-fasting) 17.9
10/27 LATEST WORK WITH ANDROGEL
T4 4.35 (5-12)
t3 64 (40-180)
FSH <.1 (.7-11.1)
LH .120 (.8-7.6)
Total Test 1442 (250-1100)
Free Test % 3.59 (1-2.8)
Free Test 517 (35-155.0)
I dont have estradiol from the latest, but the doctor wanted to REDUCE my Androgel to
every other day (EOD) because the free and test are so high. He did not suggest
ANYTHING for the low fsh and lh, and I cannot understand what has happened. Any
insight would be great. the bloodwork looks like I am ON something, but could 50mg of
androgel have those results. And shouldnt I be taking HCG right now because of the low
fsh and lh?
That is a spectacular result from using a single packet of Androgel. It is supraphysiological, which
is a concern.
When free testosterone is high, then SHBG is low. This means there may be one or more
hormonal problems besides testosterone. SHBG is lowered by low thyroid, low estrogen, low
progesterone, high testosterone, high DHEA, high insulin (as in diabetes type 2), high growth
hormone.
When external testosterone is given, there will be a reduction in LH and FSH via negative
feedback to the brain. This results in reduction in sperm production and testosterone production,
and atrophy of the testes. HCG is used then as a substitute for LH (but not for FSH), to help
return testosterone production from the testes and to help restore testicular size.
__________________
Re: Dry Skin
Quote:
Originally Posted by Megazoid
Just a quick post guy's.
While on TRT i didn't feel too great, even on 2 tubes of tesim a day. My body seem's to be
hyper-sensative to the gels and creams so i have stopped taking them. I got alot of bad
reactions and decided to stop TRT (by the doctor's orders).
My doctor's want to see what my own "natural" level/production goes back too.
I have been off TRT for about 3 day's and i have noticed my skin is dry. This only seem's
to occur on thin skin areas such as my knuckles, elbows, knees, scrotum and foreskin.
I have also noticed a large amount of spots appearing on my back (near the original
testim/gel application site). It look's almost like acne on my back. I also do have alot
more spot's since being on the TRT and i can only think this is E2 related somewhat. Not
sure if it's "peaking" and causing the spots. These aren't all near the application site but
all over my back and arms.
What would cause this dry skin? I have heard your E2 being too low can cause this. What
are the other signs of low e2?
I did notice it was really difficult to get an erection today (and keep it) but i haven't been
flushing or anything (I haven't really flushed for a good few weeks). This could be the low
testosterone though causing the problems now.
My E2 was sitting right on the lowest range for a guy when on Androgel (only 1 packet a
day though). My ranges looked good but i still didn't feel much better. I think my original
level was somewhere in the 30/40nmol range. Not sure how this balanced out with
regards to E2 and such like.
Each day i take the following:
- One A-Z Multi Vit
- Two Vit E (800mg in total)
- 50mg Zinc
- 1/2 Pints of pure fresh orange juice a day
Just wondering if anyone has any ideas on this? Should i try to eat more food's which will
raise my E2 to avoid this dry skin? Strangly before i suffered from this low testosterone
problem my diet was full of sweets and fatty food's and i never had one single problem. I
wonder if my body is more suited to higher E2. Also should i apply some kind of cream to
smoothen the skin?
Low estradiol can cause dry skin.
Low thyroid can cause dry skin.
etc.
Re: callin marianco and swale please!!
Quote:
Originally Posted by ironaddict69
hello to both of you, and thanks again for helping with this site. your greatly appreciated!
i have a few questions
im on TRT and my doc recently lowered me to 100 mg a week, he felt 200 was too high
and it had me around 1500 on the test chart, free was over the range too
1. can anti aromatase drugs like aromasin decrease sex drive? i can get erections if i
really want them, its just my sex drive is BAD. however im on day 3 of thyroid armour
and feeling a little better, and starting isocort soon due to low cortisol.
2.can low cortisol lower it too? i know being hypothyroid it will be lowerr but i wasnt
sure about cortisol.
3. how can you lower progesterone? mine was slightly over the top range, even with
estradiol being normal.
1. TRT ideally should have a target of getting total testosterone to at least 650 ng/dl, while trying
to keep the testosterone mostly within the physiologic range, i.e. max 1000 ng/dl. This can be
difficult with some forms of TRT. For example, an oil-based testosterone cream can have peaks
of testosterone up to 4000 ng/dl, with a half-life of about 12 hours. But the peak is very short-lived
in this case and can be acceptable if not a good treatment for many men.
2. If problems such as decreased sex drive persist when total testosterone is over 650 ng/dl, then
testosterone itself is not the problem. There are other neurotransmitter/hormone/immune system
cytokine problems occurring - which need to be evaluated and treated.
3. Having an appropriate amount of estrogens, particularly estradiol (the most potent one), is
important for sex drive. Estrogens provide sexual aggression - which means it contributes to the
desire to have sex. An estradiol level gives a good indication of the total estrogen activity since all
the estrogens actually determine estradiol level (when not done as a fractionated estrogens test).
4. An aromatase inhibitor can drive estradiol too low, causing a loss of sex drive. When estradiol
is too low, testosterone many even increase blood pressure rather than reduce blood pressure.
5. Thyroid hormone deficiency can reduce sex drive, as well as energy.
6. Cortisol deficiency - e.g. from adrenal fatigue - can reduce sex drive. Cortisol deficiency
impairs the mind's ability to reduce norepinephrine levels. This is necessary to relax a person.
Sex is a resting function as opposed to a fight-or-fllight function.
7. High progesterone levels can excessively sensitize a person to estrogens, which can lead to
reduced sex drive. Progesterone can also reduce DHT production by blocking alpha-reductase
enzyme. This may lead to a reduction in sex drive, particularly if total testosterone is low and
DHT's influence is necessary to promote sex drive.
8. Progesterone is primarily produced in the adrenal glands, along with the rest of the adrenal
cortex hormones in response to ACTH, which is released in response to stress or reduced energy
levels (such as from hypothyroidism) with higher need for cortisol production. Progesterone
production is largely independent of estradiol production.
9. To reduce progesterone, one has to reduce external stress levels as well as address
hypothyroidism and cortisol deficiency/adrenal fatigue.
10. Adequate progesterone is needed to have sex drive.
11. Testosterone pellets can work well with many men. It keeps total testosterone at nearly
absolutely even levels. There is no roller coaster effect. By gradually releasing testosterone, one
nearly completely avoid problems with estradiol and DHT. Testosterone pellets however ties the
person to their physician, making the person dependent on their physician. One can't travel for
extensive periods of time, for example, since one has to have the pellets inserted surgically about
once every 3 months. The person has less independence from their physician. There are few
physicians that do the pellets because it is a more invasive procedure and many disagree with
that philosophy, calling it a primitive form of medicine. However, for the person that can live with
the physician dependency, travel limitations and the idea of having an invasive procedure
regularly done, testosterone pellets actually can be the best form of TRT since it greatly simplifies
treatment and can be very effective.
12. If one can correct thyroid and adrenal problems first - completely optimizing thyroid hormone
and adrenal gland function - which unfortunately is not often done - then one can have good sex
drive with lower levels of testosterone and with lower levels of testosterone replacement. This is
one reason the Endocrine Society's guidelines for TRT indicate that one must not just treat low
testosterone levels when there is not symptom of a deficiency. Treat the person not the labs - as
one of the important lessons in physician training states.
__________________
Re: callin marianco and swale please!!
Quote:
Originally Posted by HeadDoc
and last but not least, let's not forget that primal ingrediant: romance.
Yes!
And to have romance, we have to be able to produce adequate amounts of the hormone,
Oxytocin.
Unfortunately, if a person grew up neglected, such a person may not be able to produce enough
oxytocin. Sometimes optimizing the hormones may restore this.
It took Harry Harlow's monkeys five generations to compensate for the early neglect. I wonder if
this may be offset by providing consistent, secure attachment. My wife and I have varying
degrees of success with the feral kittens we raise. They have taught me quite bit about adrenal
functioning.
__________________
Re: callin marianco and swale please!!
Quote:
Originally Posted by ironaddict69
how to you optimize that hormone?
marianco what dose do you put your patients on with trt? my dr just lowered me to 100
mg this week and i took a dive. i felt much better on 200 mg. he freaked out because my
test was 2200, but it was because i spiked my dose to 800 mg a week for a while. it was
stupid, lets not evne go there, but i feel like i need more than what he lowered me to.
being as its only 64 actual miligrams of test due to the ester weight
The starting dose for testosterone cypionate or testosterone enanthate injections is 100 mg/week.
Depending on the half-life of testosterone, the dose is adjusted up or down.
The target is a total testosterone of about 650 ng/dl, while attempting to keep the peak under
1000 ng/dl
One way to estimate the half-life of testosterone is to inject 200 mg of ester then measure the
total testosterone about 4 days later. The total testosterone should be 1000 ng/dl - for T.
enanthate. If it is about 600 ng/dl, then the half-life is about 3.5 days. The weekly dose would then
be about 200 mg/week.
If the person has hypothyroidism, and thyroid hormone treatment is started, this will raise SHBG
levels. This will then lengthen the half-life of testosterone and increase total testosterone level. A
lower dose of Testoserone cypionate or enanthate is then needed to keep a person within the
reference range.
A physician would freak out with a total testosterone of 2200 ng/dl. This takes the patient to
unknown territory. The risks include hypertension, hyperlipidemia, diabetes, etc., etc.
__________________
Re: callin marianco and swale please!!
Quote:
Originally Posted by thebigEZ
Is there any good way to raise oxytocin in men. I am curious on what yall's thoughts are
on injectable oxytocin.
Oxytocin has to be raised indirectly using psychological interventions or optimization of other
neurotransmitters/hormones such as estrogens, progesterone, cortisol, testosterone, dopamine,
etc. Oxytocin is meant to have variable levels depending on the circumstance. Keeping Oxytocin
raised would only create problems, some of them potentially lethal. Oxytocin further lasts only
minutes, making constant elevation a problem with externally applied oxytocin
Alternatives to Cortef
Quote:
Originally Posted by ironaddict69
marianco, your by far the wisest doctor ive been in contact with.
where do you practice?
would you put someone with a morning cortisol of 16 (8-25) on cortef?
my dr. wont, and i know i need it. my adrenals are effed.
Please read my profile.
I would place a person on cortef or other adrenal treatments if the diagnosis of adrenal fatigue or
adrenal insufficiency can be established. A single morning cortisol of 16 is only one clue and
cannot establish a diagnosis. More information is necessary from other labs and the history and
physical exam.
Cortisol (hydrocortisone or Cortef) is not the only glutocorticoid that can be used as part of an
adrenal treatment. Cortef, for example, has some mineralocorticoid activity (e.g. it retains salt),
which may not make it the best treatment in a person with significant hypertension, without other
compensitory medications to lower blood pressure. Cortef also has a short half-life - which makes
it difficult for teenagers or college-age students to adhere to treatment. An artificial glutocorticoid
steroid in these cases and others may then be an option. Methylprednisolone, for example, has
almost no mineralocorticoid activity and a long-half life. Prednisolone is another long lasting
glutocorticoid with similar activity to Cortef. These are much more potent than Cortisol and thus
need to be used in much smaller doses. They cannot be easily used when one needs to adjust
glutocorticoid dose quickly or frequently - for example, when I add additional doses to be used as
needed, or when fine tuning needs to be done. When small or rapid changes are needed, Cortef
is still best because the half-life is so short. The treatment with these and other alternatives still
has to be customized to the person.
__________________
Re: callin marianco and swale please!!
Quote:
Originally Posted by ironaddict69
so what tests exactly would you run?
the ACTH test?
any other ones?
im asking because im going to request them.
so you keep people on their cortisol medication, or do you take them off after a few
months and have them go onto isocort?
Tests for adrenal fatigue and associated conditions include: Cortisol AM, Cortisol PM, DHEA-s,
progesterone, fasting glucose, electrolytes (sodium, potassium, bicarbonate, chloride), albumin,
BUN, creatinine, total testosterone, Free T3, Free T4, TSH, hemoglobin A1c, fasting insulin.
Additionally it is useful to do saliva tests for Cortisol four times in a day, and DHEA two times in a
day; and urinary neurotransmitter testing (serotonin, dopamine, GABA, norepinephrine,
epinephrine, glutamate, histamine (when available)).
There are numerous options for treating adrenal fatigue. I customize the treatment to the person.
Isocort can become extremely expensive when it has to be used in high doses, for example. It
also has to be paid out-of-pocket. Hydrocortisone and other glutocorticoids can be inexpensive,
generic, and covered by health insurance. Treatment will depend on numerous factors including
the patient's needs, their ability to afford treatment, their ability to adhere to treatment (e.g. shortacting glutocorticoides such as hydrocortisone/cortisol are more difficult for college-aged adults to
use), etc. Some conditions such as severe hypertension may rule out the use of hydrocortisone.
An alternative may need to be used.
Whether or not a patient continues their adrenal fatigue treatment depends one the treatment of
associated conditions such as thyroid problems, age-related DHEA decline, testosterone
deficiency. It also depends on whether or not the person can improve their psychological skills to
adapt to stress, whether or not the person can modify their environmental stresses, whether or
not the person can resolve the problems caused by past trauma, etc. For example, if a person
can change their lifestyle to reduce stress enough that the adrenal glands can fully recover, then
they may not need continuous treatment. Some people cannot escape extreme stresses - for
example, people who have had severe childhood trauma and live in poverty. These people may
need lifelong treatment. Some people can stop treatment one day, some people can't. The
treatment depends on the person and their circumstances.
__________________
Re: callin marianco and swale please!!
Quote:
Originally Posted by ironaddict69
marianco, do you know a direct way to lower progesterone?
whats the highest dose of armour youve ever had somebody on? i hear for some it takes
up to like 10 grains.
im just curious, not that im addressing my thyrod and adrenals with isocort, im
wondering how to lower progesterone. its the only thign outta wack and its ruining my
sex life.
As far as I know, there is no direct substance to reduce progesterone production.
Norepinephrine is the signal for the presence of stress. ACTH is produced in response to
norepinephrine. ACTH from the brain triggers the production of all the steroid hormones from the
adrenal glands including progesterone. However, only cortisol gives negative feedback to the
brain. High progesterone usually indicates high stress.
Progesterone is an anti-stress hormone. It has protective effects on the brain. It improves the
speed of nerve signal conduction. It has calming and antidepressant effects. It promotes nurturing
behaviors. It is a mild diuretic, helping reduce fluid build-up. It blocks estradiol's inhibiting effects
on thyroid hormone. It helps reduce blood pressure. One needs adequate progesterone for
sexual function.
Reducing stress can lead to reduced progesterone production.
Adrenal fatigue from excessive stress can lead to reduced progesterone production.
High progesterone may be a sign of high stress level.
It is the high stress level that impairs sexual function, not progesterone (particularly at levels
below about 2.5 ng/ml in men)
The highest dose for Armour Thyroid is 5 grains or 300 mg a day. If a person has heart disease,
one has to be very careful about any dose above 120 mg a day.
__________________
Re: Pellets - Why aren't YOU on them???
Quote:
Originally Posted by eeso
Everything I've read about pellets says they're good - low estrogen, low DHT
converstion, stable Testosterone released, only have to see doc 3-4 times a year. And the
few people who have posted who are on them have great results.
So why aren't more of you people on them??? I know if i were to go back on TRT I'd be
jumping on them pronto.
So what's stopping you?
Some possible reasons:
1. Few doctors do pellets.
2. The idea of having a surgical procedure done 4 times a year
3. The view that pellets are invasive/primitive
4. The idea of being less independent of (of being dependent on) the doctor
__________________
Re: Pellets - Why aren't YOU on them???
Quote:
Originally Posted by eeso
Everything I've read about pellets says they're good - low estrogen, low DHT
converstion, stable Testosterone released, only have to see doc 3-4 times a year. And the
few people who have posted who are on them have great results.
So why aren't more of you people on them??? I know if i were to go back on TRT I'd be
jumping on them pronto.
So what's stopping you?
Some possible reasons:
1. Few doctors do pellets.
2. The idea of having a surgical procedure done 4 times a year
3. The view that pellets are invasive/primitive since it puts a foreign object inside one's body
4. The idea of being less independent of (of being dependent on) the doctor
If one does not have these reasons, then pellets are a viable way to get testosterone
replacement.
__________________
Re: Low Cortisol and TRT
Quote:
Originally Posted by kincaiddave
If you have low cortisol, 9.9 in the AM with a ref range of 8.7 - 22.4, should that be dealt
with first before starting TRT?
The more I look into it, it looks like it should have been dealt with first. Since it wasn't, do
I need to stop TRT and get adrenal and thyroid levels in the desired ranges first and then
go back on TRT? I sure would hate stopping TRT (it would feel like backing up), but
whatever it takes.
Since starting T shots, I have learned that they often drive cortisol lower. I don't need
that. I have been supplementing with Isocort and am up to 8 pills. I have also learned
that Isocort is sometimes/often inadequate for most with low cortisol.
I requested all the tests that SWALE recommends before TRT, but relative to thyroid, only
TSH was tested - 1.18. So I don't know how my thyroid hormones are.
I have read probably hundreds of posts that talk about feeling better right after the
weekly shot of T and not so good just before the next. I don't experience that. I'm
wondering if the benefits of elevated T in the days right after my shot is offset by lower
cortisol at the same time.
Any thoughts/advice? My doc is supposed to consult with SWALE on my treatment, but it
has not happened yet. I'm just trying to learn what I can for now.
When adrenal hormone (cortisol, DHEA, aldosterone, progesterone) activity and thyroid hormone
activity are optimized, then less testosterone replacement is needed to accomplish the desired
goals.
When testosterone replacement therapy is already in place, it is not necessary to stop it while
adjusting adrenal and thyroid hormones. However, it will be useful to monitor testosterone, DHT
and Estradiol to help determine if problems can occur. For example, as thyroid hormone levels
increase, there will be more SHBG made, which will increase the half-life of testosterone. The
longer duration of testosterone may mean the total testosterone may rise, leading to problems of
testosterone excess - including high DHT (with acne and other problems), increased in lipids, etc.
As adrenal function improves, adrenal testosterone production may increase, total testosterone
production may increase.
__________________
Re: adrenochrome - marianco? HeadDoc?
Quote:
Originally Posted by JustOne
I just had a 4 hour phone conversation with my cousin who is a retired doctor (medical
science) and most of the conversation was about HRT, one thing he mentioned wich
concerned me was adrenochrome problems wich can throw you into psychosis.
I just quickly looked it up and found this.
It is highly questionable if Adrenochrome - a metabolite of epinephrine - can cause psychosis. I
would not worry about it in regard to hormone replacement therapy.
The last MedLine article containing the term "adrenochrome" and "psychosis" was in 1968. There
are only 5 such articles in all of the articles in MedLine. The articles were also minor articles,
where adrenochrome was not the main subject.
Epinephrine itself is a minor neurotransmitter in the brain.
Schizophrenia is a complex neurodevelopmental - neurodegenerative disease. There is incorrect
development of the brain such that certain brain cells are missing and certain brain cells are in
excess. It is more than just an excess or deficit of some neurotransmitters. This is why the best
antipsychotics on average reduce symptoms by 4% (!!!!) in chronically ill patients with
schizophrenia.
Psychosis is a complex condition. It may be caused in some but not all circumstances by
excesses of certain neurotransmitters or hormones - e.g. excess dopamine, glutamate, cortisol,
serotonin, etc.
__________________
Re: Question for Marianco
Quote:
Originally Posted by mkl13
One study with arimidex called for no st. johns along with some other drugs that increase
cytocrome 450 (i.e. ant-convulsants, etc.). From what I can find, st. johns increases,
while arimidex inhibits. I wanted to insure no interaction before starting the st. johns
wort.
Even when medications interact, the question would be what risk does that entail. If the benefits
significantly outweigh the risks (since everything has risks), then a person may then decide what
course of action may be of most benefit to oneself.
If a person wants absolutely no interaction between two medications, I think that person will find
few such medications. Every intervention or non-intervention entails risks.
Let's look at Arimidex and St. John's Wort at a greater depth - i.e. more than the initial two-step
chess answer that I gave before.
Arimidex blocks aromatase so that Estradiol and Estrone are reduced. However, this may force
testosterone through other enzyme pathways such that total estrogens (with other forms of
estrogen) may increase - albeit with much weaker estrogens.
Arimidex by reducing overall estrogen activity (since estradiol is the most potent estrogen), can
lead to an increase in LH production and an increase in testosterone production.
Estradiol and other estrogens act like monoamine oxidase inhibitors - antidepressants. This
means they can raise some neurotransmitter levels: Serotonin > Norepinephrine > Dopamine.
Estrogens have about 399 other actions.
Using Arimidex then will reduce overall levels of serotonin, norepinephrine and dopamine via
reduction in estrogen activity.
However, the increase in testosterone will help increase dopamine activity.
The increase in testosterone may either reduce or increase thyroid hormone activity.
The increase in testosterone may also reduce cortisol production (via reduction of pituitary ACTH
production and via direct inhibiting effects on the adrenal gland itself).
The reduction in cortisol production may lead to an increase in norepinephrine production to try to
compensate for the energy loss. This may lead to an increase in anxiety.
These are some of the neurotransmitter and hormone cascades that may occur, without
describing the immune system changes.
St. John's Wort apparently works by increasing serotonin and norepinephrine to reduce
depression and/or anxiety.
Excessively increasing serotonin can lead to a decrease in dopamine production in dopaminereleasing cells. This can also then lead to an increase in norepinephrine production in
norepinephrine-releasing cells, which were controlled by the dopamine-releasing neurons.
Increasing norepinephrine excessively can lead to adrenal fatigue - including deficiencies in the
production of cortisol, DHEA, progesterone, aldosterone, and testosterone from the adrenal
glands. This can lead to depression and anxiety symptoms.
St. John's Wort also increases the activity of Cytochrome P450 3A4 - the most common enzyme
to metabolize (via oxidation) toxins, medications, and steroid hormones and other substances.
St. John's Wort and Arimidex (via reduction of estrogen activity) may potentially cancel each
other out, depending on each other's dose, in regard to neurotransmitters. The medication with
the dose which is more potent will decide the direction.
St. John's Wort (through increased Cytochormone P450 3A4 and oxidation of estrogens) and
Arimidex may have additive effects in reducing estrogen activity.
St. John's Work, however may reduce testosterone levels as well as cortisol, progesterone,
DHEA and other steroid hormones by increasing the activity of P450 3A4; while Arimidex
increases testosterone level by increasing LH production.
These are just some of the potential interactions.
Whether or not to use both together depends on what one wants to accomplish and the dose of
each to use, and vigilence to the interpretation of the side effects one experiences so one can
interpret what is happening and modify treatment as necessary to improve functioning.
Perhaps St. John's Wort can then at some dose help reduce depression and anxiety,
counteracting some of Arimidex's actions. However, of concern would be its effects on hormone
levels with or without Arimidex. If those are significant enough - which depends on the person - it
would give one pause. If those are not significant enough - which again depends on the person then the use of St. John's Wort may be O.K., particularly if found effective.
If a person finds the potential benefits outweighing the risks, then it may be of benefit to give
things a trial run - so long as one is willing to take the risk or take a leap of faith. The answer will
depend on the individual.
The usual psychiatric answer is: "It depends."
Re: Question for Marianco
Quote:
Originally Posted by mkl13
Marianco, this would also seem to apply to most medications that are metabolized via
P450 pathway. Examples include, trazodone, dilantin, certain benzos, and a host of
others. Should Individuals modify these types of medication to ensure maximal sucess in
raising low testosterone (i.e. looking for alternatives that are metabolized differently)?
Thanks again for all the great info.
In an ideal world, we can have all the alternatives possible so we can maximize success by
avoiding interactions, and that these alternatives are effective.
However, we do not live in an ideal world.
When interactions are possible, we work with them, for example: adjusting dosing as necessary
depending on the interaction seen, when particular combinations are used.
Re: Bran, Licorice, working out?
Quote:
Originally Posted by DrmChld
Me again...
Last Labs results came in after being off Androderm for 2 weeks.
10/17/06 354ng/dl Range: >245
Previously off Androderm for 1 week, crashed really hard.
9/27/06 464ng/dl Range >245
Initial Lab Results from new Endo while on AndroDerm for over 6 months
8/22/06 398ng/dl Range >245
Endo now wants me off the patch again for 1-2 weeks and is then going to send the blood
drawn to an outside lab called Quest. These results are really confusing me.
I feel like crap when I am off that patch, I don't know if it is just a placebo or what. When
I was off for the first week my Testosterone went up which doesn't make any sense to me.
I figured that being on Androderm would give me much more of a boost than the 398ng.
I am to the point where I want to self-treat at 125-150mg Test-E per week. Delimia is
wife doesn't want me to do this. She read that Testosterone was an abused substance(I
have abused pain killers before) and doesn't want me doing anything like this. The
second part is I will be moving to Canada in 6 months on a student visa (while waiting
for immigration papers to be approved) and can only use health services for emergency
(can't be a burden or show lot of medical problems, might cause them to deny my
immigration)
I know there are sources in Canada for Testosterone, however I cannot risk being caught
and being deported and not allowed back into the country. Which would mean my wife
stays there. I am then in the US, wifeless and homeless.
Now about the topic... I figure if I can lower my Testosterone close to the range my Endo
would then prescribe Testosterone shots (which I would then explain I can do at home,
etc...) and then get the vials for myself.
What type of Bran to eat? What kind of licorice and how much? For working out, overtrain? Do full body work outs? Don't breathe right while working out?
OT: If I do get a prescripe to the vials, has anyone had any experience with flying and
going through customer have Testosterone vials and sryinges in their luggage?
thanks in advance as always!
(ps: I never proof read)
Some people require 2-3 patches in order to overcome the drop in natural testosterone
production to raise testosterone level significantly while on Androderm. For example, three
patches applied at 10 PM can cause the morning testosterone level to be about 750 ng/dl.
When traveling with medications and syringes, it is important to have labels which prove they are
prescribed.
Black licorice is at times used to treat adrenal fatigue. It lengthens the half-life of cortisol. The
problem is that the adrenals need to be able to vary the production of cortisol quickly in response
to stress. Licorice makes this more difficult. It can help under some circumstances. However,
there are times when the cortisol abruptly drops when licorice stops working. I have had patients
who would then go into acute adrenal insufficiency when this happens - they would become
confused, dizzy to the point of falling, etc. This and how often nausea occurs with licorice is why I
do not often advise its use.
Note that per Endocrine Society guidelines, the target of testosterone replacement is a total
testosterone of 650 ng/dl. If that level is not achieved, the dose needs to be increased or
treatment route needs to be changed.
__________________
Re: My lab results!
Quote:
Originally Posted by JustOne
woopty woop finally got my results back.
Prolactin: 272 mIU/L (0-500) (performed using Abbot method)
Cortisol 11am: 350 nmol/L (AM138-650 PM70-325)
Oestradiol: 36.1 pg/ml (<46.1) (performed using Roche method)
FSH: 11.6 U/L (1-9.2)
LH: 7.2 U/L (2-8)
Total Testosterone: 551 ng/dl (231-1096)
SHBG 18 nmol/L (10-50)
Free Androgen Index 106% (20-130)
Free testosterone: 56 pmol/L (43-138)
Total PSA: 0.51 ng/mL (0-2.5) ((performed using Abbot method)
TSH 1.08mIU/L (0.3-4)
T3 and T4 was withheld because of normal TSH level
IGF-1: 24 nmol/L (24-102)
Homocysteine 9.3 umol/L (6.0-14.0)
Fasting Insulin 5.9 mU/L (0-20)
Plat Count 158 x10^9/L (150-450)
Cholestrol 4.2 nmol/L (3.9-5.5)
Triglycerides 0.8nmol/L (0.5-1.7)
Bilirubin 21 umol/L (0-20) *better then last time
AST & ALT 13 U/L (0-40)
Metabolic Panel pending cause of screw up in pathologist not know what he was doing.
Comments anyone?
Anything I can do about my low Plat count?
Cortisol AM = 12.6 mcg/dl
Oestradiol = 36.1 pg/ml
FSH = 11.6 U/L (1-9.2)
LH = 7.2 U/L (2-8)
Total Testosterone = 551 ng/dl
SHBG = 18 nmol/L (10-50)
TSH = 1.08mIU/L (0.3-4)
T3 and T4 was withheld because of normal TSH level
IGF-1: 24 nmol/L (24-102)
Fasting Insulin 5.9 mU/L (0-20)
Plat Count 158 x10^9/L (150-450)
Here is a conversion calculator: http://www.globalrph.com/conventional_si.htm
It would help to translate the SI to Conventional units so that the albs would be more
understandable to those of us in the U.S.
It is important to obtain the fasting glucose value to correlate it with the insulin level.
IGF-1 is an indirect measure of growth hormone. It is influenced also by Testosterone, DHEA and
Estradiol levels. Optimizing these and other hormones affected by growth hormone makes it
clearer if there is a growth hormone deficiency.
The Free T3 and Free T4 are more important than TSH to help diagnosis hypothyroidism. The
history and physical exam are far more important.
SHBG which is low is most correlated with high insulin levels (such as in diabetes). However,
SHBG is influenced by multiple hormones such as those that increase it (such as thyroid
hormone, estrogens, and progesterone) and those that decrease it (such as androgens, growth
hormone, and insulin).
Cortisol level is useful in determining the presence of adrenal fatigue. But when doing lab tests, it
is also important to correlate it to DHEA-s, Progesterone, blood glucose, Albumin, sodium,
potassium, and other lab studies to determine if there is adrenal fatigue. A physical exam and the
history would also be highly useful.
__________________
DHT and E2
Quote:
Originally Posted by masterpp
i never used to understand why my e2 was so high when i was off gels, ie natural
hypergonadal. but from another post, someone explained that excess lh and fsh converts
very quickly to estrogen, hence why when i was off trt my e2 was higher than when i was
on it.
the second point, i could never understand why my dht was so high, but i had no sex
drive. i used to think that it was because e2 was too high, but actually i believe the
reverse is true, and that my gels cause dht conversion, and suppress e2 conversion, so im
actually lacking e2 and may try rubbing some test on my stomach to see what happens
cheers
Estradiol is made from testosterone via aromatase enzyme.
Luteinizing hormone increases testicular testosterone production.
Luteinizing hormone also increases aromatase enzyme production, leading to a converstion of
testosterone to Estradiol.
Estradiol is as much as 10,000 times more potent than testosterone in its effects. It is a fine
balance that needs to be done at small levels, to maintain function with estradiol in men. Too little
or too much will impair functioning.
The brain measures how much testosterone (with the help of progesterone) and estradiol to
determine how much Luteinizing hormone to produce. This is the negative feedback mechanism.
If there is too much testosterone and estradiol together, then LH production is lowered.
Dihydrotestosterone is made from testosterone via the alpha-reductase enzyme.
Dihydrotestosterone is about 7 times more potent than testosterone at testosterone receptors
(except in muscle - which is why dihydrotestosterone is not anabolic).
Since Dihydrotestosterone is more potent than testosterone, it can make the brain think there is
enough testosterone so that it reduces LH production, leading to a reduction in testosterone
production, and hence estradiol production.
Dihydrotestosterone may inhibit the aromatase enzyme - but I am not sure of this point - to
reduce estradiol conversion from testosterone.
Dihydrotestosterone can do some things the opposite of testosterone. For example, it can
increase abdominal fat - rather than reduce abdominal fat as testosterone does. It can cause
scalp hair loss as opposed to hair growth as testosterone can. Dihydrotestosterone can cause
insulin resistance as opposed to reducing insulin resistance.
Dihydrotestosterone can either improve function or impair function - it can be a good hormone or
bad hormone. Because of this dual nature of DHT, I prefer to minimize its production to avoid
negative side effects.
Having a lot of body hair indicates there is a lot of alpha-reductase in the skin. DHT does promote
body hair growth (not scalp hair growth).
If a reduction in DHT production is desired, then testosterone injections or pellets are the
preferred route of administration.
If DHT acts as a good hormone, then transdermal gels or creams can be used. It is up to the
physician and patien to decide if this is happening.
__________________
Re: Finally an explanation?
Quote:
Originally Posted by kimura
I don't have all my test results- I'll get more in the next couple weeks. I'm just so
desperate for an explanation I want to ask you if these numbers look a little suspect.
LH: 7 (2-9)
FSH: 5 (1-18)
Testosterone: 660 (240-950)
Free Test: 15.8 (9-30)
Some basic info:
38 yrs. No AAS. Very fit up until 2 yrs ago. (road cycling, gym, and mma)
I've had a horrible time rehabing an injury that no doctor has been able to figure out. It's
a soreness/tightness deep inside my hips or pelvic area. The more I try to rehab the
tighter it gets. Nerve pain down the left leg also. Depression has been getting
increasingly worse. Only rarely do I get morning wood (unfortunately I never really
thought much about this until reading here).
I'll keep reading and will post later with full results and intelligent questions but for nowwhat do you think?
When doing testosterone replacement for a testosterone deficiency, a good starting target is to
get the total testosterone level to 650 ng/dl. If any problems remain, then other hormones or
neurotransmitters or immune cytokines may instead be causing the problem.
__________________
Re: All results are in
Quote:
Originally Posted by kimura
38 yrs. No AAS. Very fit up until 2 yrs ago. (road cycling, gym, and mma)
I've had a horrible time rehabing an injury that no doctor has been able to figure out. It's
a soreness/tightness deep inside my hips or pelvic area. The more I try to rehab the
tighter it gets. Nerve pain down the left leg also. Depression has been getting
increasingly worse. Only rarely do I get morning wood (unfortunately I never really
thought much about this until reading here).
TSH: 1.96 UIU/mL (0.34-4.82)
LH: 7 IU/L (2-9)
FSH: 5 IU/L (1-18)
Testosterone: 660 ng/dL (240-950)
Free Test: 15.8 ng/dL (9-30)
% Free Test: 2.4 % (2.0-4.8)
Prolactin: 14 ng/mL (3-13) <- high
Estrone: 44 pg/mL (10-60)
Estradiol: 28 pg/mL (10-40)
PSA: 0.88 ng/mL
Free T3: 3.2 pg/mL (2.3-4.2)
Free T4: 0.97 ng/dL (0.61-1.76)
Cortisol (24hr urine): 40 ug/24hr (<105)
DHEA (blood): 636 ng/dL (146-850)
Ferritin: 170 ng/mL (22-322)
Thanks to all for the help.
1. A testosterone level over 650 ng/dl yet with continued problems indicates other
neurotransmitter/hormone/immune-system-cytokine problems are present.
2. If relying on labs, a TSH > 2.0 miu/ml OR a Free T3 < 3.3 pg/ml OR a Free T4 < 1.0 ng/dl are
clues that hypothyroidism may be occurring. This can then be confirmed by the history and
physical exam. Hypothyroidism may most reliably be diagnosed using only the history and
physical exam since there are people who have signs and symptoms of hypothyroidism and all
the consequences, yet have normal thyroid tests (Hypothyroidism type 2, a mitochondrial
disease). There are not many physicians who can do a classical diagnosis and treatment
hypothyroidism based solely on the history and physical, using the lab as confirmatory rather than
diagnostic. If you find one, then keep him/her.
3. A salivary DHEA and Cortisol test multiple times in a day is the most sensitive test for adrenal
fatigue.
4. A 24-hour urine Cortisol is not sensitive enough - only catching the most severe forms of
adrenal fatigue, or adrenal insufficiency. The fact that the reference range does not include a low
value indicates the test used by the lab is not sensitive enough for low values.
5. If using 24-hour urine tests, a more useful test is of the metabolites since these will indicate
how well the body is using a particular hormone. For adrenal hormones, then, the metabolites of
cortisol, DHEA, aldosterone, and progesterone are ones to help the evaluation. A deficiency in
the metabolites gives a truer indication of a hormone deficiency.
6. A blood DHEA-s is better than obtaining DHEA itself. DHEA varies tremendously in level from
moment to moment, thus does not give a good indication of the overall level of DHEA. DHEA-s,
the storage form for DHEA, is a better indicator of DHEA production.
7. When it comes to sexual problems, it is important to consider insulin (when severely high), then
testosterone, then cortisol, then thyroid hormones before considering estrogens as a problem optimizing the most important hormones first will help correct problems with the other hormones.
8. When prolactin level is high, dopamine production may be low. It is important to determine if
there is a pituitary tumor via MRI which is affecting prolactin production.
9. When dopamine production is low, it is important to determine if there are neurological
problems, such as Parkinson's Disease, which affect dopamine levels.
10. When dopamine levels are low, extrapyramidal symptoms/motor movement problems can
occur. This includes muscle cramps and muscle stiffness, tremors, slowed movements, etc.
11. Depression is a complex condition involving problems with
neurotransmitters/hormone/cytokines such as: low serotonin, low dopamine, low norepinephrine,
low thyroid, low cortisol, low DHEA, low estrogens, low testosterone, low progesterone, low PEA,
or high inflammatory cytokine levels, or a mixture of problems.
12. Morning wood requires at least good testosterone levels, good thyroid hormone activity, good
adrenal hormone activity (good cortisol, aldosterone activity), a predominantly resting
neurotransmitter balance (e.g. an emphasis on serotonin, dopamine, and GABA activity
compared to norepinephrine and histamine) - meaning there is predominant parasympathetic
nervous system tone - and a person is thus not in a stressed state. Sex is a resting activity as
opposed to a fight-or-flight activity.
__________________
Re: Finally an explanation?
Quote:
Originally Posted by kimura
Thanks for the info.
It looks like this is not a simple case of "take this and you'll feel better". More tests and
expertise are required.
Here's my dilemma (same as most others' I'm sure)
The docs I've seen over the last couple years have just been "checking the box" and
unwilling to work to find the cause. This (new) PC is a refreshing change. She has been
very willing to work with me and order the tests I've asked for but openly admits that she
is not an expert in this area (also nice to see the ego is not a limiting factor).
Marianco- would you be willing to consult with my PC or do you recommend I see an
endo or anti-aging? I'm in the mid-new england area if anybody knows good resources.
I think an endocrinologist would usually be completely lost in attempting to treat you.
One way to test if a physician may be able to help you: If you can find an endocrinologist or other
physician who can diagnose hypothyroidism using only the history and physical exam - without
using blood tests, then that person can help you since such a physician will have a higher skill
level and understanding of disease process than a physician who has to rely on lab tests for the
diagnosis. You can ask them if they can.
If you were to look for a local or near local physician, I think an "Anti-Aging Board-Certified"
physician would be best - not just an "anti-aging" physician. An anti-aging board-certified
physician would have to study a lot to understand anti-aging principles, not just dabble in it.
You can look up anti-aging doctors at the directory of A4M at http://www.worldhealth.net
__________________
Re: Is simply living with low Testosterone actually dangerous?
Quote:
Originally Posted by dunbar
According to what my doctors told me my T levels which are always around 300ng/dl are
okay and they all made it look like getting TRT was some sort of risk. But when I look at
how much testosterone 60-65 year old men have then they're still much higher than me!
And since low T is linked to many diseases this actually means that if I don't get TRT I am
putting myself at a higher risk, right? Does this mean that not getting TRT would be
risking my health?
But I just don't know what to do. Wether to simply give it a try or not and once I'm on
TRT it's also hard to stop if I decided to stop, isn't it?
Here is an interesting article about declining T in American men.
This is really funny. They complain that the 60-65 year old men only have 450ng/dl and
say that the men in the late 20ies peak testosterone. But I'm 25 and already have much
lower T than those 65year olds...
http://health.yahoo.com/news/168226
Conventional medicine is slowly realizing that men with low testosterone levels die at an early
age. The problem is that conventional physicians do not have any direction on how to intervene
yet. The causes of death of men with low testosterone is too varied (i.e. complex) for conventional
physicians to make sense to them, since they often think simplistically, in cook-book style.
There are numerous reasons testosterone levels are declining.
For example, hypothyroidism is rampant in the U.S., with about 40% of people having
hypothyroidism. Yet, even if hypothyroidism is diagnosed (and only via lab testing), the person
remains undertreated and symptomatic. The majority of people with hypothyroidism are
undiagnosed and untreated. Hypothyroidism reduces testosterone production.
As another example, Insulin resistance (i.e. Metabolic Syndrome) and diabetes are ramptant in
the U.S. Metabolic syndrome occurs in about 30% or more of people. Insulin resistance and
diabetes results in lower testosterone production. Insulin resistance is not treated. Only the
symptoms and signs of insulin resistance - such as hypertension, hypercholesterolemia, obesity,
and heart disease - are addressed. These are bandages to the problem.
Additionally, adrenal fatigue is a very common condition since societal stresses are much higher
today than in the past. About 25% of women and about 17% of men have been traumatized by
sexual abuse. Trauma also occurs from emotional abuse and neglect. Sixty percent or more of
the children in some counties live in poverty. Poverty and homelessness are long-term traumatic
stresses.
Adrenal fatigue can lead to higher sympathetic nervous system tone, which leads to a reduction
in dopamine production, which leads to a reduction in testosterone production, among the other
neuroendocrine and immune system cascades it causes. For example, adrenal fatigue can lead
to sugar cravings and obesity (alternatively it can also lead to loss of appetite and severe weight
loss). The obesity can lead to insulin resistance and a reduction in testosterone production.
There are many estrogenic toxins and other toxins in the environment and in the foods we eat
which can lead to hormonal imbalances such as hypothryoidism and lower testosterone
production.
Since the reasons are so numerous, it is difficult for conventional physicians to recognize them
together as a cause of lower testosterone production and to come up with a comprehensive
treatment plan for addressing the issues. Conventional physicians (and even endocrinologists)
also do not often understand how hormones, neurotransmitters, and cytokines work together to
cause health or disease. It's not in the training. Of the medical specialties, anti-aging doctors
come closest to this understanding (for myself, anti-aging medicine and endocrionlogy are
actually a subset of psychiatry).
__________________
Re: Symptoms, painful hotflushes?
Quote:
Originally Posted by JustOne
Is it normal for hotflushes to become slightly painful? it is hard to explain but when I get
hot flushes I get a really dull pain in my chest, it doesnt feel like its coming from my
lungs, and its not heart burn, and it only happens when I get hot flushes.
Also recently I have been getting a slight feeling of motion sickness(that not quiet nuasea
not quiet a headache feeling) wich will last for about 2 hours then gradually go away,
just wondering if this can be related to hormones.
"Hot flushes" may actually be at least two different phenomena.
Hot flushes traditionally can occur with estrogen withdrawal. Estrogen withdrawal can result in a
reduction in serotonin, leading to serotonin withdrawl symptoms, which may include vertigo - a
sensation of the room spinning or movement.
Hot flushes can also be caused by surges in norepinephrine levels that can occur when one has
adrenal fatigue. The increase in norepinephrine can precipitate anxiety symptoms, which may
include chest pain. It is important, however, to be checked to make sure the chest pain does not
represent angina - or coronary artery disease - and an impending heart attack.
Low cortisol production resulting from adrenal fatigue may result in dizziness and nausea, among
other symptoms.
__________________
Re: Symptoms, painful hotflushes?
Quote:
Originally Posted by Megazoid
Be sure to get yourself checked out buddy. I had something similar myself but it was more
like muscle pain in the chest area with me. It would be worth going into hospital to find
out what's going on (even if they run a few chest test's to make sure they can safe
everything is good).
Regarding these "hot flushes", i have a question regarding this.
When i first injuryed my last remaining "good" testicle due to a varicocele forming (due
to injury). One of the first symptoms of low testosterone was bad "night" flushes after
about two day's of the initial injury. I am talking whole body flushes soaking my bed right
through! At this time i wasn't on TRT and taking no other medications.
Just wondering what would have caused this at the time. Was this testosterone "battling"
E2 or something?
Estradiol is made from testosterone. As testosterone levels fall, estradiol levels fall as well. This
results in estrogen withdrawal - a hot flush.
Reduction in testicular steroid production (such as testosterone) may also result in a lowering of
thyroid hormone activity (via multiple pathways, including reduction in testicular thyroid releasing
hormone production), which can result in a higher norepinephrine level as the brain compensates
for the loss of energy from lower thyroid hormone by driving adrenal hormone production. This
increase in norepinephrine may result in a hot flush.
If a person's adrenal glands are already working hard, the loss of thyroid hormone with then
increased demand for adrenal hormone production or the reduction in testosterone - which acts to
limit overactivity of the adrenal glands - may tip the scale toward adrenal fatigue developing
suddenly, resulting in a fall in glucose production along with a compensatory increase in
norepinephrine or histamine production, resulting in a hot flush.
These are some possible pathways that may result in a hot flush.
__________________
Penile Anatomy and Hot flushes
Quote:
Originally Posted by JustOne
I know its not heart related, I have had chest muscle inflamation before(lungs brushing
up against ribs) and angina, and its nothing like that at all.
The hot flushes I get are around the arms, chest and upper back, and then the face, it all
started about 8 months ago when I coincidently took a lot of antacids then a lot of speed,
it was an intense pulsating hot flush wich lasted for the whole night, I just asumed the hot
flushes were a lingering side effect from the speed and antacid reaction but I havent
touched antacids or speed since then and theres no other explanation.
marianco, refering to this thread http://forum.mesomorphosis.com/mens...134246679.html
Is there a tendon wich runs a long the top of the penis? The doctors are telling me its a
tendon but I am pretty sure the penis only has 1 tendon and thats underneath, I am
thinking it has to be a nerve or lymph vessel.
Methamphetamine abuse most often causes adrenal fatigue. Methamphetamine increases both
dopamine and norepinephrine release. The Norepinephrine release causes adrenal fatigue.
Adrenal fatigue can take months to years to recover from. It can result in the hot flush reaction.
Regarding the anatomy of the penis, look at this site:
http://www.webmd.com/content/article/7/1680_50125
The penis has no classic "tendon" - which is a cord of connective tissue that connects bone to
muscle.
Rather, the penis has connective tissue, called the tunica albuginia, which forms three sausageshapped balloons, held together in an inverted triangle formation. The bottom balloon contains
the urethra and corpus spongiosum - a sponge-like vein; and the two top balloons contain the
corpus cavernosum - also sponge-like veins.
To achieve erection, the outflow from the penis is slowed down, causing the blood to back up and
fill the corpus spongiosum and cavernosum. These erectile tissues then fill up until limited in size
by the tunica albuginia.
Unlike a balloon, which can stretch until it bursts, the tunica albuginia is like Kevlar. It will fill until
the balloons are hard then will stop expanding, allowing the erection to be rock hard.
Penile enlargement techniques try to stretch the tunica albuginia so that the penis can be larger
on erection. It takes a long time and dedication to cause the tunica to stretch and allow a larger
erection since it is very tough connective tissue.
__________________
Re: lab Results
Quote:
Originally Posted by Dutch Buster
The doc called back there was a place sooner because i said it was urgent.
Went there talked for 2,5 hours ! (where do you find a doc that's taking so much time )
after 30 min she say's do you want to do a test i says okay what ?
take this prednisolone after 5 min. my hand got warmer i got more relaxed that was soon.
This is the first doc that says you are realy sick and no a littele...
Dont't drink pipewater anymore buy a osmose filter not water in bottles there not good
and not controled.
buy only bio fruit and vegatebels
why because every body get poisend of the heavy metals and pesticide and drugs in water
EEK!
monday back to belgium for blood drawn,(42 bloodtests) and after that i may start
hydrocortisone 10mg in the morning and 10 mg at noon
30-11 back for results
I think that i finally found a good doc after 6 times it is all between your ears !
I'm glad you were able to find someone to help you. It was nice for Thierry to give you alternative
doctors to contact. I regard Thierry Hertoghe as the best European doctor for the evaluation and
treatment of hormone problems.
__________________
Re: Does this make sense???
Quote:
Originally Posted by Kanecore
Hi everyone! I've been taking 60 mg of T cyp every three days along with 100 iu of HCG
a day. My estradiol is normal but my total Es are high. I am supposed to take Arimidex at
.25 mg every other day to drop m total Es but this makes me feel horrible. So I've been
taking it as needed or when I feel anxiety and/or prostate pain. This isn't working either.
My sex drive sucks! When I do have sex, I don't even need to take Arimidex for the next
few days because it seems to lower my hormone levels significantly and I experience no
estrogen related side effects. After sex, I have no recovery and can't get another errection
for hours. Also, if I stop taking the HCG for a few days, I feel like crap. And if I stop the
HCG and take Arimidex on those days, I feel like death. I also get bad prostate pain, but I
don't have an elevated PSA. I've already had two biopsies for red spots, but they turned
out to be non cancerous. My thyroid and adrenals (24 hour urine) was optimal. My TT
and FT are in the upper normal range and my DHEA, LH, prolactin and SHBG are in
optimal range. I'm so frustrated because I've been going through this for over ten years!
The labs say I should be like a bull but I always feel like crap! Can anyone offer some
advice?
1. Prostate pain - is it truly prostate pain or is it rectal pain?
2. Estradiol level is a better measure of estrogen activity than total estrogen level. This is because
each estrogen has a different potency. Estradiol level is a sum of the estrogen activities of the
estrogens skewed toward estradiol, the most potent estrogen.
3. The other estrogens are fairly weak - so weak that they may even reduce estrogen activity by
blocking estradiol from estrogen receptors. Estriol does this, for example. This is why Estriol can
be viewed as an anti-estrogen, protecting a woman from breast cancer, when in the presence of
estradiol.
4. When estradiol level, then, is normal. There is no reason to use Arimidex. Using Arimidex may
lower estradiol level excessively, causing symptoms including loss of sex drive, depression,
anxiety, etc.
5. Estradiol is necessary for sex drive. Estradiol provides sexual aggression and thus drive.
Estradiol also determines the number of testosterone receptors made, making testosterone more
potent.
6. Excess estradiol can reduce sex drive. Estradiol, for example, acts as a monoamine oxidase
inhibitor, which can primarily drive sertonin levels up. HIgh serotonin levels can inhibit sex drive
directly or by reducing dopamine production - where dopamine is the most direct determinant of
libido, sexual desire/drive.
7. The sympathetic nervous system triggers orgasm. This may occur via an increase in
norepinephrine - the sympathetic nervous systems main chemical messenger - made primarily in
the group of neurons called the locus ceruleus in the brain stem.
8. Dopamine production is reduced during and after an orgasm. This results in the Refractory
Period - during which achieving another erection and sex drive are inhibited. The dopamine
reduction causes an increase in Prolactin. Lower dopamine and higher prolactin can reduce
testosterone production - reducing sex drive further.
9. If the refractory period is long - such as when men age - this means dopamine levels do not
return to their basal levels quickly because production is slow. This may also mean there were
low dopamine levels to begin with, and orgasm lowered the levels even more.
10. As humans age, dopamine neurons die off. There are only about 50,000 of them in the brain.
They control huge chunks of function and behavior.
11. Other neurotransmitter/hormone/and immune-system cytokine problems can cause a
lowering of dopamine production, makes the refractory period longer.
12. Note that dopamine levels need to vary with time so that the brain can sense dopamine.
13.. Increasing dopamine to high levels artificially may result in insensitivity to dopamine. This
may occur when testosterone levels are too high - since testosterone increases dopamine
production. Low dopamine levels, such as from prolonged testosterone deficiency, may result in
suprasensitivity to dopamine. This may cause the initial and transient euphoric effects of
testosterone when TRT is started.
14. Thyroid and adrenal testing via 24-hour urine testing may not be sensitive enough to find
problems. For thyroid tests, it is far better to obtain blood TSH, Free T3, and Free T4. For adrenal
testing, obtaining a blood Cortisol - AM, DHEA-s, Progesterone, Albumin, fasting glucose as well
as obtaining multiple Saliva Cortisol and DHEA levels would give a better idea as to the presence
of adrenal fatigue as a factor in sexual function.
15. Neurotransmitters, hormones, and immune-system cytokines are highly linked in function.
16. When total testosterone is in the upper normal range, other neurotransmitter, hormone, or
cytokine problmes are present to cause the problem.
17. High normal free Testosterone may actually be a clue that there are other hormone problems
occurring.
18. Even with normal thyroid hormone levels, some people are still hypothyroid. They have
thyroid hormone resistance caused by mitochondrial problems. There is not test for this
mitochondrial problem. Thus it is highly important to look at the history of a person and perform a
physical exam to determine if hypothyroidism is present, even with normal thyroid tests. For such
a person, treatment with thyroid hormone replacement is necessary. The goal of treatment is to
reduce the signs and symptoms of hypothyroidism, not to treat the lab test since it would look like
the person is becoming hyperthyroid on the lab test, but they are still hypothyroid clinically based on the exam and history. With many hormone problems it is not simply enough to look at
the lab test.
19. For 24-hour urine tests, it is highly important to evaluate the hormone metabolites to
determine what is actually occurring. Even with a normal urine cortisol, if the metabolites are
deficient, then the person may actually be deficient in cortisol since the cortisol in the urine
represents cortisol which has not been used or has been active.
20. It is also important to look at the person to determine if there is a particular hormonal problem.
For example, a person who appears obese may appear to have a high growth hormone level (via
high IGF-1 of 300). However, such a person may actually be deficient when obesity is taken into
consideration. Similarly with hypothyroidism as discussed above.
21. Neurotransmitter levels can be obtained using a urine test. It can be ordered by a health care
provider from NeuroScience, Inc. or Sanesco, Inc. The neurotransmitter levels then can be
correlated with the signs and symptoms and other hormone and cytokine levels to determine
what is happening. There is a good correlation between urine neurotransmitter levels and brain
neurotransmitter levels. But this is not always so. For example, 90 percent of serotonin is
produced by the gut's nervous system. It is up to the skill of the physician to determine what a
particular neurotransmitter level means both alone and in concert with other chemical
messengers.
22. "Optimal range" depends on the person evaluating the lab test. It would be nice if you would
provide us with the actual levels from your lab tests so we can see for ourselves whether they are
optimal or not. As Cuban Gooding said, "Show me the money!"
__________________
Re: Health Insurance
Quote:
Originally Posted by thefantom1
Could this be SPAM !!!!!!
This appears to be an effort to collect your name, phone number, address, and email number.
The insurance advertised in the link is not free.
Health insurance is not actually free. Someone has to pay for it. Or there are substantial
limitations in the services.
Where there is universal health insurance - such as in some countries - one pays for it through
higher income tax. There are significant limitations in the services you may obtain.
Some poor people in California can receive Medi-Cal health insurance for "free". The main
limitation is that one has to remain poor, e.g. one can't have more than $3000 in cash or personal
property (e.g. a car). To not remain poor results in a loss of health insurance and potential loss of
health - which may not be covered by the job that one gets to pull oneself out of poverty. This
places many people in a bind - for which many have to choose to remain poor - particularly when
they have chronic illnesses which are expensive to treat (e.g. major mental illnesses, diabetes,
heart disease, etc.). One may be even denied when having such an illness by insurance
companies when attempting to buy one's own health insurance. California is a state where health
insurance companies can deny insurance due to pre-existing conditions. Washington State is not.
Etc.
Re: periodic stop TRT with short PCP
Quote:
Originally Posted by hoochyman1
I had the same question awhile back, but haven't attracted any response.
The reason I had asked about this is that so many people who have used testosterone
experience shut-down of the HPTA, sometimes for a long time. I gather that this is mostly
younger men who have taken much higher dosages than you would ordinarily use for
TRT (I'm injecting 100 mg test E every 5 days). Since I'm older (67) I wondered whether
my age might make me more susceptible to HPTA shut-down, even at this relatively low
dose, should I ever have to stop TRT (e.g., because of polycythemia, etc.) I wondered
whether periodic respites might restart my HPTA, and avoid extended or permanent shutdown in the event I have to stop TRT some day.
My serum testosterone before TRT wasn't 'officially' hypogonadal (it was around 450)
but I had strong signs of androlpause anyway. The TRT has been extremely effective. I
also wonder, though, whether I'm not driving my serum T up too high (over 800 ng/DL 5
days after injection, range is 200-1000). Free test also high, outside 'normal' range),
around 50. Am I taking too high a dosage? I don't aromatize all that much, estradiol is
30 ( a good number, optimal thought to be 20-30).
Thanks for following up on this question.
1. What were the signs of andropause? The question I would have is whether nor not the signs of
andropause were caused by other hormonal problems than testosterone.
2. The Hypothalamic-Pituitary-Testicular axis will always be suppressed with testosterone
replacement therapy (including HCG therapy). In order to raise testosterone level over the
baseline enough testosterone has to be added to overcome the reduction LH production from the
pituitary from testosterone replacement. The testes will atrophy stop testosterone production from
the loss of LH production - unless HCG - an LH analog - is used to prevent testicular atrophy.
Whether or not the HPT axis can bounce back to full activity will depend on many factors
including one's age. Past the age of 60 or even younger ages, for example, the testes may not
respond to LH or HCG. Past the age of 50 or even at younger ages, the pituitary of many men is
too old to preduce enough LH to drive testosterone production.
3. One does not have to completely stop TRT due to polycythemia. The dose can be reduced or
blood can be donated or removed, etc. to reduce the risk of polycythemia.
4. Free Testosterone is determined primarily by the level of Sex Hormone Binding Globulin
(SHBG) because albumin production is fairly stable - unless dehydration or dietary protein
insufficiency is present. SHBG is increased by thyroid hormone, estradiol, and progesterone.
SHBG is reduced by testosterone, DHEA, insulin, growth hormone, Dihydrotestosterone, and
other androgens.
5. A high free testosterone with high-physiologic total testosterone implies there are other
hormone problems besides testosterone. Common problems include hypothyroidism, insulinresistance (which causes high insulin levels), adrenal fatigue, etc. Testosterone treatment alone
may not fully correct these problems in many men. One is lucky if it does since it can in some
men.
6. Due to age-related changes which can be irreversible, I do not think the HPT axis can be fully
restored in older men (e.g. those over 40). Thus periodic withdrawal of TRT may be an exercise
in exposing a person to problems caused by low testosterone.
7. Early treatment with growth hormone might slow down the deterioration in the HPT axis.
Growth hormone drops quickly after the age of 30.
8. Optimal treatment of hypothyroidism and insulin resistance may help restore some of the
testosterone production lost due to these problems - to thus see what one's true capacity to
produce testosterone is before embarking on TRT as a solution.
__________________
Re: Enanthate or cypionate???
Quote:
Originally Posted by the/rock
Which one to use????They are so simular???
What are the pros and cons???
Testosterone Enanthate has an average half-life of between 7-9 days.
Testosterone Cypionate has an average half-life of around 7 days.
The half-life varies per person. Some have a half-life much shorter than 7 days. Some longer.
Testosterone Enanthate can have slightly more even blood levels than T. Cypionate.
Testosterone Enanthate is in a much thicker solution than Testosterone Cypionate.
It is harder to push T. Enanthate through a small gauge needle (e.g. 25 gauge) than T.
Cypionate.
It takes longer to inject T. Enanthate through a small gauge needle (for less pain) than T.
Cypionate.
Testosterone Cypionate is less expensive than Testosterone Enanthate.
Otherwise, they are similar. 200 mg/ml of either one gives you the same amount of testosterone.
__________________
Re: Enanthate or cypionate???
Quote:
Originally Posted by tres
i have read in many spots that enanthate is a couple days shorter acting than cyp.
but to be honest who cares!!!
my quetsion i can i inject .50 on monday then .50 on thursday???
Twice a week dosing is my preferred schedule for doing depo-testosterone injections with either
T. Cypionate or T. Enanthate. The peaks are smaller, the valleys are smaller, the overall
testosterone level is much more stable within a smaller range. Twice a week dosing also takes
into account those men who have a short-half-life for testosterone - necessitating twice a week
dosing to avoid problems. Twice a week dosing also reduces the high peaks which result in high
DHT or Estradiol levels. For some patients, for example, the DHT level can be below the pretreatment/baseline level when twice a week dosing is used. There would therefore be less need
to use an alpha-reductase enzyme inhibitor to control DHT.
The half-life of testosterone is between 10 minutes to 100 minutes - a huge range. Thus not every
schedule will fit any particular person. The twice a week dosing works for most men, not all. If
every day dosing is necessary, then perhaps testosterone pellets would be an alternative to
consider.
Once every 2 week dosing results in large supraphysiologic levels in the beginning for
testosterone, DHT, and estradiol. The estradiol levels remain supraphysiologic long after
testosterone has significantly declined - creating potential problems.
Once a week dosing is a compromise which works for the average man, but does not work for
those with short-half-life testosterone.
For twice a week dosing, a dose on Monday and Thursday can be done. Some do it on Monday
and Friday with decent effects. The timing needs to take into account the person's schedule.
Note that the peak testosterone level with injections occurs between 24-48 hours after the
injection.
__________________
Re: Nolvadex and Sex drive
Quote:
Originally Posted by Andromeda
To treat gynecomastia and lower my estrogen levels I've been taking Nolvadex since Sept
11 this year. Initially the first month saw me take just 10mg a day. At the 1 month
followup review this has since been upped to 20mg a day.
In the first few days since upping the dosage my sex drive improved greatly. eg: Face to
face contact with attractive females at supermarket or in the office led to partial erections
and pre-cum production (depending on situation)
However approx 2 weeks after starting the higher dosage I find my sex drive is as poor as
ever, and I'm rarely getting aroused in the aforementioned situations where I normally
would. I recently read a great reply Marianco made to this thread
http://forum.mesomorphosis.com/mens-...134246742.html and note that estrogen levels
are needed for arousal and sexual proactivity. Is it possible that the Nolvadex which now
must be at fairly high levels in my system, is somehow suppressing sex drive. eg: blocking
estrogen receptors in the brain that are responsible for arousal? Or is it actually leaving
my brain saturated with too much fake estrogen which is then disturbing sex drive?
Any advice will be much appreciated as I have my followup review soon where I have a
chance to make treatment alterations....
Thanks in advance,
Nolvadex can block estrogen receptors in the hypothalamus resulting in an increase in LH
production, which then increaes tesotsterone. But Nolvadex can block estrogen receptors in the
brain which affect sex drive, which can be experienced at higher doses. When it comes to
estrogen, a balance (not too low or not too high) is necessary.
Nolvadex is an option to testosterone deficiency. However, the long-term risks are not well known
in men. The risk for blood clots is also a concern, among the side effects.
__________________
Re: Symptoms, painful hotflushes?
Quote:
Originally Posted by JustOne
Is it normal for hotflushes to become slightly painful? it is hard to explain but when I get
hot flushes I get a really dull pain in my chest, it doesnt feel like its coming from my
lungs, and its not heart burn, and it only happens when I get hot flushes.
Also recently I have been getting a slight feeling of motion sickness(that not quiet nuasea
not quiet a headache feeling) wich will last for about 2 hours then gradually go away,
just wondering if this can be related to hormones.
"Hot flushes" may actually be at least two different phenomena.
Hot flushes traditionally can occur with estrogen withdrawal. Estrogen withdrawal can result in a
reduction in serotonin, leading to serotonin withdrawl symptoms, which may include vertigo - a
sensation of the room spinning or movement.
Hot flushes can also be caused by surges in norepinephrine levels that can occur when one has
adrenal fatigue. The increase in norepinephrine can precipitate anxiety symptoms, which may
include chest pain. It is important, however, to be checked to make sure the chest pain does not
represent angina - or coronary artery disease - and an impending heart attack.
Low cortisol production resulting from adrenal fatigue may result in dizziness and nausea, among
other symptoms.
__________________
Re: Symptoms, painful hotflushes?
Quote:
Originally Posted by Megazoid
Be sure to get yourself checked out buddy. I had something similar myself but it was more
like muscle pain in the chest area with me. It would be worth going into hospital to find
out what's going on (even if they run a few chest test's to make sure they can safe
everything is good).
Regarding these "hot flushes", i have a question regarding this.
When i first injuryed my last remaining "good" testicle due to a varicocele forming (due
to injury). One of the first symptoms of low testosterone was bad "night" flushes after
about two day's of the initial injury. I am talking whole body flushes soaking my bed right
through! At this time i wasn't on TRT and taking no other medications.
Just wondering what would have caused this at the time. Was this testosterone "battling"
E2 or something?
Estradiol is made from testosterone. As testosterone levels fall, estradiol levels fall as well. This
results in estrogen withdrawal - a hot flush.
Reduction in testicular steroid production (such as testosterone) may also result in a lowering of
thyroid hormone activity (via multiple pathways, including reduction in testicular thyroid releasing
hormone production), which can result in a higher norepinephrine level as the brain compensates
for the loss of energy from lower thyroid hormone by driving adrenal hormone production. This
increase in norepinephrine may result in a hot flush.
If a person's adrenal glands are already working hard, the loss of thyroid hormone with then
increased demand for adrenal hormone production or the reduction in testosterone - which acts to
limit overactivity of the adrenal glands - may tip the scale toward adrenal fatigue developing
suddenly, resulting in a fall in glucose production along with a compensatory increase in
norepinephrine or histamine production, resulting in a hot flush.
These are some possible pathways that may result in a hot flush.
__________________
Re: Low T - Dealing with Doctors/Family/Friends
Quote:
Originally Posted by JustOne
I have learnt to completely ignore it when my doctors tell me my T level is normal,
My 1st GP agreed it was low(400ng/dl), my urologist ordered a 2nd blood test wich was
higher and said it was normal 547ng/dl. An anti aging doctor agreed it was low, and my
oncologist asked me how long I hadnt shaved in.
It is imposible to convince my sister I need HRT, but I was able to convince my brother.
The few friends I have told defenetly believe me because all of a sudden I am declining
offers to go out, I will go one place with them, then decline to go somewhere else
afterwards because I have no energy.
1. When testosterone is "normal" and problems are still present, then there are other
neurotransmitter/hormone/immune-system cytokine problems occurring that are the cause of the
problem. Testosterone is only one of numerous neurotransmitters/hormones/cytokines that
determine sex drive. Using testosterone as the only measure misses what may be the actual
cause of problems.
2. A total testosterone of 547 ng/dl is high enough and a level of 400 is still high enough that other
problems are probably present and are MORE important to determine and treat.
3. Social withdrawal or loss of energy or loss of confidence are some of the symptoms associated
with adrenal fatigue and/or hypothyroidism (which can lead to adrenal fatigue). There are
complex changes in neurotransmitters when these conditions are present that contribute to the
behavioral changes.
4. When energy is an issue, then thyroid hormone or adrenal hormones are at the center of the
problem. If there are other hormone problems, then they all usually end up influencing thyroid
hormone or adrenal hormones as the common final pathway to determining energy problems.
5. When the production of testosterone results in a reduction in energy level, it is not testosterone
itself that is the problem. Often, a thyroid hormone deficiency or insulin excess (insulinresistance) or adrenal cortisol deficiency is the simultaneous problem. If these other problems are
not addressed, then even with testosterone replacement, energy level can remain low.
6. When testosterone replacement increases energy level, it may do so by stimulating thyroid
hormone production. However, in many people, testosterone actually instead causes a reduction
in thyroid hormone production. Thus testosterone can reduce energy instead of improving it.
Addressing the thyroid problem directly is more likely to help address the energy problem.
Best wishes in finding a solution.
Re: Gels to Injections T amounts?
Quote:
Originally Posted by magic8989
I am just starting to switch from the gels to the injections. I was on 10g of androgel daily
and this made my levels flucuation. On some lab results i would get in the 600 for total T
and a few i was almost over the top for total T. I made sure to take a shower before
getting my lab results each time as well to make sure the gel was not on my arms. My
question is my doc said the conversion from the gel to injections can be hard and he is
starting me on 100mg of depo test twice weekly. Is 200mg a week too high of a dose? I
know everyone is different but from most of what i have read on here many do not go this
high. I also asked about E2 and he said it is possible and will see me again in 8 weeks. As
a precaution i am going to keep taking my DIM/Indplex and TMG though as i have been
taking this for a bout 4 weeks. My E2 a few months ago was 29 so i am a little worried
about it.
Thoughts?
100 mg a week of Depo-testosterone is a good starting dose and is often equivalent to 10 grams
of Androgel a day, in achieving a good total testosterone level.
Re: Gels to Injections T amounts?
Quote:
Originally Posted by magic8989
Thanks for you input. I know most docs are stupid but i wonder why mine started me off
so high. Thus far he has been very good about my HRT with the gels at least and he does
not base everything off of the lab results so this makes me wonder.
The primary guidelines for testosterone replacement using Depo-testosterone use a starting dose
equivalent to 100 mg/week. I am not sure if your doctor is aware of this. 200 mg a week for a
starting dose would only be appropriate for a person proven to have a short half-life of about 3-4
days for Depo-testosterone.
__________________
HCG and Fertility
Quote:
Originally Posted by DAVID
I'm on HRT since 10 year's, five year's ago I have a baby with my wife with one shot of
200 mg of testosterone eveyr three week !!!!
But at this time my wife want another baby but it's more difficult... I'm on testosterone gel
and my spermogram is oligospermia...
The physician put me on HCG 1500 IU with FSH 3 time a week. I stop after two month
because I have bloating, my libido go down, I'm sweating all the night, big water
retention. I try clomid or proviron with that but I feel depress. I look like smooth with no
libido. GREAT...
Thank you for your help. Can I take my testo gel with small dosage of HCG like 250 IU ,
do that work for fertility ? I remember that I have a baby with testosterone, and when I
don't take testosterone my life is a misery.
I've bad experience with femara too, my estradiol with only 1/4 of femara go to 60 pg to
< 9 pg.
I've reading that too much oestradiol or too litlle estradiol kill spermatogenesis. Some
guy said in this board that arimidex doesn't kill to much estradiol. Are the true ?
I take also many vitamins, minerals and control all the hormone on my body to have a
good balance.
Thank you for your help...
1. When taking HCG, one needs to watch for excessive estradiol production since HCG increases
aromatase enzyme production. Excessive estradiol can not only reduce sex drive but can also
increase thyroid binding globulin production, which traps thyroid hormone and causes a relative
hypothyroid state. This not only further reduces libido, but may lead to a surge of norepinephrine
production as the brain tries to compensate for the energy loss by forcing the adrenal glands to
work harder. This and ups and downs in estradiol level can lead to hot flashes or sweating.
2. When taking HCG, it is thus important to control estradiol excesses using, for example,
Arimidex. The starting dose can be 0.5 mg a week, given the long half-life.
3. When taking HCG, it is important to optimize thyroid hormone.
4. Estradiol is necessary for sperm production. Excessive reduction in estradiol may impair sperm
production and sex drive.
5. One will need to monitor sperm production to determine if the use of HCG or Clomid works.
__________________
Re: HCG and Fertility
Quote:
Originally Posted by DAVID
thank you for thsi answer Marianco. Do you think arimidex lower too much estradiol like
femara. In fact, after only 1 tabs of femara (1/4 of tablets 2 times a week for 2 weeks) put
my estradiol level near to zero. Do arimidex is different ?
And one more question. For people who have hypogonadism from hypothalamus, the mix
of HRT with androgel and hcg are effective or not for male fertility ?
Because I suppose that hcg alone isn't great for arousal, libido and well being for
hyponadism
One will have to measure sperm production to determine if the mix of androgel and HCG affects
fertility. It cannot be determined without measurements. Many men on HRT are still fertile, with
estrogen contributing to sperm production, not just FSH.
The affect of Arimidex or Femara depends on the person. One cannot truly know until the effect is
measured, given variability in response. Both are aromatase inhibitors.
__________________
Re: HCG and Fertility
Quote:
Originally Posted by Andrew Androgen
Is it just estradiol that does these things, or is it the elevation in the other estrogens as
well? If it's just estradiol, then taking Indoplex/DIM would be a big help for someone on
HCG.
When using Arimidex or other aromatase inhibitors to reduce estradiol level, what is interesting is
that total estrogens may rise to very high levels as testosterone is metabolized through other
pathways. Yet these estrogens do not contribute much to impairing sex drive or causing side
effects of estradiol. They are weaker than estradiol.
Indoplex/DIM does block the enzymes which convert estradiol into other proliferative estrogens,
reducing the effects of growth inducing estrogens (such as cancer risk), by shunting estrogen
metabolism to the non-proliferative estrogens.
Indoplex/DIM may be useful if the proliferative estrogens can be shown to contribute to sexual
dysfunction. Urine tests for estrogen metabolites would be needed to measure the effects of
Indoplex/DIM.
In Serious need of help.
Quote:
Originally Posted by roro
IUp to the age of fifteen, I was completely normal (uncontrollable erections and thoughts
of sex 24/7). However I got a urinary infection, my semen changed in appearance, and all
I could think was “**** me, I’m going to lose my sex drive and become impotent. I
worried intensely about this for years, and surprise surpise these things manifested
completely.
I am now 33, I don’t have a libido at all. I only really masturbate to try and make sure
nothing ‘shuts down’. I never get full erections, and only RARELY get soft morning
erections.
For the record, there is nothing wrong with my secondary sexual characteristics, and 2
months working out gets back a great physique.
The serum testosterone and SHBG ended up being done twice as it took 3 visits to get all
the tests done that I requested.
Serum Testosterone 18.1 nmol/L (10.0–31.0) 31/07/06
Serum Testosterone 22.7 nmol/L (10.0–31.0) 07/08/06
Bio-available Test’ 15 nmol/L unknown
DHT 2.62 nmol/L (0.9-2.9) unknown
SHBG 13.8 nmol/L (13.0-71.0) 31/07/06 (ammended report?)
SHBG 17.1 nmol/L (13.0-71.0) 07/08/06
FSH 2.9 iu/L (0.8-13.0) 31/07/06
LH 3.9 iu/L (0.5-10.0) 31/07/06
Oestradiol 128 pmol/L (0-206) 31/07/06
Prolactin 167 mIU/L (53-360) 31/07/06
Cortisol 356 nmol/L (138-690) 07/08/06 (morning sample)
TSH 3.07 mIU/L (0.3-4.1) 07/08/06
Albumin 43 g/L (35-50) 31/07/06
Triglycerides 0.7 mmol/L (0.8-1.7) 31/07/06 (only included as low)
Ten years ago, this incredibly in-depth investigation was done……………
Serum Testosterone 26.2 nmol/L (10.0–31.0) 04/06/96
I have never done any steroids.
To help those of us in the U.S. understand the labs better, it is important to convert the units from
SI to conventional units:
Total Testosterone = 22.7 nmol/L = 649 ng/dl
Dihydrotestosterone = 2.62 nmol/L = 75 ng/dl
Sex Hormone Binding Globulin = 17.1 nmol/L
FSH = 2.9 iu/L
LH = 3.9 iu/L
Estradiol = 128 pmol/L = 35 pg/ml
Cortisol = 356 nmol/L = 12.9 mcg/dl
TSH = 3.07 miu/ml
Albumin = 43 g/L = 4.3 g/dL
Triglycerides = 0.7 mmol/L = 62 mg/dL
1. When total testosterone is good, but problems remain (e.g. sexual dysfunction), then the
problem lies elsewhere. This means there are other neurotransmitter/hormone/immune-cytokine
problems that are present to cause the problem.
2. A total testosterone of 649 is high enough to indicate that there is no need for testosterone
replacement. The problem lies elsewhere.
3. Sex Hormone Binding Globulin is increased by thyroid hormone, estrogens, and progesterone.
It is lowered by androgens (e.g. testosterone, DHEA), growth hormone, and insulin.
4. Low sex hormone binding globulin can occur most commonly with insulin-resistance/diabetes
type 2 (with high insulin levels), and with hypothyroidism. Low estrogen and progesterone may
also contribute.
5. Clues to insulin-resistance/diabetes includes a fasting blood glucose over 102 mg/dl, a high
fasting insulin, high glucose and insulin levels on a 3-hour glucose tolerance test, a triglyceride
(mg/dl) to HDL cholesterol (mg/dl) ratio > 3.5.
6. High estradiol may impair sexual function. Estradiol increases the production of thyroid binding
globulin, which then reduces the activity of thyroid hormone. Estradiol itself competes with thyroid
hormone at the thyroid hormone receptor. This causes a relative state of hypothyroidism which
reduces libido.
7. Estradiol is important for sex drive. Excessively low estradiol levels will contribute to a lack of
libido. Estradiol is necessary for the production of numerous neurotransmitters - such as
serotonin, dopamine. etc. Estradiol itself contributes to sexual aggression - hence sex drive.
8. It is far more important to address testosterone production, thyroid hormone activity, and
adrenal hormone activity first before considering estrogen as a problem - because most often it is
not estrogen that is the problem. When total testosterone is around 650 ng/dl, estradiol can be as
high as 50 and a person can still have good sexual function - so long as there is adequate thyrod
hormone and adrenal hormone activity.
9. Often, when sexual function improves because of the use of an aromatase inhibitor, the
lowering of estradiol ends up improving thyroid function, which then improves sexual function.
The thyroid dysfunction is the original problem. Once thyroid hormone is optimized, then estradiol
control becomes much less of an issue.
10. A morning cortisol of around 18-20 mcg/dL is about ideal. When the morning cortisol is low,
adrenal fatigue or adrenal insufficiency may be occurring - causing fatigue, anxiety, and a loss of
sex drive - among other symptoms.
11. Lab clues to adrenal fatigue include: low normal fasting blood sugar (e.g. < 93 mg/dL), low
sodium, low potassium, low or low normal progesterone, low albumin, low DHEA-s, low normal
cortisol AM and PM, low saliva cortisol levels. Additionally, in post-menopausal women: low
testosterone, low estradiol.
12. Hypothyroidism causes sexual dysfunction. It can also lead to insulin-resistance and diabetes;
as well as adrenal fatigue; depending on the stresses a person experiences in their life.
13. Clues to hypothyroidism include: TSH > 2.0 mIU/mL OR a Free T3 < 3.3 pg/mL OR a low
Free T4.
14. The Free T3 is the most important measure since it represents the most active thyroid
hormone and the hormone measured by the brain to determine TSH. Unfortunately, for various
reasons, the TSH is often wrong. For example, with age or brain injury, the brain cannot produce
enough TSH, leading to hypothyroidism despite a "normal" TSH. TSH is the brain's opinion of
how much T3 is available. Unfortunately, the brain can be wrong.
15. There are people who have a mitochondrial disease which causes thyroid hormone
resistance. For them, they have completely normal thyroid hormone levels but they are clinically
hypothyroid - having all the signs and symptoms of hypothyroidism. For them, a trial of thyroid
hormone treatment is indicated - since they need higher than normal thyroid hormone levels to
treat their signs and symptoms.
16. When it comes to the diagnosis of hypothyroidism, it is important to see a physician who can
diagnose hypothyroidism strictly by history and physical exam - without relying on lab tests. This
is a physician who has not lost his/her skills at physical diagnosis, and will most likely be able to
help the person suffering from hypothyroidism.
17. If the physician has to rely on the lab test for the diagnosis, then that physician will be blind to
the adequate treatment of hypothyroidism. If treated, the patient will improve but will not be fully
well.
18. Unfortunately, too many endocrinologists are willing to keep a person hypothyroid than to risk
getting optimum treatment out of fear of letting the person become hyperthyroid. To do this keeps
the person at high risk of obesity, diabetes, heart attacks, strokes, cancer, sexual dysfunction and
mental illness. Since hyperthyroidism is obvious to diagnosis, and one needs very high doses of
thyroid hormone to achieve a hyperthyroid state, I think this is an unfounded fear. Also, if one
uses Armour Thyroid, rather than T3 or Cytomel, to obtain T3, safety is enhanced. Unfortunately,
many endocrinologists view Armour Thyroid as a primitive treatment - yet it is highly standardized
in dose (30 mg of Armour thyroid has 19.5 mcg of T4 and 4.5 mcg of T3).
By the way, if you are in Europe, the best physician there for addressing hormone problems is
Thierry Hertoghe, M.D., in Belgium. He is fabulous. He comes from a long line of famous
endocrinologists. He is a true anti-aging physician.
__________________
Re: Hypogonadal recovery time?
Quote:
Originally Posted by JackBauer
How long will it normally take for erectile health / quality to return once T levels are
raised back to real levels?
Is it a matter of weeks, months? I've had low T levels for over 3 years, and I think I'm just
getting them back to higher levels... I'm not yet seeing it in the erectile area though.
Thank
If total testosterone is at least 650 ng/dl and erectile problems are still present, then there are
other factors causing erectile problems.
This includes thyroid hormone deficiency, cortisol and other adrenal hormone deficiencies,
excess or deficient estradiol, circulation problems, diabetes or insulin resistance, nervous system
problems, etc.
Assuming there are no other health problems or other neurotransmitter, hormone, or immune
system cytokine problems, then correcting testosterone levels can increase sex drive in a matter
of hours or a few days.
The problem is when total testosterone is low, there are usually multiple health problems present
which either contribute to low testosterone or are results of low testosterone (which then further
contributes to low testosterone). Thus for many men, testosterone replacement alone will not
solve their problems. It is important to at least examine the entire endocrine system to determine
where problems lie.
__________________
Re: Hypogonadal recovery time?
[QUOTE = Anonymous]As you will know from seeing my most recent thread, i went downhill
pretty fast. Is free testosterone the most important value to monitor when on TRT? To the best of
my knowledge this is responsible for maintaing flaccid penis size and the ability to get erections.
Have you ever dealt with a man who has low testosterone and a varicocele? Have you ever
witnessed a man having this repaired and seeing improvements in testosterone levels (both total
and free)?
What controls the ability to "maintain" these erections and control the recovery time between
orgasms? My penis feel's numb for a while (hour's infact) while in the past (when i had a large
functioning testicle) it would only take maybe 20/30 minutues before i could "go" again and get
another erection. Now it seem's like almost a day is needed.
When my testicle started shrinking, the problems started. The first thing i noticed was lack of
morning erections and also reduced erection strength. Everything started going downhill from that
point. I am not even sure what caused the actual testicular shrinkage other than the varicocele
and blockage of the spermatic cord. I am seeing a urologist this week who is going to look into
varicocele surgery as an option to restart my own system. Because both testicles have atrophied
(and underlying problem still isn't fixed) would you recommend HGC as a way to quickly restore
testicular size or would you simply wait and see if my own system would restart on it's own? I feel
it might be best to stop putting more chemicals into my body and just wait to see if nature take's
it's course.
I started on TestoGel (AndroGel) but i have been getting a bad full body itch and skin irritation
(full body - lots of rashes, etc). For the time being i have stopped TRT to see if this reaction will
clear. How long does it take (on average) for the TestoGel to "flush" out of your blood
stream/system? I am going to stay off everything (even if i feel bad) to see if this skin reaction
clears up.
I have been told to try Testim instead (which has a different formula) and shouldn't give as bad a
reaction (fingers crossed).
Is it more dangerous to come off of TRT all together to see if these problems "heal" or is it best to
switch to Testim right now to help my immune system get more testosterone to "fix" the
problems?
Any advice you can give on the above would be great.[/quote]
I can't give you advice since you are not a patient or client of mine.
1. Total testosterone is the most important value to monitor when on TRT. Bioavailable
testosterone is second.
2. I have not yet dealt with varicoceles.
3. Maintaining an erection is a complex process involving having an adequate parasympathetic
nervous system tone (i.e. a greater brain emphasis on resting functions over fight-or-flight
functions - and sex is a resting function), adequate balance between testosterone and other
reproductive hormones, adequate energy, a patent nervous system to the penis, adequate
circulation in the penis, and intact smooth muscle function in the penis.
4. The recovery time between orgasms is determined primarily by dopamine levels, which drop
after an orgasm, causing an increase in prolactin and prolactin’s neuroendocrine
cascade/consequences.
5. HCG, by acting as an LH analogue, helps maintain testicular size when LH production is
reduced.
6. Androgel or Testim provides an external supply of testosterone to the body. How long Androgel
or Testim lasts depends on the person’s ability to metabolize testosterone. Usually by about the
third or fourth day, after stopping its use, the testosterone level is close to baseline.
7. Androgel and Testim have other ingredients to which some people may be allergic.
8. Using an external supply of testosterone will reduce LH production by the pituitary, as the brain
senses the extra testosterone levels. This results in atrophy of the testicles.
Outside of sexual problems and atrophied testicles, what other problems are you experiencing?
This may help determine if it is more than testosterone deficiency that is the problem. Often, it is a
multi-hormone/neurotransmitter problem that is occurring to cause a person's problems. When
one hormone becomes deficient, there are often other hormones also causing problems.
__________________
Re: Grape seed extract a natural aromatase inhibitor
Quote:
Originally Posted by Andrew Androgen
In my research for safe alternatives to drug aromatase inhibitors, I discovered that grape
seed extract both inhibits aromatase & downregulates its expression:
Grape seed extract is an aromatase inhibitor and a suppressor of aromatase
expression.Kijima I, Phung S, Hur G, Kwok SL, Chen S.
Department of Surgical Research, Beckman Research Institute of the City of Hope,
Duarte, California, USA.
Aromatase is the enzyme that converts androgen to estrogen. It is expressed at higher
levels in breast cancer tissues than normal breast tissues. Grape seed extract (GSE)
contains high levels of procyanidin dimers that have been shown in our laboratory to be
potent inhibitors of aromatase. In this study, GSE was found to inhibit aromatase activity
in a dose-dependent manner and reduce androgen-dependent tumor growth in an
aromatase-transfected MCF-7 (MCF-7aro) breast cancer xenograft model, agreeing with
our previous findings. We have also examined the effect of GSE on aromatase expression.
Reverse transcription-PCR experiments showed that treatment with 60 mug/mL of GSE
suppressed the levels of exon I.3-, exon PII-, and exon I.6-containing aromatase mRNAs
in MCF-7 and SK-BR-3 cells. The levels of exon I.1-containing mRNA, however, did not
change with GSE treatment. Transient transfection experiments with luciferasearomatase promoter I.3/II or I.4 reporter vectors showed the suppression of the promoter
activity in a dose-dependent manner. The GSE treatment also led to the down-regulation
of two transcription factors, cyclic AMP-responsive element binding protein-1 (CREB-1)
and glucocorticoid receptor (GR). CREB-1 and GR are known to up-regulate aromatase
gene expression through promoters I.3/II and I.4, respectively. We believe that these
results are exciting in that they show GSE to be potentially useful in the
prevention/treatment of hormone-dependent breast cancer through the inhibition of
aromatase activity as well as its expression.
PMID: 16740737 [PubMed - indexed for MEDLINE]
This is interesting and potentially useful information.
__________________
Re: Enanthate or cypionate???
Quote:
Originally Posted by the/rock
Which one to use????They are so simular???
What are the pros and cons???
Testosterone Enanthate has an average half-life of between 7-9 days.
Testosterone Cypionate has an average half-life of around 7 days.
The half-life varies per person. Some have a half-life much shorter than 7 days. Some longer.
Testosterone Enanthate can have slightly more even blood levels than T. Cypionate.
Testosterone Enanthate is in a much thicker solution than Testosterone Cypionate.
It is harder to push T. Enanthate through a small gauge needle (e.g. 25 gauge) than T.
Cypionate.
It takes longer to inject T. Enanthate through a small gauge needle (for less pain) than T.
Cypionate.
Testosterone Cypionate is less expensive than Testosterone Enanthate.
Otherwise, they are similar. 200 mg/ml of either one gives you the same amount of testosterone.
__________________
Re: Enanthate or cypionate???
Quote:
Originally Posted by tres
i have read in many spots that enanthate is a couple days shorter acting than cyp.
but to be honest who cares!!!
my quetsion i can i inject .50 on monday then .50 on thursday???
Twice a week dosing is my preferred schedule for doing depo-testosterone injections with either
T. Cypionate or T. Enanthate. The peaks are smaller, the valleys are smaller, the overall
testosterone level is much more stable within a smaller range. Twice a week dosing also takes
into account those men who have a short-half-life for testosterone - necessitating twice a week
dosing to avoid problems. Twice a week dosing also reduces the high peaks which result in high
DHT or Estradiol levels. For some patients, for example, the DHT level can be below the pretreatment/baseline level when twice a week dosing is used. There would therefore be less need
to use an alpha-reductase enzyme inhibitor to control DHT.
The half-life of testosterone is between 10 minutes to 100 minutes - a huge range. Thus not every
schedule will fit any particular person. The twice a week dosing works for most men, not all. If
every day dosing is necessary, then perhaps testosterone pellets would be an alternative to
consider.
Once every 2 week dosing results in large supraphysiologic levels in the beginning for
testosterone, DHT, and estradiol. The estradiol levels remain supraphysiologic long after
testosterone has significantly declined - creating potential problems.
Once a week dosing is a compromise which works for the average man, but does not work for
those with short-half-life testosterone.
For twice a week dosing, a dose on Monday and Thursday can be done. Some do it on Monday
and Friday with decent effects. The timing needs to take into account the person's schedule.
Note that the peak testosterone level with injections occurs between 24-48 hours after the
injection.
Re: Selenium (from yeast) is helping with my low libido a lot.
Quote:
Originally Posted by chip douglas
I know selenium can indirectly affect Testosterone :
Selenium is localized in the mitochondrial capsule protein and is involved in biosynthesis
of testosterone (Bedwal RS, Nair N, Sharma MP, Mathur RS, Selenium--its biological
perspectives., Med Hypotheses 1993 Aug;41(2):150-9).
Do you guys know of other reasons why selenium has this consistent and fast effect on
me, like within 3-4 hours after I take it in ?
Selenium is used by the enzymes which activate thyroid hormone (converting T4 (thyroxine) to
the more active T3 (triiodotyronine). Thyroid hormone in turn stimulates testicular steroid
hormone synthesis (e.g. increasing testosterone production).
Often people have diets deficient in selenium.
Selenium has many uses. For example, it is the most active antioxidant mineral. It helps reduce
the risk for prostate cancer. It helps (along with zinc) in reducing stress-related hair loss.
The usual dose is 200 mcg a day when used as a supplement.
Some people are allergic to yeast. They would need to take a yeast-free selenium product.
L-selenomethoinine as a source of selenium has a bad odor. Sodium Selenite is something I
would prefer instead.
__________________
Re: benzodiazepines
Quote:
Originally Posted by DaVinci2
http://www.inchem.org/documents/pims/pharm/pim926.htm
Does this mean that benzos can be responsible for the inability to lose fat? I take a benzo
(2mg) for insomnia.
The usual psychiatric answer is "it depends".
Whether or not benzodiazepines cause certain side effects on a particular person depends on
multiple factors including the person's genetic tendency for the side effect, the other
neuroendocrine and immune problems a person has, the person's systemic response to the
benzodiazepine. It's a complex matter.
Benzodiazepines work by increasing the sensitivity a person has for GABA, by modifying the
GABA receptor. This then leads to multiple possible outcomes depending on the amount of
GABA available and dose of Benzodiazepine, among other factors. For most people, they want
the antianxiety or sedative effect - the primary effect. However, benzodiazepines may also have
other effects including disinhibition and agitation if (for example) frontal cortex functions are only
partially inhibited compared to other parts of the brain. Benzodiazepines can reduce various
neurotransmitter production - then either helping or hurting the person. For example, reducing
dopamine production allows Benzodiazepines to help antipsychotic treatment. Reducing
serotonin production, however, may lead to depressed mood or reduced thyroid hormone
production. These are some example of the complex cascade of effects that benzodiazepines
can have.
Benzodiazepines - due to their transient effects and the development of tolerance - are primarily
bandage treatments.
One question I would ask, then, is why is the person using the benzodiazepine in the first place?
For example, Benzodiazepines treat insomnia. But the cause of insomnia remains. Perhaps the
actual cause of insomnia, then, is the primary factor contributing to obesity.
Insomnia may be caused by a relative increase in stimulant neurotransmitters (such as
norepinephrine, epinephrine, glutamate, histamine) and/or a relative decrease in inhibitory
neurotransmitters (such as serotonin, GABA, dopamine). Insomnia may also occur with hormone
problems such as hypothyroidism, adrenal fatigue (with lower cortisol, DHEA, progesterone
production), etc. All of these factors interact.
Two of the most common causes of insomnia are hypothyroidism and adrenal fatigue.
__________________
Re: Depression leads to lower T levels ?
Quote:
Originally Posted by chip douglas
Dr. John told me that depression in and of itself increases pro inflammatory cytokines
inhibiting both GH and Testosterone.
So this would mean Dysthymia can be a cause for low TT in the 400 range ?
Why then if depression can bring on low T, that we see so many men on TRT ?
My point among those men (if my above correlation is not wrong) with low T, part may
originate from depression, while others from overt low T.
Marianco, would you be so kind as to shed some light on this, so I better understand
which comes first ?
Thankfully
It is not really useful to determine which came first. It is more useful to determine what is deficient
or in excess to indicate what treatment would be best.
Depression can have multiple contributing factors. There may be a genetic tendency for having
low serotonin levels, for example. There may be problems involving other neurotransmitters,
hormones, and immune system cytokines such as dopamine, norepinephrine, GABA, glutamate,
PEA, thyroid hormone, estrogens, testosterone, progesterone, DHEA, etc., etc. Only one of these
contributing factors is testosterone. Depression can reduce GH and testosterone production.
However, depression is often the endpoint of multiple system problems occurring at the same
time.
Testosterone decreases with age, generally past the age of 30 in men. Depression does not
always occur. A low testosterone may not be due to depression so much as genetic fators and
age and other hormone imbalances, etc.. Testosterone deficiency can thus be also a multiple
system problem, aside from age-related decline.
In many patients, a multiple system treatment would best address their problems. It would be nice
if adding testosterone will solve everything. But this obviously is not the case with many patients.
They still have problems even with high testosterone levels.
__________________
Re: akathisia- Marianco
Quote:
Originally Posted by DAVID
Marianco I've just reading your nice board about akathisia- You speak about high
serotonin and low dopamine.
I have no difficulty to fall asleep very quickly the night. My brain say : I think it's a good
night. But one hour after my eyes is open. I feel agited, I turning MY leg in bed for falling
a sleep. Do this problem is akathisia ?
What the best strategy to increase the ratio dopamine/serotonin. I read that the best way
is to take testosterone. But I take the HRT but this problem is here depiste testsoterone
When you have this problem is look like ADD in the day. What do you think about ritalin
for akathisia ? Do you think is ritalin is a dangerous drug ?
Many physicians said that is bad for the brain but when you read Dr Amen, this good
physician is good for ADD. What your idea about that ?
Thank you for your time and help
I have observed that akithisia most commonly is a side effect of serotonergic medications or
dopamine antagonists when the medication reduces the activity of dopamine so much that
restlessness or agitation occurs. This may impair one's ability to fall asleep. The actual
pathophysiology causing akathisia is not entirely known. Norepinephrine, histamine, and
glutamate excesses may also be involved. This may be why Beta-blockers (blocking
norepinephrine receptors), sedatives, and anticonvulsants may be also useful in treating
akathisia. Dopamine mimic medications or medications that increase dopamine release can
reduce symptoms of akathisia.
When a person is able to fall asleep, but later wakes up and feels agitated or restless, the
question I would have is why? It is less likely akathisia since akathisia is usually a constant
condition. From my observations, waking up agitated or anxious may occur as a result of a surge
in norepinephrine or glutamate or histamine production in response to lower glucose production
than the brain desires, resulting from tiring of the adrenal glands.
There is a separate condition called restless legs syndrome. It is unclear what causes it.
However, since dopamine mimicking medications help reduce symptoms, perhaps it is caused by
lower dopamine levels. But I think the actual situation is more complex. It appears to be a
separate syndrome from akathisia since dopamine mimicking medications (which are agonists at
D3 receptors) reliably reduce symptoms, whereas I have not found them useful in treating
akathisia.
Ritalin and the amphetamines increase both dopamine and norepinephrine release. The
dopamine component may help reduce akathisia, but the norepinephrine component may worsen
it - both directly in the brain itself (contributing to agitation or anxiety) or by contributing to adrenal
fatigue (and its consequences). I haven't found it useful for treating akathisia.
In the wrong hands, Ritalin, any other medications or substance (including water), is dangerous.
There is always a risk in taking anything. Even eating food can potentially be lethal if certain e coli
bacteria have contaminated it. Just driving a car, for example, kills more people in the USA each
year than the number of American soldiers killed in Vietnam. The key is understanding the risks
and making an informed risk assessment so one can make the best decision about treatment or
non-treatment.
When testosterone level is at least 650 ng/dl with therapy yet problems remain, the other
hormones, neurotransmitters, and/or immune system cytokines are involved.
Dr. Amen has defined subtypes of ADHD such as ADHD bipolar type, ADHD depressive type,
etc. I don't agree with these distinctions. I would rather call "ADHD bipolar type" as simply "bipolar
disorder", for example.
There is ADHD which is caused by dopamine resistance. In such a person, there is high
dopamine production to compensate for dopamine resistance. This may be THE true ADHD as
an illness.
ADHD-like symptoms can occur with many other conditions where there may be lower dopamine
production relative to other stimulant neurotransmitter production (e.g. norepinephrine, glutamate,
histamine). This includes depression, anxiety, hypothyroidism, adrenal fatigue, hypogonadism,
diabetes, etc.
Treatment with Ritalin may help ADHD symptoms by increasing dopamine levels, but the
tendency for Ritalin to increase norepinephrine may in the long-run worsen the condition, unless
this is also taken into account in the treatment - e.g. by instituting an adrenal treatment.
Currently, the best way to increase the dopamine to serotonin ratio is to use a stimulant such as
methylphenidate or amphetamine or to use an anabolic hormone such as testosterone or DHEA.
However, each method does have its risks (such as excessive norephenrine with stimulants).
I usually do not encounter people with high serotonin levels. Rather, serotonin is usually low in
people with mood disorders such as bipolar disorder, depression, or anxiety disorders; or
endocrine problems such as hypothyroidism and adrenal fatigue. Thus, I would want to increase
both dopamine and serotonin.
__________________
Re: akathisia- Marianco
Quote:
Originally Posted by 1cc
Yes, the main point I was trying to make was that many conditions are being described as
psycological even though they are hormonal in origin. Such may be the case with a
number of guys here on the board that described themselves as having ADHD.
Your point is well made.
From my point of view, the mind is the sum of the functions of the nervous system, endocrine
system, and immune system. These three systems are actually one single system. As such, there
is very little separation if at all between psychological, neurological, endocrine and immune
system problems. They are all part of one system - the mind.
A problem occurs when we look at a problem as being only due to one of these systems. For
example, if we consider ADHD as only a nervous system problem or worse, as only a
"psychological problem" - which means there is no physical component to the illness, no nervous
system component to the illness. When looked at from only one point of view, the physician or
other practitioner will totally miss the other components that contribute to the problem. Further, as
a result of missing the other contributing components to an illness, more effective treatments may
be missed.
Adrenal fatigue is not exactly only a hormone problem. It is an mind problem. The adrenal glands
are part of the sympathetic nervous system. And they play a large role in the immune system.
When I see adrenal fatigue, I may see multiple areas of impairment. There often is relatively
reduced serotonin, reduced dopamine, reduced GABA, high norepinephrine, and possibly high
glutamate, and high histamine levels. There is reduced production of cortisol, DHEA,
progesterone. Further, there may be increases in pro-inflammatory immune system chemical
messengers (cytokines) such as IL-6 and IL-12. These cytokines may in turn influence the
production of serotonin and other neurotransmitters, and influence the hypothalamic-pituitaryadrenal system. Thus adrenal fatigue is a much more complex condition than just cortisol, DHEA,
or progesterone deficiency. It is not just a hormonal problem.
Treatment of adrenal fatigue can be as simple as a behavioral modification - thus treating the
nervous system component only, or as complex as a total mind treatment involving behavior,
nervous system, endocrine system, and immune systems.
Years ago, as a psychiatrist, we use to be able to hospitalize a person for two years and give
them only psychotherapy. This treatment relieved the person of external stresses (including
responsibilities). Usually, such a person came out psychologically much more healthy.
Essentially, their adrenal fatigue was essentially totally treated by psychological means.
Without such an extreme intervention to reduce external stresses (essentially a 2 year vacation
with a large staff to take care of one), treatment of adrenal fatigue may have to involve the other
systems. Treating it with psychiatric medications alone may not be then enough. Adding
endocrine and immune system treatments may then result in a stronger regimen - which is
missed if the condition is only considered a nervous system/psychological problem.
__________________
Re: akathisia- Marianco
Quote:
Originally Posted by DAVID
Thank you so much for all answers.
Marianco, I've learning more from you than Wilson (adrenal fatigue) or Jefferies (safe
use of cortisol) about adrenal fatigue.
May be because I've adrenal fatigue and your answer in the board about adrenal is
integrated with all the hormones/neurotransmetteurs/cytokines.
Dr Amen or Dr Braverman never speak about adrenal fatigue that is very important
about brain chemistry.
Do you write a book about adrenal or article ? Do you known another book that it's
different that Jefferies or Wilson or Herthoghe for understanding the cause and the
physiology of adrenal fatigue ? When you look at PubMed there are not so much
informations about that.
Why the "dogmatic medecine " never speak about this important problem ?
All those mentioned provide pieces of the puzzle the results in a fuller understanding of mental
and physical health.
Thierry Hertoghe comes closest. He focuses primarily, though, on specific hormone deficiencies
and nutrition, not linking them to whole organ systems nor to nervous system and immune
function. When he talks about cortisol, aldosterone, DHEA, progesterone deficiency, in a way, he
is talking about adrenal fatigue. He does use the strongest tools - hormone therapies and
nutritional interventions - though some patients with severe problems (particularly those with
mental illnesses) may need the psychiatric and immune system treatments also - a coordinated
treatment.
Low Libido despite high testosterone.
Quote:
Originally Posted by Joe Chop
As I posted in another thread (test cyp first cycle)I have been experiencing low libido and
wood. I just got blood test results back and was surprised that I have test levels of total
740 and free 14. Estradiol was at 33 which I believe could be causing the problems. With
test levels that high do I really need to use hcg again? Will nolva bring estradiol levels
down or should I use something else? Thanks
When testosterone is over 650 ng/dl, and lack of libido persists, I would look for problems with the
other hormones.
The most important ones to look at first are the adrenal hormones and thyroid hormones.
Testosterone provides sex drive. Estrogens provide for sexual aggression - and thus contribute to
sex drive. However, with adequate adrenal AND thyroid function, there is not enough energy for
sex drive, and thus no drive. Also, the brain reacts to inadequate energy levels by increasing
stimulant neurotransmitters such as norepinephrine, while reducing production of dopamine and
other calming neurotransmitters. This results in the brain being in a flight-or-fight state. This then
cuts down on libido - a resting function - no matter how high testosterone (which increases
dopamine levels ) is.
High estradiol levels (over physiological range) does affect libido. It increases thyroid binding
globulin production - inactivating thyroid hormone. It also competes with thyroid hormone at
thyroid hormone receptors. Thus high estradiol reduces thyroid hormone function, reducing sex
drive. Estradiol also functions as a monoamine oxidase inhibitor in the brain - generally increasing
serotonin levels > norepinephrine > dopamine. If serotonin levels go too high or if norepinephrine
levels go too high (resulting in adrenal fatigue), then sex drive is impaired.
Increasing thyroid hormone, on the other hand, increases sex hormone binding globulin. This
then traps estrogens, reducing the activity of estradiol. (This results in hair loss in women who
don't have enough estrogen).
Reducing estradiol levels too low also can reduce sex drive - since sexual aggression is lost.
If estradiol levels are within physiologic range and are not causing overt side effect such as
gynecomastia, it is more important to look at adrenal and thyroid function for the answer to the
continued lack of libido.
There are many such interactions that create a 3-dimensional web of influences among the
hormones, neurotransmitters, and immune system cytokines, that determines a person's
functional state.
__________________
Re: Low Libido despite high testosterone.
Quote:
Originally Posted by zumper
When you say inadequate adrenal you mean low adrenal hormones like low cortisol,low
DHEA and such?
Normal to high Cortisol is good?
Yes, inadequate adrenal means inadequate production of cortisol, DHEA, etc.
Transiently high cortisol production is often necessary in response to high stress levels. Cortisol
reduces CRH production, which then reduces norepinephrine production which had signaled the
presence of high stress.
The question is - can the adrenal keep up with the demand for cortisol production particularly
when high stress levels are constant? Many times, it cannot and adrenal fatigue results. The
adrenal glands were not designed to provide constant energy production. Rather they provide a
boost in energy over and above the energy from thyroid hormone production, in response to
transient increases in stress level.
Excessively high cortisol production - such as from an adrenal tumor - is not healthy since there
are side effects of prolonged high cortisol production. Chronicly high cortisol activity - such as that
emulated by the use of corticosteroids such as Prednisone - cause similar problems.
__________________
Re: catch up growth and going on shots
Quote:
Originally Posted by masterpp
hey guys,
i was wondering for those of us who never properly completed puberty, can trt go
someway to taking us up, to where we should have gone, or are the receptor channels
closed, and we will just have to be content with being more virilised versions of our
current selves
also just thought id say that im trying test enan next week, as ive been dissapoointed with
the gels, particularly the anabolic function which has been non existent
AFAIK, once the bone growth plates are replaced by solid bone - sometime during the end of
adolescence - the bone cannot grow longer. Thus the person can no longer grow taller
Re: Adrenal fatigue, does it really exist?
Quote:
Originally Posted by Legenden1999
Yes, I know it exists, but according to many of the doctors I have seen, there is no such
thing as a illness called "adrenal fatigue", cause it has not (yet) been scientifically
proved, and there is no ICD-10 code for it. This has made me wonder. How come is this
syndrome not more recognised amoung doctors? If it has been known by some dotors for
a long time, why has nobody done a study on it? and why has noone tried to get it
internationally known, and gotten an ICD-10 code for it?
Any thoughts?
JH
Adrenal fatigue use to be well known in medicine in the late 1800s and early 1900s.
One problem is that lab tests were developed to measure cortisol and other hormone levels.
Another problem is that endocrinology was developed as a specialty which recognizes only the
extremes of hormonal deficiency or excesses as illnesses. Generally, this means only the bottom
2.5 percent and top 2.5 percent of people (those exceeding the reference range) are considered
ill. Most of medicine has decided to follow along with this idea of what an illness is.
And another problem is that medicine was designated to treat illnesses. To prescribe something,
it has to be for a recognized "illness". Unfortunately, many conditions are not recognized as
illnesses. Treating these conditions prevents the development of illness. But medicine hasn't
progressed to the point of thinking about promoting "wellness" as opposed to treating illness.
Despite all the talk about doing more preventative medicine, such as preventing heart attacks and
strokes, etc., doctors do little preventative medicine. To do so risks being considered doing
malpractice because there is no defined "illness" being treated. Lawyers have to be blamed for
this.
For example, there is no "illness" called Insulin Resistance. This is also called "pre-diabetes".
There is no ICD number for insulin resistance. There is one for elevated fasting glucose. But this
is not an illness.
For coding adrenal fatigue, I just use the code for Other Specified Disorders of the Adrenal
Glands - which I call Adrenal Fatigue.
Studies are very expensive to do. Few people other than drug companies can afford to do large
studies.
There are studies on adrenal fatigue. One, for example, was a study in the American Journal of
Psychiatry, where patients with posttraumatic stress disorder were treated with 10 mg a day of
hydrocortisone. The patients improved. Unfortunately, the authors of the article - being unfamiliar
with endocrinology - made the wrong conclusions.
Posttraumatic Stress disorder is the poster child for adrenal fatigue. There are numerous articles
on how low cortisol levels are in PTSD. However, because conventional psychiatrists are overly
focused on neuron function, they cannot see how the adrenal glands are the primary organs
affected by PTSD. Treatment with cortisol is not a recognized treatment of PTSD as a result.
Chronic and severe stresses can also create a hormonal picture of PTSD with the same
symptoms. However, the suffering person won't be diagnosed with PTSD sicne the stress is not
life threatening.
__________________
Re: Blood Labs In - Please Advise
Quote:
Originally Posted by swordfish
I'd like to include a better description of my ill feelings:
I got very sick the first day of high school (maybe anxiety), couldn't eat, for weeks, very
sick in the mornings, thought I had the flu.
This went on for the 12 years and I had some good days and some bad, but never
completely normal.
After becoming an anti-depressant guinea pig, i foudn this forum and start reading about
Adrenal fatigue and hormonal issues.
I am convinced that I may have adrenal insufficiency and am waiting on the saliva test to
come in.
I am not going to stop until I wake up in the morning craving french toast and ambtion! I
know I can get there and thank for the support here.
I was able to eat well on Remeron for the past 2 years, but anti-depressants are not my
answer. I have been off for over 2 weeks now and have been feeling very run down,
losing weight, no appetite, etc.
Thanks for the support and let me know what you think of the first set of lab test here.
If lack of energy is a problem, then the two most common areas to examine are thyroid function
and adrenal function. Please see my previous posts on these two subjects. The thyroids and
adrenals are the two organs affected by every other neurotransmitter and hormone deficiency
that can reduce energy.
For the evaluation of adrenal fatigue, helpful would be also a morning Cortisol, DHEA-s,
Progesterone.
It is important to also have a physical evaluation to help support the history and lab evaluation.
Often, with thyroid problems, for example, the labs may look completely normal, yet the person
will be clinically hypothyroid and will often never get adequately treated. It is interesting for me to
examine people physically to see what hormonal deficiencies are present even before asking
them questions. Often it correlates with their complaints and lab findings.
For many patients, I also like to see are an analysis of urinary neurotransmitters such as
Serotonin, GABA, Dopamine, Norepinephrine, Epinephrine, and Glutamate. These are affected
by hormonal deficiencies. And neurotransmitter problems themselves affect hormone balance.
For example, lack of serotonin reduces thyroid hormone production. Lack of dopamine reduces
testosterone production. Lack of thyroid hormone reduces serotonin production. Lack of
testosterone reduces dopamine levels. Etc. It is highly useful to help tease apart the nervous
system's and endocrine system's roles in causing a person's mental health problems.
__________________
Re: Regarding balding and hypogonadism
Quote:
Originally Posted by The_Skeptic
I think it is well-documented that hormones play a role in male-pattern balding because
studies of casstrated men have shown that they don't go bald. But how certain are we that
DHT is the sole hormone responsible for MPB?
I've been hypogonadic since before puberty because of a serious head injury I suffered as
a child. So despite the fact that I started puberty late and never even completed puberty,
stalling at Tanner Stage IV, I've had a receding hairline since my teen years.
Granted, the men on both sides of my family have widow's peaks that gradually recede,
but not to the point of complete baldness. But even though I was never tested for DHT, it
must have been extremely low because I experienced very little virilizatiion until I got on
TRT at the age of 26, when my T levels were tested at 236.
Over the last 12 years, I've lost a little more hair, which is probably a result from the
TRT as well as normal aging. I've used Rogaine on and off over the years and this may
have kept more of my hair from falling out.
I am now 38 and still have a widow's peak, meaning I still have most of my hair, but I
notice is getting thinner on the top.
But I'm wondering if E2 of low T plays a role in baldness because I had started to lose
my hair even before I got on TRT.
Hair loss can occur with hormone imbalances, including:
1. High Dihydrotestosterone
2. Low Thyroid hormone
3. Low Estrogen
4. Low Progesterone
5. Low Cortisol
6. Low Testosterone
7. Low DHEA
8. Low Growth Hormone
Dietary deficiencies also promote hair loss, including deficiencies in:
1. Protein
2. Omega-3 Fatty Acids - such as fish oil
3. Zinc
4. Magnesium
5. Vitamin C
6. Selenium
7. Vitamin B6
8. Folic Acid
9. Vitamin B2 (Riboflavin)
10. Manganese
11. Calcium
__________________
Re: Despaired skinny-fat endo with low testosterone needs help!
Quote:
Originally Posted by James23
Man, I hate to be a downer, but my body looks EXACTLY like yours. I, too cannot build a
chest or do pushups, and I also (for some odd reason) have a problem with a receeding
hairline.
Here's the bad news: I've been on TRT with good doctors for the past three or four years,
and I have seen absolutely NO improvement.
Like you, I have the normal free T, and the low SHBG. That's the problem -- the SHBG.
You have a very rare case of hypogonadism and regular TRT isn't going to fix it. When
you put T into your body, your low SHBG will let too much of it become free (like 4000%
of normal) and your pituitary will detect this and send DHEA, cortisol, and E2 all over
the fucking place!
I'm not suggesting that you give up. I'm just reccomeding that you save your time and
find a doctor that knows how to deal with LOW SHBG AND LOW T COMBINED.
Otherwise, you'll waste years and years, get even balder, your hair will thin AND receed
at the same time, and you'll get puffy nipples, just like me.
Seriously, you need to raise SHBG to normal levels or NOTHING will balance for you.
Low SHBG / High Free Testosterone can occur many conditions including the following:
1. Low thyroid (e.g. hypothyroidism)
2. Low progesterone (e.g. adrenal fatigue)
3. High insulin (e.g. insulin resistance or diabetes)
4. Low Estradiol/Estrogens (e.g. low aromatase activity)
5. High DHEA (e.g. acute stress)
6. High Testosterone
7. High DHT
8. High Growth Hormone
Addressing these may help restore SHBG to higher levels.
__________________
Re: Despaired skinny-fat endo with low testosterone needs help!
Quote:
Originally Posted by James23
T3, Progesterone - Hmm, as Dr. Crisler did my labs, I think my T3 and progesterone
levels are fine.
High insulin - I have mild hypoglycemia at times (blood sugar drops to 89 on a glucose
meter if I'm eating incorrectly) so I know I can't be diabetic, right?
Low E2 - Well, I have gynecomastia, so no.
High DHEA - Yes, so high that Dr. Crisler had to ask if I was taking DHEA
supplements. However, he knows of no way to lower DHEA. Do any of you? If it's caused
by stress, I must have been constantly stressed from age 13 through 26.
High T - No, all low.
High DHT - They're midrange levels, but they make me lose hair. Does that mean they're
too high for my body?
High GH - Crisler did my labs so I assume it is fine.
There are a lot of assumptions you are making on the lab results.
It would be interesting to all of us, as well as educational, to give us the actual levels: Free T3,
Free T4, TSH, Progesterone, DHEA, Estradiol, IGF-1, IGF-BP-3, DHT, fasting glucose, Cortisol,
Total Cholesterol, Triglycerides, HDL Cholesterol, Total Testosterone, Hemoglobin A1c, Sodium,
Potassium, Albumin, SHBG, Prolactin, etc.
With the actual levels, we can then see for ourselves whether or not they are O.K. or not.
Insulin resistance can be present even with low blood sugars. It would be hidden by adrenal
fatigue.
It is still possible to have hypothyroidism even with normal thyroid hormone levels. It's a condition
involving resistance to thyroid hormone. Normal thyroid hormone levels act like low thyroid
hormone levels in this illness. One goes by the symptoms and signs of hypothyroidism when
making the diagnosis. The treatment is the same - adding more thyroid hormone until the signs
and symptoms resolve. Signs of low thyroid activity include low morning arm pit body
temperature, dry skin, thickening of skin, generalized hair scalp loss, etc.
Adrenal cortex hormone production is triggered by ACTH. All the hormones are made at once.
Only Cortisol has negative feedback to the brain to reduce ACTH secretion. ACTH is released in
response to stress. Cortisol, DHEA, Progesterone, Adrenal Testoterone production increases in
response to ACTH. DHEA has no negative feedback control. There really isn't a way to reduce
DHEA production other than to reduce stress levels. The question I would have is: Is the
production of DHEA out of proportion to the cortisol level, progesterone level, etc.? If it is much
higher than the others, then perhaps some metabolic pathways that use DHEA to produce other
hormones (e.g. Estradiol, Testosterone) is being blocked, leading to an accumulation of unused
DHEA. DHEA has hormone signaling functions independent of other hormones. But it is also is a
precursor for other hormones. If the metabolic pathway is discovered, then perhaps by stimulating
it, DHEA would then be lowered.
There are many hormonal factors possible for hair loss, not just DHT. For example,
hypothyroidism results in a diffused, generalized hair loss, which does not fit male pattern hair
loss. High DHEA could potentially cause hair loss - though this is most often seen in women.
__________________
Hypothyroidism, Adrenal Fatigue, and Hypogonadism
Quote:
Originally Posted by dunbar
Hi!
I think you and me have very similar hormonal levels. Fascinating. Once I also had DHT
tested and it was also pretty low. Do you have a lot of hair? My legs are totally hairy
while my upper body isn't but in the past few months something's changing and I'm
getting annoying hair on my shoulder and chest...really great.
By the way I also had my thyroid hormones checked and they seem to be normal:
TSH 1.71 Norm 0.4-2.5
fT4 pmol/l 16.8 Norm 10.3-24.5
fT3 pg/ml 3.0 Norm 1.8-5.2
But what I noticed now is that he didn't test Estrogen, only Estradiol. Why didn't he also
test Estrogen? This seems completely silly to me. Maybe my Estradiol levels are okay but
my Estrogen levels are going through the roof, who knows?
Of the thyroid tests, the free T3 is the most important. It indicates the amount of active thyroid
hormone that is working. Free T3 is the most active of the thyroid hormone and is the hormone
measured by the brain to determine how much TSH to produce.
If a person has a history of lack of energy and weight gain, then the two organs center of
determinining energy level and metabolism to be evaluated are the thyroid gland and the adrenal
glands. Other hormone deficiences have to affect one of these two in order to reduce energy and
metabolism.
If a person has a history and physical exam (i.e. signs and symptoms) consistent with
hypothyroidism and the Free T3 is less than or equal to 3.2 pg/ml, I would consider treatment with
thyroid hormone. If a person has a history and physical exam consistent with hypothyroidism (e.g.
low body temperature, etc.), I would consider treatment no matter what the lab test result may be
- at least a clinical trial of thyroid hormone to see if this improves a person's level of functioning.
There are many cases of thyroid resistance (a mitochondrial illness) where thyroid tests are
normal but a person has all the symptoms of hypothyroidism. This occurs because the body does
not respond well to normal thyroid hormone. More is needed.
Low thyroid hormone or Low adrenal function both can lead to sexual dysfunction even if
testosterone levels are optimal. If low thyroid or low adrenal function is present, it may be very
difficult to lose weight since the signals to allow weight loss may not be present.
__________________
Re: Despaired skinny-fat endo with low testosterone needs help!
Quote:
Originally Posted by pmgamer18
I just wish this was a faster process I have been on Isocort now for 10 week and on
Armour now for 6 weeks still have low engery. I am not doing 90 mgs of Armour and my
Isocort = 20mgs. of cortisol a day. I am at a good Temp all day 98.4 to 98.6 then one day
it droped down to 97.7 and I felt bad sweating and bad fatigue. So I upped my dose of
Armour 15mgs and got my temps back up and feel better. Still my morning Temp before
getting up taken under my arm is 97.0.
Do you think High E2 has an effect on this it seams when my E2 starts going up I am
short of breath and feel like crap. How long does this take I have been house bound sence
winter and just walking is very fatiguing. Yet I am much better then I was 3 months ago.
Dam time goes so slow when you don't feel good.
Drops in energy during a day accompanied by sweating is more indicative of adrenal fatigue still
being present. Sweating is due to the increased norepinephrine output from the brain, which is
trying to increase adrenal production to improve energy level.
Treatment of adrenal fatigue takes time. Over time, thyroid hormone also improves adrenal
function by increasing the production of mitochondria in adrenal cells.
It takes 4-6 weeks from the LAST increase in Armour Thyroid to get the maximal benefit from the
change. This occurs because T4 has a long half-life and takes 4-6 weeks to peak. The T3 is
active the day it is taken.
There is a risk to going too high on Armour Thyroid - e.g. indicated by high body temperature and
too fast a pulse. Risks of going into a hyperthyroid state include atrial fibrillation.
The risk of going up too fast on Armour Thyroid includes worsening adrenal fatigue.
This worsens fatigue, lowers blood sugar. It causes the brain to react by increase norepinephrine
production and reduce the production of calming neurotransmitters - as it attempts to increase
adrenal production to improve energy. The side effect of this brain response is depressive and
anxiety symptoms including sweating.
The adrenal glands have to be healthy enough to take the higher workload that thyroid hormone
demands of them. Over time, thyroid hormone makes the adrenal glands stronger. But there is a
balance to be maintained as both are treated.
__________________
Re: Despaired skinny-fat endo with low testosterone needs help!
Quote:
Originally Posted by dunbar
@ marianco
I asked him about hashimoto thyreoditis and he did an ultrasound and said that the
thyroid looks normal and also isn't enlarged. Does fT3 stand for free T3? Do I not have
enough free T3?
A thyroid ultrasound looks for possibly cancerious nodules in the thyroid as well as look for
structural abnormalities such as the size.
Hashimoto's Thyroiditis - a common cause of hypothyroidism - is an illnesses where the immune
system attacks the thyroid gland. The diagnosis is established by measuring the level of
antithyroid antibodies. These include thyroglobulin antibodies and thyroid peroxidase antibodies.
A thyroid ultrasound which is normal will not rule out Hashimoto's Thyroiditis.
fT3 is Free T3 - I assume.
I have given my general thoughts about T3 in a previous post on this thread.
__________________
Re: Despaired skinny-fat endo with low testosterone needs help!
Quote:
Originally Posted by James23
I figure people will be interested in my labwork, since I am have the same problems as
MacDonnell and dunbar.
Keeping my testosterone in the exact middle of the range, using only 60mg of
testosterone cypionate every week:
Total T: 520ng/dl
Bio T: 427pg/ml (< 400)[HIGH!]
SHBG: 9 (7 - 50) [LOW]
E2 is unknown, but there are no signs of elevated E2. Everything else is normal.
Specifically:
ACTH: 10 (7-50)
Progesterone: 1.3 (<1.4)
DHEA was near the top of the range.
Cortisol was normalized.
Pregnenelone was low.
[I don't have exact values, as this was extracted from an e-mail from Dr. Crisler.]
If I could simply raise SHBG, I could get my free T and serum T to be normal, something
I have never experienced! I don't know what on earth Shippen is talking about. Free T
isn't a magic bullet. It can be metabolized quickly and then you are left with serum T that
is low end empties TWICE AS QUICLY since SHBG isn't high enough to store an
appropriate amount -- thus your stamina and libido are shot under normal
circumstances.
Suggestions?!
The midrange testosterone level is 650 ng/dl (when using the range of 300-1000 ng/dl).
When to measure this level varies between practitioners. Some (e.g. Endocrine society) want it
measured at the midway point between injections. Others want to measure it at the trough level
(meaning the time just before an injection).
It is better to get the exact level rather than state it is near the top of the range. The problem is
the range chosen depends on what illness one is measuring for. I prefer for example, using the
range of 300-1000 ng/dl for total testosterone rather than the lab's range, because that is a
common range for "normal" used in the literature.
DHEA-s range depends on sex and age. Knowing the level and the range used gives more
important information. If the wrong range was given by the lab, for example, then one can have
the impression that the level is in high normal, when it is actually low instead.
A Cortisol level that is "normalized" is not clearly normal. Cortisol level depends on the stress a
person experiences and the internal stress signals (e.g. norepinephrine levels) generated by the
brain at that moment. A person can look like they have a normal cortisol at a single point in time,
but when examined across the day with multiple cortisol samples, a clearer picture shows.
Often, it may be possible to obtain lab results directly from the lab itself.
__________________
Free Testosterone, Adrenal Fatigue.
Quote:
Originally Posted by cjsabbath
My latest labs revealed the following:
DHT 69 ng/dL Reference Range 30 - 85
Estradiol 47 Reference Range 3 - 70
LH 0.3 mIU/mL Reference Range 1.5 - 9.3 (Low)
FSH 0.3 mIU/mL Reference Range 1.4 - 18.1 (Low)
Testosterone, Serum 784 Reference Range 241 - 827
Testosterone, Free 28.0 pg/mL Reference Range 8.7 - 25.1 (High)
Progesterone 0.2 ng/mL Reference Range 0.3–1.2 ng/mL (Low)
DHEA Sulfate 92 Reference Range 95–530 µg/dL (Low)
PSA 1.0 ng/dL Reference Range 0.0 - 4.0
Of course, I knew that my LH/FSH would be low given that I'm on Androgel. My total
testosterone level is fine. However, I note that my "free" T level is high.
My doctor (a member of the American Academy of Anti-Aging Medicine) said that it
wasn't a problem. She was more concerned with my DHEA Sulfate levels, however, and
wrote me a prescription for 25mg DHEA Sulfate once per day.
She said that low DHEA levels can cause unwanted problems and may also contribute to
major depression. I have bouts of major depression so perhaps this will help.
At any rate, would anyone care to weigh in on the "free" T issue? I've noticed a
significant increase in strength/size since coming off Dilantin (which is notorious for
lowering T levels)
CJ
I've written about Free T in previous posts.
I don't think Free Testosterone is useful for deciding on the dose of testosterone replacement.
Free Testosterone does not represent total testosterone activity. Testosterone weakly bound to
albumin is also active. Testosterone bound to SHBG is active at SHBG receptors.
Free Testosterone is determined by how much SHBG is present since Albumin production tends
to be stable.
SHBG is itself determined by multiple hormones including:
Hormones that increase SHBG: estrogens, thyroid, progesterone
Hormones that reduce SHBG: testosterone, DHEA, insulin, growth hormone, other androgens
Thus, Free Testosterone actually represents the sum of all of these hormone activities.
If Free testosterone is too high or too low, it may mean a problem with any of these hormones not
just testosterone.
If Free testosterone is high, for example, it may mean that a person is low on estrogens, low on
thyroid, low on progesterone, high on insulin (insulin resistance), or high on testosterone, DHEA,
growth hormone or other androgens.
Thus, Free Testosterone is an indicator that something is wrong. It just doesn't say what is wrong.
I think it is incorrect to assume that Free Testosterone is THE active testosterone and is the
determinant of testosterone's activities. It can be normal or high even with very low testosterone
levels (e.g. < 300 ng/dl - particularly when SHBG is low - this is a common finding with insulin
resistance), yet a person has sexual dysfunction.
To determine the testosterone replacement dose, the best measure is total testosterone.
Bioavailable testosterone (free T plus weakly bound T) is a good second measure.
If Progesterone and DHEA-sulfate are low or low normal, I would generally suspect adrenal
fatigue. It would then be usetul to also check Cortisol levels (best is a saliva test four times in a
single day to check activity across an entire day), fasting blood sugar, albumin, sodium,
potassium (and testosterone and estradiol in women), aldosterone (sometimes), hemoglobin A1c,
insulin, cortisol binding globulin, urine adrenal hormone metabolites, etc. to help determine the
diagnosis. A physical exam and history would be very useful.
__________________
Re: Free Testosterone, Adrenal Fatigue.
Quote:
Originally Posted by cjsabbath
Thanks Gents (and Doctor):
Yes, my progesterone was low - as was DHEA. My fasting blood sugar is fine - but I have
been under a lot of stress lately (teenage son) - and do have generalized anxiety disorder.
So, I'm "wired" for stress as it is. I have often wondered whether I suffer from Andrenal
Fatigue.
At any rate, I will ask my doctor to check Cortisol levels the next time I see her.
She also said she wanted to check Insulin Like Growth Factor?
You guys are awesome - I really appreciate the feedback.
CJ
Insulin-like Growth Factor (IGF-1) is an indirect way to measure growth hormone.
If measuring IGF-1 by blood, it is useful to also measure IGF-BP3 (the main IGF binding protein)
to help interpret the IGF-1 level.
IGF-1 is dependent on other hormones including DHEA. A low IGF-1 may represent, for example,
low DHEA rather than low growth hormone.
Growth hormone affects the other hormones, which can cause problems if they are not first
optimized before growth hormone treatment is started, and adjusted after they change with
growth hormone treatment.
The most important hormones to optimize before treatment with growth hormone include:
Thyroid Hormone
Cortisol
Aldosterone
Progesterone
Testosterone
DHEA
Insulin
Estradiol
Melatonin
__________________
Re: Transdermal Application Sites
Quote:
Originally Posted by mkl13
I just recieved a 10% compounded gel (switching from androgel). Where are the best
places to apply the gel to maximize absorbtion and minimize E2 conversion. Thanks..
The biceps and shoulders are some of the best places.
If a person doesn't have too much facial hair and has treatment to prevent hair loss (e.g.
finasteride), then the face and neck are good areas for absorption.
If a person has difficulty in absorbing transdermal testosterone, one problem may be thickening of
the skin which occurs with hypothyroidism.
__________________
Re: Transdermal Application Sites
Quote:
Originally Posted by The_Skeptic
Does applying test to the face increase DHT more than in other areas?
Areas where there is a lot of hair growth such as the beard area will cause an increase in DHT
larger than other areas.
The rationale for using the face is that wherever a person blushes, there is a lot of circulation
underneath the skin. This allows more of the testosterone to be absorbed.
Using gel on the face can be inconvenient, however. It can be sticky. The face and neck is one
alternative for some men that may otherwise have absorption in the usual areas such as the
arms, flanks and shoulders.
If the face or neck is used, an alpha-reductase inhibitor such as finasteride should be considered
to avoid scalp hair loss.
Alpha-reductase inhibitors do have their risks in use - such as sexual dysfunction or anxiety in
some men. In some cases, they can impair brain function by reducing myelin production through
blocking the conversion of progesterone to allopregnenolone in the brain. Women are much more
susceptible to the negative effects of Finasteride.
One anti-aging doctor I know, however, applies testosterone gel to his scalp while using
Finasteride to prevent hair loss. The scalp applied testosterone helped regrow his hair. I don't
think this will work with everyone - but his scalp is pretty full and thick now. If the Finasteride
doesn't adequately stop DHT production, the scalp application would have instead resulted in
balding. This is why I wouldn't generally recommend this technique unless one wants to risk
going bald in order to see if one can gain hair. That is a tough decision to make.
__________________
Re: Latest Test Interpretation?
Quote:
Originally Posted by Andromeda
Since 11 Sept 2006 Ive been taking 10mg of Tamoxifen (Nolvadex) daily to get rid of my
gynecomastia. It has progressed, albeit slowly, and just today I had my followup Dr visit
to review my ongoing treatment.
At this visit we reviewed my latest blood tests to monitor hormonal changes since starting
the treatment. Now these results were stunning. My estrogen levels were actually higher
than before starting the Nolvadex
At the same time testosterone was slightly higher , with bound testosterone showing itself
to be even higher relative.
For those who want to see/compare raw figures I have the following.
Pre Nolva: 3 weeks Post Nolva:
Testosterone - 35
Free T: 68 69
P4: 200 300
E2: 198 300
I have recently had an ultrasound of both my testicles and chest. So far the testicles are
fine, and I assume the Endo would have called if the chest results (not held at the time)
came back unusual... so it seems to rule out the possiblity of an E2 secreting tumour.
Please come forward with your suggestions on how this has come about as my Dr has no
idea till we see the next set of tests. I'm now taking double the amount of Nolvadex (20
mg now) with followup tests to be done again in about 3 weeks.
Any advise on this mystery would be appreciated...
Cheers in advance,
Measuring Estradiol alone is going to be thrown off when taking Tamoxifen (name brand:
Nolvadex).
Tamoxifen acts essentially as a mild estrogen. It blocks estrogen receptors in some tissues
(particularly breast) so that the stronger breast-tissue growing estrogen (estradiol) cannot act on
the tissue. Tamoxifen acts like an estrogen in other areas of the body (which is why it may cause
blood clots and in some cases, cancer).
Measuring estradiol alone is actually a measure of all the estrogen activity, heavily weighted for
estradiol - the most potent estrogen. Since Tamoxifen acts as an estrogen, it raises the
measurement for estradiol.
Measuring estradiol alone when taking Tamoxifen is thus not accurate.
To measure estrogens when taking Tamoxifen, it is better to obtain Fractionated Serum
Estrogens - where the estrogens are separated into the different estrogens then each is
separately indentified. This will reduce the influence of Tamoxifen.
Estrogens raise SHBG. I would not be surprised that SHBG is raised by Tamoxifen, since
Tamoxifen acts like an estrogen.
The brain measures the level of estrogen and testosterone to determine how much Luteinizing
Hormone (LH) to produce. LH production leads to an increase in testosterone production.
Estrogens are then produced from testosterone via the aromatase enzyme.
Tamoxifen - by blocking stronger estrogens in the brain - gives the brain the false impression that
there is less estrogen available. The brain then raises LH production, which then raises
testosterone production.
As a side note, when progesterone is available, the brain more easily senses testosterone levels.
__________________
Re: Help With Test Results
Quote:
Originally Posted by Lockk
I have read those posts already JanSz thank you, my question is still the same are the last
(3) test results so definitive that there is no need for a Testosterone test and is that
possibly why the doctor didn't order one?
The short answer is no. LH, TSH, and Prolactin do not definitively indicate that testosterone
production is normal.
LH is the brain's opinion of how much testosterone, DHT, and estrogens are present. The brain
can often be wrong - e.g. secondary hypogonadism.
Prolactin production is controlled by brain dopamine. When dopamine levels are high, prolactin is
low. Dopamine helps determine testosterone production. However, there are so many other
neurotransmitters and hormones that determine testosterone production, that dopamine or
prolactin alone does not indicate whether or not there is adequate testosterone production.
TSH is the brain's opinion of how much thyroid hormone is present (particularly T3). The brain
can often be wrong. This is why Free T3 is a better test for thyroid hormone activity. T3 is the
most active thyroid hormone. Thyroid hormone helps determine testosterone production.
However, there are so many other neurotransmitters and hormones that determine testosterone
production that TSH alone or T3 or T4 measurement will not indicate that there is adequate
testosterone production.
Other determinants of testosterone production include: norepinephrine, cortisol, insulin,
epinephrine, serotonin, cholesterol, DHEA, progesterone, etc.
If there is a brain problem so that LH, TSH are wrong, and primary hypogonadism (e.g. aged
testes that do not respond to LH well), then measuring Prolactin, TSH, and LH will not indicate if
there is adequate testosterone production.
It is far easier to just measure total testosterone to find out if there is adequate testosterone
production.
__________________
Re: What do these thyroid resuts mean?
Quote:
Originally Posted by griffinannie
Tsh 3.49 0.4 - 4.0
T3-f 4.90 1.5 - 4.1 High
T4-f 1.10 0.8 - 1.9
Assuming these have standard units in the U.S., i.e.:
TSH = 3.49 mIU/L (0.4-4.0)
Free T3 = 490 pg/dl (150-410)
Free T4 = 1.1 ng/dl (0.8-1.9)
Then the results don't say much unless they can be correlated with the clinical history and
physical exam.
The possibilities run from the person having normal thyroid function to hypothyroid symptoms, to
hyperthyroid symtoms.
It can be speculated that:
1. TSH > 2.0 is suspicious for hypothyroidism type 1.
2. Free T3 490 is suspicious for hyperthyroidism.
3. There may be thyroid hormone resistance, particularly at the pituitary gland, such that high T3
does not reduce TSH to a lower value.
4. etc.
Sleep apnea and testosterone
One has to be more careful if sleep apnea is present when doing testosterone replacement
therapy. The problem is that if one develops polycythemia while on TRT, it can make breathing
more difficult if one has sleep apnea. Follow up labs are thus important to decide dosing. TRT is
one option in treating sleep apnea, however - given its ability to help reduce fat, which contributes
to sleep apnea.
__________________
Re: Why Test Cyp
Quote:
Originally Posted by fenstermaker
I have noticed that the only Test that is suggested here is Test Cyp. Is there a reason or
are there better versions of Test available with less side effects? I am currently on
Androgel and I do not feel like I am getting much response. As I have been reading up on
Test, It seems there are several versions that claim different results and different (or less)
side effects than Test Cyp. How do you determine the right kind of Test would be the best
for you?
Thanks for anyones insight on this.
Testosterone Cypionate is commonly used because it is inexpensive.
Testosterone Enanthate is the alternative injectable long-acting testosterone. It is the one
commonly used in research. It is a little more expensive.
The two generally have similar half-lives of about 7 days. But the actual half-life in an individual is
different from person to person. Some have shorter, some have longer half-lives.
There are several different delivery systems for testosterone - e.g. injectables, commertical gels,
pellets, compounded alcohol gels, compounded alcohol creams, oral. Which one is best for the
individual depends on the individual's response and preference. Side effects may vary which
each preparation. Which ones will occur varies with the individual.
Generally, a good goal in replacement therapy is to achieve a total testosterone of 650 ng/dl - per
Endocrine Society guidelines.
If problems persist at such a dose - such as lack of libido - then other hormones need to be
examined for deficiencies or excesses (e.g. thyroid, cortisol, DHEA, estradiol, DHT, etc.). It is not
lack of testosterone that is the problem.
Some estimate that 100 mcg of Levothyroxine is roughly the same as 60 mg of Armour Thyroid.
__________________
Re: Why Test Cyp
Quote:
Originally Posted by fenstermaker
Thanks guys....this should really help.
I have been on Androgel for about six weeks....started on 2.5 and my Test went down the
first four weeks....then I have been on 5 and I suspect I am still low. Not feeling any
improvements so I am guessing my Dr might put me on Test injections. I am going to ask
to try Armor also.
Thanks again for the help.
A person cannot suspect they are low until it is measured.
What is interesting is how the symptoms of low testosterone, low thyroid, low adrenal hormones,
and insulin resistance can overlap so much that one can't tell until it is measured what is off.
__________________
Re: better but still not great
Quote:
Originally Posted by masterpp
hey guys since going on trt my labs have come back much better.
my dht is a little high, but my T is pretty good and my estrogen in in range
and yet i still get anxiety and my figure hasn;t changed at all. i haven't shifted any of the
stubborn fat on my chest and belly and my arms are still puny.
more importantly, my sex drive is still crap.
what should i investigate yet. how would my adrenals effect things
cheers
also, has anyone had any luck with anything to aid weight loss. i know there are no
miracle cures but hasnt any one had any luck though with any products or supplements
Once testosterone is in good range, yet a person is still having problems, then it is important to
look at optimizing the other hormones. Next in line would be the adrenal hormones and thyroid
hormones.
DHT with transdermals tends to be high. It can be a problem with some people because high
DHT can increase belly fat, increase hair loss, etc.
High DHT with testosterone injections can be reduced by more frequent injections, e.g. twice a
week injections with divided doses (such as 50 mg twice a week instead of 100 mg once a week).
It would certainly be educational to have your lab data shared with others on the board.
__________________
Re: Sudden Rapid Hair Loss
Quote:
Originally Posted by adam12
I just turned 30 and since May ( now September) my hair has started falling out 8 times
as fast. Previous to May I would wash my hair and find maybe 5 hairs in the lather. Now
I'm finding at least 40 at a time. Previous to May I had lost some of my temporal lobes
and none of my crown, now I have a bald spot starting to come in on my crown and from
my crown to the front of my head.
Could what I started taking in May, increase my DHT levels. Specifically my Essential
Fatty Acid supplements.
In May I started taking per day:
12.5 mg - Seroquil a day ( for tics ).
1 - One-a-Day Men's Helth Formula Muliti Vitamin
Omega 3,6,9 Essential Fatty Acid supplements
The fatty acid supplements totaled per day:
1200mg Flaxseed Oil
1200mg Borage Seed Oil
1200mg Fish Oil ( 50% Omega-3 )
These three oils composed of this this per day
Omega 3 = 660mg ALA ( Alpha Linolenic Acid ), 360mg EPA ( Elcosapentaenoic Aicd ),
240mg DHA ( Docosahexaenoic Acid )
Omega 6 = 540mg Linoleic Acid, 264mg GLA ( Gamma Linoleic Acid )
Omega 9 = 456mg Oleic Acid
Also in March I had my test levels taken. 405 ng/dL was my total and the free test was
101.6 pg/Ml which is 2.51%.
Any ideas?
Hair loss has many possible causes including:
1. Dihydrotestosterone excess - male pattern baldness
2. Thyroid hormone deficiency
3. Cortisol deficiency - hair loss in patches
4. Progesterone deficiency
5. DHEA deficiency
6. Estrogen deficiency
__________________
Re: Androgel now in use - how soon will effects be noted?
Quote:
Originally Posted by infoseeker
OK, it looks like my husband may never get around to posting here but he does read
some.
He got his hands on the Androgel (10 mg. each day) and he said it's like spreading two
entire ketchup packets everywhere. He knows how to let it dry, etc., all that protocol with
laundry, etc.
It's only been two days now. He has had hot and cold spells. Would the hot flashes be
from dropping estrogen or something else? His lab total testosterone was only 200; this
is what prompted the Rx in addition to the usual constellation of high glucose, (avg. AM
110-130, post-meal 140-180 or higher at times, A1C of 7 and later 6.1, a substantial
amount of belly fat, little weight loss despite ideal diet and exercise and pretty good
bloodwork re: cardiac markers. Just bringing anyone up to speed who has not read my
posts - oh yes, he's 45 and has about 40 lbs. to lose, already lost 20 or 25 but SO slowly.)
One big reason for prescribing this Androgel is in the hopes that it will give him a weight
loss or at least fat loss / muscle gain (although he looks plenty muscular) push. The fat is
just not coming off. We hope that will change.
Are the sweating sessions from his metabolism changing? Also, he has not seen a return
of the A.M. friend "Mr. Happy " (LOL - I think someone here typed that one time), but it's
only been one full day of usage, so could that still improve in a few days, or is it not likely
to improve if it hasn't yet?
We were hoping for blood sugar levels to improve immediately (that's one other reason
the dr. thought it would be a good idea) but it seems like the same-old, same-old (Oh
yeah, and he's been on Metformin for more than a month and it's hardly bringing blood
sugars down.) Any other beneficial or adverse effects he should watch for? Thanks.
Androgel has to be spread in as large an area as possible in order to maximize the absorption of
testosterone into the fat layer of the skin. From the fat layer, testosterone is then gradually
released into the body. Too small an area of application can cause the fat layer of the skin to be
saturated with testosterone. Then the rest of the testosterone will be absorbed directly into the
blood stream - which does not bode well for steady levels since testosterone lasts a short time in
the blood. Too small an area of application, on the other hand, can impair absorption as the
testosterone dries on the skin without being absorbed.
Transdermal testosterone reaches its peak steady state level in about 1-3 days. There are
immediate effects should it be absorbed optimally. 10 grams of Androgel generally has a good
chance of getting good testosterone levels. Should there be no other serious hormonal
imbalance, the higher amount of testosterone can directly improve sex drive, allow morning
erections, etc. The metabolic effects such as weight loss and improvement in blood sugar control
may take a while to manifest. With a transdermal testosterone, one can get follow up labs as
soon as a week after starting to track total testosterone, estradiol, DHT, etc.
Testosterone can increase metabolism (e.g. stimulate thyroid activity) and skin blood flow
contributing to a flushing or heat sensation.
If a person has drops in estradiol level, then a hot flash can occur during TRT. This is more
frequently seen with injections of testosterone. But it can occur with transdermals when there are
not steady blood levels of testosterone - such as with high potency testosterone gels or creams or
with problems with absorption (such as with thickened skin due to hypothyroidism).
Note that testosterone can also reduce thyroid activity in some people - thus follow up to assess
response is important - since in this case, testosterone can cause weight gain rather than weight
loss. Also, excessive dihydrotestosterone (DHT) can also increase belly fat and weight.
Excessive testosterone (this depends on the person) can increase fasting blood sugar rather than
reduce fasting blood sugar.
There are numerous interactions to pay attention to in order to optimize response. The presence
of other hormone imbalances can change one's response to testosterone. Thus a multi-hormone
evaluation and treatment ( if needed) is important. Follow up labs and adjustments of these other
hormones may be necessary if treatment with testosterone does not work as expected.
__________________
Re: Androgel now in use - how soon will effects be noted?
Quote:
Originally Posted by infoseeker
Just me - the buttinsky here - ;o) I think he's asking about weights because he's already
been doing the walking 45 mins. or greater for years, (we have four kids including
young'uns and you know how they keep you busy and active) he can do a lot of hiking
even as of recently, including hills and stuff, and thus is in pretty good condition, good
blood pressure etc. except that the dr. discovered high heart rate which he's a little
concerned about and will follow up on in Decmber.
I know that the dr. wants him to get his total T checked in late November. Of course he
didn't write any estrogen on the lab slip but maybe he can ask the dr. to do that. It makes
sense.
We have some weights and he's been using them all along too, but not consistently. I
guess he wants to get serious so that's why he's asking. Typically he's been the type who
just touches a weight and his muscles bulk up. All right, I may be embarrassing him and
I'll shut up now.
Our teenage boys like to use the weights also, so it's a family activity.
Again - thanks - you guys are great.
A total testosterone is the one test done in a basic protocol - such as the Endocrine Society's
Guidelines for Testosterone Replacement Therapy.
A basic set of follow up labs to help determine what is happening with testosterone replacement
includes:
Total Testosterone
Dihydrotestosterone
Estradiol
Free T3
Cortisol AM
DHEA-s
Fasting glucose
It's important to drink 0.5 to 0.75 liters (about 2 to 3 cups) of water prior to the lab test to avoid
getting artificially higher levels due to dehydration.
__________________
Re: Androgel now in use - how soon will effects be noted?
Quote:
Originally Posted by Andrew Androgen
Marianco, why do you say that a total testosterone test is the best one to carry out, when
SWALE says they are notoriously inaccurate? SWALE says that a free testosterone test is
best for determining testosterone status.
Actually, Dr. Crisler (A.K.A. SWALE) wrote that Free Testosterone is often inaccurate. The
reason being that it measures a very small amount of the total testosterone. Measuring small
amounts results in a higher risk for error.
He uses bioavailable testosterone (testosterone bound to albumin plus free testosterone) as the
measure for testosterone's activity - in addition to total testosterone.
Free Testosterone is not accurately measured by labs. It also does not measure all of
testosterone's effect on the body. Free testosterone is also not just a measure of testosterone but
is the sum effect of multiple hormones including thyroid, estrogens, progesterone, insulin, DHEA,
growth hormone, and testosterone, etc.
If total testosterone is low yet free testosterone is high, then there may be significant problems
with these other hormones for which treatment with testosterone is not a complete treatment.
Bioavailable testosterone is a better measure of testosterone's activity. The testosterone bound to
albumin is loosely bound and is active.
Total testosterone (I believe) is an even better measure because testosterone bound to SHBG is
still active. It is active on SHBG receptors, not testosterone receptors.
Re: Blood work has me confused. Referred to an Endo
Quote:
Originally Posted by rmx
Hello all, I was hoping to get some thoughts on my lab result.
I am 31, 6'4 195 about 8% BF
I like to go annually to the dr. to get a physical and this year I asked her to test my Test
levels with my blood. Here is some of the report:
CBC was normal
Glucose, Serum = 94 mg/dL (65-99)
BUN = 27 mg/dL (5-26)
AST (SGOT) = 49 IU/L (0-40)
ALT (SGPT) = 41 IU/L (0-55)
Testosterone, Serum (Total) = 252 ng/gL (241-827)
TSH = 1.104 uIU/mL (0.35-5.5)
Cholesterol, Total = 130 mg/dL (100-199)
Triglycerides = 68 mg/dL (0-149)
HDL Cholesterol = 47 mg/dL (40-59)
VLDL Cholesterol Cal = 14 mg/dL (5-40)
LDL Cholesterol Calc = 69 mg/dL (0-99)
LDL/HDL Ratio = 1.5 (0-3.6)
I also need to note I was currently using a herbal product that does not aromatase and
naturally boosts t levels. It is not an AI. I was on it 2 weeks at the time of test. Also it is
important to not that I have never taken any type off AAS/PH type product.
So the doc says no problem with your test besides the liver counts and they are not
terrible. She asked numerous times about PH products and admittedly it does look that
way but honestly I have not used any. She said my test levels where normal and I held the
BS flag high and said we need another test but this time add free. We scheduled. I was off
the supplement for a few days (half life is 8 hrs) and ran milk thistle for my liver. Here
are the new test results that are about 3 weeks later.
LH = 2.9 mIU/mL (1.5-9.3)
FSH = 3.5 mIU/mL (1.4-18.1)
Testosterone, Serum = 164 ng/dL (241 - 827)
Testosterone, Free = 7.38 ng/dL (5-21)
% Free Testosterone = 4.5% (1.5-4.2)
Glucose, Serum = 86 mg/dL (65-99)
BUN = 38 mg/dL (5-26)
AST (SGOT) = 40 IU/L (0-40)
ALT (SGPT) = 42 IU/L (0-55)
Bilirubin, Direct = .13 mg/dL (0-.4)
Prolactin = 6.1 ng/mL (2.1-17.7)
Doc says test levels are fine and actually my free test is high. She said to call her in a few
months and we will run it again. I held up another B.S. flag and she agreed to send me to
see and Endo. I told her that 164 is bad for total test and that the 241 limit is retarded for
a 31 year old. So anyway I have an appt in a few week to see an endo. Any words of
advice? Can anyone decipher this stuff for me. Lastely I am not sure if this relates at all
but I did have a kidney failure about 8 years ago. This is freaking me out a bit . I am
super pissed because every search I do it keeps coming back like I abused AAS. If I did it
fine but I am a big tall stick man. Couple other notes to finish my rant. I have been
diagnosed with depression for many years, always tired, low sex drive (but not gone),
penis hardness is not always that hard, etc.
Again thanks and I am learning so much from this site. It is a wonderful tool.
Free Testosterone is not a useful measure for determining the appropriate level of testosterone.
The problem is that free testosterone is the sum effect of numerous hormones such as thyroid
hormones, estrogens, progesterone, testosterone, DHEA, growth hormone, and insulin, among
others. Free testosterone also does not determine all of testosterone's activities. Free
testosterone is only a small percentage of testosterone. It is the testosterone not bound to SHBG
and not loosely bound to Albumin. Bioavailable testosterone (free T plus T bound to Albumin) is a
better measure of testosterone's activities. Bioavailable testosterone is active testosterone. I think
total testosterone is an even better measure. SHBG-bound testosterone still has active signaling
functions.
If total testosterone is low yet free testosterone is high, then high free testosterone may occur
when there there is low thyroid, low estrogens, low progesterone (as in adrenal fatigue), high
insulin (as in insulin resistance or diabetes), high DHEA (as in stressful conditions), etc. It is
important to search for these other conditions since they may also contribute to depression, lack
of sex drive or function, fatigue, etc.
When one has sexual dysfunction and a total testosterone under 300, then one has testosterone
deficiency/hypogonadism for which treatment is legitimate for an endocrinologist - hopefully. It
really depends on whether or not the endocrinologist is familiar with testosterone replacement
therapy. Many are not. For those that are not, hopefully they can follow the Endocrine Society's
clearly written guideline for treatment of testosterone deficiency - where the goal is to achieve a
midrange total testosterone (i.e. 650 ng/dl on a scale of 300-1000).
Ideailly, LH and FSH are going to be in the upper range when testosterone is low. If they are on
the low side, then one has at least secondary hypogonadism. Then the question shifts to looking
for the reasons why. For example, insulin resistance (high insulin levels), results in an impairment
in the production of LH, leading to lower testosterone production. Low thyroid hormone can lead
to insulin resistance. Low thyroid can lead to eventual adrenal fatigue, which can impair sex drive.
Etc. There are multiple hormone and neurotransmitter cascades that occur with imbalances of
single hormoens. Searching for and correcting these other problems may help improve clinical
response over and above treatment with testosterone replacement alone.
If the brain is already off in regard to producing LH and FSH, how reliable is the TSH? It may not
be reliable as a measure of thyroid function. It would be better to get a Free T3, Free T4 to
assess thyroid function.
__________________
Re: dopamine sensitivity
Quote:
Originally Posted by DAVID
After some year's of Test therapy, I don't have the good feeling rush of dopamine the day
you take it. I hope that Marianco help for this problem.
May be there are a down regulation of DA receptors ? and there are a strategy tto
increase DA sensitivity ?
The following is fairly speculative.
High levels of testosterone for long periods of time, can, I think, result in tolerance to the higher
levels of dopamine in the brain. The initial almost euphoric feeling that initial TRT can eventually
wane to a lesser level. When at hypogonadal levels for a long time, there may be suprasensitivity
to dopamine that develops from the dopamine deficit of hypogonadism. This contributes to the
high that results from TRT at the onset.
A problem for testosterone therapy is that there is no therapy that really mimics the daily
fluctuations in testosterone production. Testosterone tends to be highest in the morning and fall
gradually through the day. This means the dopamine levels in the brain will also follow a similar
pattern. Testosterone treatment generally follows either a many day decay in level after a large
peak (e.g. injections) or a very steady state level (e.g. transdermals or pellets).
Dopamine is one neurotransmitter that clearly can result in tolerance when present at high levels.
Dopamine is a neurotransmitter that needs to vary in concentration hour by hour. On of its
functions is to provide a feeling of reward on certain events. A reward cannot last forever, it has to
have a finite life or one cannot differentiated it as a reward. TRT generally does not have the
frequent fluctuations in dopamine level during the course of the day that natural testotserone
production lends.
Dopamine sensitivity improves once a deficit is created.
Going off TRT periodically, which is done by ASIH, for example, would then allow dopamine
sensitivity to return.
In a way, if dopamine insensitivity is an issue, then one other possible solution would be to have
once a month injections such as a colleague of mine uses for her TRT clients. This causes a
large peak and then a return to baseline hypogonadism before the next injection. Dopamine
levels follow the testosterone curves - in this case having large changes in levels through the
month.
The thought of giving a person their whole 4 week supply of testosterone in one injection gives
me pause - for example out of concern for a roller coaster experience. The large dose of injection
also is a concern. Problems with supraphysiologic levels of testosterone and other hormones at
the onsent of treatment is a concern. From her experience, her technique works well for her
clients. Perhaps this is one technique that maintains dopamine sensitivity since dopamine levels
are constantly changing rather than remaining at the same high levels.
A third approach would be doing TRT in such a way as to avoid very high total testosterone levels
- for example, going up to 400-500 ng/dl rather than 650-1000 ng/dl. This way, dopamine levels
do not remain constantly high. There then is more headroom for the brain to produce more
dopamine in the reward circuits of the brain on demend, without getting to high levels that
promote tolerance. If sexual function is not optimal, then optimizing other hormonal systems such
as thyroid and adrenal hormones may return sexual function at the lower target testosterone
levels. As an example, with good thyroid and adrenal function, sex drive often persists to fairly
low levels of testosterone.
__________________
Re: dopamine sensitivity
Quote:
Originally Posted by pmgamer18
Sounds good but lower levels in men like me cause joint and muscle pain at one time I
was house bound could hardly walk and the pain in my back was dam bad. I was on gels
and my levels were 600. Doing shots and my levels at 900 I don't have this pain.
I need to say that my labs range is 262 to 1593 so this needs to taken as to a range of 250
to 1000.
The story is more complex.
When a high testosterone level is needed (such as levels over 1000 ng/dl), the question I would
have is what other hormone problems are occurring that a high level is needed to compensate for
the problem?
For example, testosterone can stimulate thyroid function, thus increasing one's energy. (There
are some people however, where too high a testosterone level can reduce thyroid function
instead of increasing it. ) If one is then low on thyroid to begin with, then a high dose of
testosterone is needed to compensate for the lack of thyroid hormone. But if thyroid hormone
levels were corrected, does the person need such a high dose of testosterone - which has its own
risks? A good chance not. A physiologic dose (within 300-1000 ng/dl) may serve well - with lower
risks overall.
Testosterone, thyroid hormone, and cortisol are major anti-inflammatory hormones. Progesterone
and DHEA are among the others. They help reduce pain conditions. If a person has
hypogonadism, hypothyroidism, and adrenal fatigue the person is at high risk for inflammatory
and pain conditions. A high dose of testosterone may be needed to compensate for the
deficiencies in other hormones. However, if the thyroid and adrenal deficiencies are addressed,
would this be needed? A good chance not. A physiologic dose (within 300-1000 ng/dl) may serve
well - with lower risks overall.
Testosterone can't be considered alone in a vacuum. Its effects need to be considered in terms of
teamwork with other hormones, neurotransmitters, and immune system cytokines.
__________________
Re: dopamine sensitivity
Quote:
Originally Posted by pmgamer18
Yes your right but I have seen my levels go up on the same dose as I treat my Adrenals
and Thyroid. So as I have lowed my dose my pain is coming back. Yet I have just started
on treating Adrenals and Thyroid so I do need to give it time. I am finding I don't need as
high a does of T meds now. I guess it's like you said in a post some men use the T meds
up faster then others. I am now finding I am not using them up so fast and having to cut
my dose because levels are now going to high.
An interesting note is that before physicians had lab tests to overly rely on to diagnose and treat
hypothyroidism, they had to treat hypothyroidism by signs and symptoms (which I think is the
correct way to treat it). The average dose of Armour Thyroid used then was about 180 mg a day.
The dose, of course, has to be individualized to the person. But some may need a dose as high
as 300 mg a day to reduce the signs and symptoms of hypothyroidism. I would not recommend
going to doses this high without being under the care of physician, given the risks involved.
__________________
Adrenal Fatigue and Sugar.
Quote:
Originally Posted by Caspian
Dr. Wilson writes that it is very important to avoid sugar when suffering AF. What kind
of experiences do you AF-sufferers have on this? I crave sugar very much and eating it
(candy for example) makes me feel a lot better - for a while. Anyway I avoid it as much as
I can because Wilson says it's so important - and feel awful.
C.
A person with adrenal fatigue has difficulty in producing cortisol and other hormones such as
DHEA and progesterone.
Cortisol is the signal to the liver to make sugar so the rest of the body has an energy source.
When the brain cannot get adequate sugar - as when one has adrenal fatigue - it creates the
craving for external sources of sugar. Eating sugar then compensates for the lack of adequate
Cortisol production.
A person with adrenal fatigue does - at least temporarily - feel better after eating sugar.
A problem is that the higher blood sugar levels from ingesting sugar also reduces the brain's
signals to the adrenal gland to produce cortisol. This lowered cortisol production can persist
through the day, long after the ingestion of sugar.
Thus, when ingesting sugar, one feels better (e.g. for about an hour), until the sugar dissipates.
But then one is faced with worse adrenal fatigue through the day since Cortisol production is
lowered by the sugar intake.
If anything, longer lasting, slower digesting, sources of sugar such as whole-fruits and vegetables
are better than ingesting candies, fruit juices and other quick sources of sugar when one has
adrenal fatigue.
A similar problem occurs when drinking coffee. Caffeine is a short-acting stimulant that can give
energy. However, it also causes a higher level of stress in the body that persists through the day long after caffeine has stopped working to give energy. In adrenal fatigue, this persistent stress
places a higher workload on the adrenal glands, increasing the likelihood of adrenal fatigue or
slowing recovery.
__________________
Growth Hormone Replacement
Quote:
Originally Posted by HeadDoc
There is alot of controversy on HGH treatment. AMA issued a statement through JAMA.
Here is a letter from Dr. Ron Rothenberg to JAMA. He addresses many of the issues
above.
http://ehealthspan.com/download/Resp...GH_Article.doc
When the world's largest, oldest and most respected group of endocrinologists acknowledges the
existence of adult growth hormone deficiency and even has a reasonable guideline for it
(http://www.endo-society.org/quickcon...ormoneBook.pdf), treatment with growth hormone has
been legitimized.
A problem is that so many doctors, particularly endocrinologists, are not themselves familiar with
adult growth hormone deficiency syndrome. Further, growth hormone has been given a bad
reputation due to its abuse by athletes. And a more significant problem I often encounter is that
treatment with growth hormone is often done without consideration of the many interactions it has
with the other hormone systems - thus causing problems.
Growth hormone should be the last hormone to optimize. Every other hormone should be
optimized first. Then after growth hormone treatment is started, all the other hormones need
again to be re-optimized, as growth hormone affects their values.
Growth hormone works best when all the other hormones, themselves, are optimized.
At the very least, the following need optimization first before starting growth hormone therapy:
Melatonin, Thyroid Hormone (T3, T4), Cortisol, DHEA, Pregnenolone, Aldosterone, Estrogens,
Progesterone, Testosterone, and Insulin.
Growth Hormone most often cannot be given by itself without causing problems. For example, it
automatically reduces adrenal function, causing symptoms of adrenal fatigue. Thus, when
treatment is started, it has to be coupled with an adrenal fatigue treatment (which can mean at
least 5 more different pills to take in some patients).
Growth Hormone, if given, has to be part of an integrated, multi-hormone treatment program.
__________________
Re: Growth Hormone Replacement
Quote:
Originally Posted by rockin813
When you say optimizing other hormones...how important is DHEA in the big picture of
things. If one has low DHEA should he (she) take DHEA supplements to see if there's any
response? Everything else is in the Gray area (T 400, LH 4, FSH 7 w/out TRT).
My DHEA is 160 with ref range of 80 - 560.
Thanks for any responses/comments.
DHEA and growth hormone, more than the other hormones, clearly decline with age.
DHEA has effects independent of other hormones in improving IGF-1, reducing insulin resistance,
improving immune system function, reducing blood pressure, improving mood, sex drive, etc.
DHEA is also a precursor for other hormones such as testosterone, estradiol, etc.
When one has low DHEA - which, for example, occurs with adrenal fatigue and age supplementation is important. It is part of a comprehensive adrenal fatigue treatment.
Re: Transdermal selegiline ?
Quote:
Originally Posted by JackBauer
I know some people take selegiline by mouth... But Emsam has been out for about 6
months. I'm wondering if anyone is using it to raise T successfully? (It seems to have
some real benefits over the pill version)
Emsam uses Selegiline at such a high dose that selegiline is no longer specifically increasing
Dopamine (which increases testosterone production). Rather in Emsam, selegiline acts as a full
MAOI Inhibitor - increasing primarily Serotonin, then Norepinephrine, then Dopamine. Thus many
of the side effects from increasing serotonin (e.g. sexual dysfunction) and norepinephrine (e.g.
adrenal fatigue) may be possible. Emsam is an excellent antidepressant with much less of the
risks of traditional oral MAOI inhibitors.
__________________
Re: Study on SC T Injection
Quote:
Originally Posted by Normandy
This is a great study. Thxs Vforcer2.
Although this is an area where no one can claim any real certainty to, I'd still love to
hear Marianco's thoughts on possible dangers or perhaps scenarios (pharmokinetically
speaking) of using TE sub-Q as long term therapy.
Are we talking about chemical reactions with the cell membranes of adipose tissue? Or is
there something else inherently different among the two methods.
This is an area I wouldn't mind spending hours, if not days, researching on (and bringing
relevant material back to this board) if only I had a better grasp of what's at stake here.
-- Normandy
I don't know too much at this time about using Testosterone Enanthate subcutaneously.
From this abstract, the dose used can be lower since testosterone enanthate has a longer
apparent half-life. This reduces the cost and can reduce the need for more frequent injections.
Injections in the abdomen - particularly if one's abdomen was ripped or six-packed - can be more
difficult since there won't be much subcutaneous fat.
The injections used subcutanesouly, are relatively small - 0.25 to 0.5 cc.
Note that they do not state the size of the needle used. I find 25 gauge needles the best
compromise between slowness of injection and pain. Pain is fairly minimal with 25 gauge needles
intramuscularly. Subcutaneously, however, one may need smaller gauge needles, making it more
difficult to inject the testosterone ester in oil.
This is interesting as an alternative delivery method, but more information is needed - e.g. getting
well defined pharmacokinetics, data on long-term safety of injecting oil into fat cells, etc.
The pharmacokinetics of doing subcutaneous injections would be interesting to see. I hope they
can do a well defined curve as with testosterone enanthate so one can predict the dose needed.
The pharmacokinetics of testosterone enanthate are well-defined, making clinical decisions much
easier to make to optimize dosing.
There is an alternative site to the thigh and dorsogluteal injections for intramuscular injections that
actually is best: The ventrogluteal site. This uses the gluteus medius muscle rather than the
gluteus maximums. There are fewer nerves and blood vessels in the ventrogluteal site. There is
also a more consistent fat layer over the site than in the buttocks. The upshot is that it is a site
which is doable when self-injecting, which also is safer than the thigh and dorsogluteal sites
(buttocks), and is also much less painful an area. The site is relatively well-defined. It does need
to be done in a lying position. Google for information about this site and instructions.
An interesting alternative - if it ever becomes available - is the use of Testosterone Undecanoate
intramuscular injections. Testosterone Undecanoate has a very very long half-life compared to
Testosterone Enanthate.
Instead of once a week injections, one can use once every three month injections with
Testosterone Unedecanoate.
Here's one study: http://www.andrologyjournal.org/cgi/...tract/23/3/419.
This would make testosterone injections close to the equivalent of testosterone pellet
implantations.
__________________
Re: 100mg/wk enough to fix 51ng/dl test level?
Quote:
Originally Posted by liftin4life
I'm 25 yrs old and...I've posted on this board before about my situation. I have really low
test levels due to a recently discovered pituitary tumor. My most recent and morning lab
results for testosterone is 51ng/dl total and 11ng/dl free. All other levels are normal
including prolactin and E2.
I finally was referred to an endocrinologist and saw her this past week. She ordered a full
endocrine lab workup to check liver, adrenals...everything. She said she had to rule out
possible other issues also.
Anyway, she said when the results come back she'll call me (this week) and then call in
my prescription for 100mg/wk of testosterone enanthate. Is that enough to bring me up to
a normal 25 yr old's levels??? 100mg/wk seems like nothing when you consider that
maybe 70-80 of that is the test due to the ester. I've had no sex drive for 6 months and
complete erectile dysfunction for 3 months now.
100 mg a week of Testosterone Enanthate is enough for an average male with hypogonadism to
raise their total testosterone to between 650 to 1200 ng/dl - which are in line with men in their
20s. It is used as a standard starting dose. A person has to start somewhere, and 100 mg a week
is a good rule of thumb.
Once a steady state is obtained, labs can be drawn, and the dose adjusted. Variables affecting
the ultimate dose can include a person's half-life of testosterone, half-life of testosterone
enanthate. Some men need higher doses, some men lower doses.
__________________
Re: 100mg/wk enough to fix 51ng/dl test level?
Quote:
Originally Posted by DaVinci2
If after 3 months of 100mg per week levels only increase by 100ng or 200ng should the
dosage be increased? Is there anything else to look for?
An injection of testosterone enanthate adds to the total testosterone level.
If the total testosterone level only increase creases to less than 650 ng/dl, then a higher dose is
needed or more frequent injections at the same dose is needed. Usually that occurs because the
half-life of testosterone enanthate for that person is less than the average half-life of 7-9 days.
At the onset of treatment, one way to estimate the half-life is to give the person an initial injection
of 200 mg of testosterone enanthate then get a total testosterone after 4 days. In an average
person, the level should be around 1000 ng/dl. If it is much lower, then the half-life will be lower,
and the person will need a higher dose than 200 mg every 2 weeks (or 100 mg per week).
One patient, for example, had a total testoterone of about 600 ng/dl 4 days after the 200 mg
injection. This indicated the person's half life was near 4 days rather than 7-9 days. He needed
100 mg twice a week to maintain a total testosterone of between 800-1000 ng/dl.
__________________
Androgel now in use - how soon will effects be noted?
OK, it looks like my husband may never get around to posting here but he does read some.
He got his hands on the Androgel (10 mg. each day) and he said it's like spreading two entire
ketchup packets everywhere. He knows how to let it dry, etc., all that protocol with laundry, etc.
It's only been two days now. He has had hot and cold spells. Would the hot flashes be from
dropping estrogen or something else? His lab total testosterone was only 200; this is what
prompted the Rx in addition to the usual constellation of high glucose, (avg. AM 110-130, postmeal 140-180 or higher at times, A1C of 7 and later 6.1, a substantial amount of belly fat, little
weight loss despite ideal diet and exercise and pretty good bloodwork re: cardiac markers. Just
bringing anyone up to speed who has not read my posts - oh yes, he's 45 and has about 40 lbs.
to lose, already lost 20 or 25 but SO slowly.)
One big reason for prescribing this Androgel is in the hopes that it will give him a weight loss or at
least fat loss / muscle gain (although he looks plenty muscular) push. The fat is just not coming
off. We hope that will change.
Are the sweating sessions from his metabolism changing? Also, he has not seen a return of the
A.M. friend "Mr. Happy " (LOL - I think someone here typed that one time), but it's only been one
full day of usage, so could that still improve in a few days, or is it not likely to improve if it hasn't
yet?
We were hoping for blood sugar levels to improve immediately (that's one other reason the dr.
thought it would be a good idea) but it seems like the same-old, same-old (Oh yeah, and he's
been on Metformin for more than a month and it's hardly bringing blood sugars down.) Any other
beneficial or adverse effects he should watch for? Thanks.
Re: Androgel now in use - how soon will effects be noted?
Quote:
Originally Posted by infoseeker
OK, it looks like my husband may never get around to posting here but he does read
some.
He got his hands on the Androgel (10 mg. each day) and he said it's like spreading two
entire ketchup packets everywhere. He knows how to let it dry, etc., all that protocol with
laundry, etc.
It's only been two days now. He has had hot and cold spells. Would the hot flashes be
from dropping estrogen or something else? His lab total testosterone was only 200; this
is what prompted the Rx in addition to the usual constellation of high glucose, (avg. AM
110-130, post-meal 140-180 or higher at times, A1C of 7 and later 6.1, a substantial
amount of belly fat, little weight loss despite ideal diet and exercise and pretty good
bloodwork re: cardiac markers. Just bringing anyone up to speed who has not read my
posts - oh yes, he's 45 and has about 40 lbs. to lose, already lost 20 or 25 but SO slowly.)
One big reason for prescribing this Androgel is in the hopes that it will give him a weight
loss or at least fat loss / muscle gain (although he looks plenty muscular) push. The fat is
just not coming off. We hope that will change.
Are the sweating sessions from his metabolism changing? Also, he has not seen a return
of the A.M. friend "Mr. Happy " (LOL - I think someone here typed that one time), but it's
only been one full day of usage, so could that still improve in a few days, or is it not likely
to improve if it hasn't yet?
We were hoping for blood sugar levels to improve immediately (that's one other reason
the dr. thought it would be a good idea) but it seems like the same-old, same-old (Oh
yeah, and he's been on Metformin for more than a month and it's hardly bringing blood
sugars down.) Any other beneficial or adverse effects he should watch for? Thanks.
Androgel has to be spread in as large an area as possible in order to maximize the absorption of
testosterone into the fat layer of the skin. From the fat layer, testosterone is then gradually
released into the body. Too small an area of application can cause the fat layer of the skin to be
saturated with testosterone. Then the rest of the testosterone will be absorbed directly into the
blood stream - which does not bode well for steady levels since testosterone lasts a short time in
the blood. Too small an area of application, on the other hand, can impair absorption as the
testosterone dries on the skin without being absorbed.
Transdermal testosterone reaches its peak steady state level in about 1-3 days. There are
immediate effects should it be absorbed optimally. 10 grams of Androgel generally has a good
chance of getting good testosterone levels. Should there be no other serious hormonal
imbalance, the higher amount of testosterone can directly improve sex drive, allow morning
erections, etc. The metabolic effects such as weight loss and improvement in blood sugar control
may take a while to manifest. With a transdermal testosterone, one can get follow up labs as
soon as a week after starting to track total testosterone, estradiol, DHT, etc.
Testosterone can increase metabolism (e.g. stimulate thyroid activity) and skin blood flow
contributing to a flushing or heat sensation.
If a person has drops in estradiol level, then a hot flash can occur during TRT. This is more
frequently seen with injections of testosterone. But it can occur with transdermals when there are
not steady blood levels of testosterone - such as with high potency testosterone gels or creams or
with problems with absorption (such as with thickened skin due to hypothyroidism).
Note that testosterone can also reduce thyroid activity in some people - thus follow up to assess
response is important - since in this case, testosterone can cause weight gain rather than weight
loss. Also, excessive dihydrotestosterone (DHT) can also increase belly fat and weight.
Excessive testosterone (this depends on the person) can increase fasting blood sugar rather than
reduce fasting blood sugar.
There are numerous interactions to pay attention to in order to optimize response. The presence
of other hormone imbalances can change one's response to testosterone. Thus a multi-hormone
evaluation and treatment ( if needed) is important. Follow up labs and adjustments of these other
hormones may be necessary if treatment with testosterone does not work as expected.
__________________
Re: Androgel now in use - how soon will effects be noted?
Quote:
Originally Posted by infoseeker
Just me - the buttinsky here - ;o) I think he's asking about weights because he's already
been doing the walking 45 mins. or greater for years, (we have four kids including
young'uns and you know how they keep you busy and active) he can do a lot of hiking
even as of recently, including hills and stuff, and thus is in pretty good condition, good
blood pressure etc. except that the dr. discovered high heart rate which he's a little
concerned about and will follow up on in Decmber.
I know that the dr. wants him to get his total T checked in late November. Of course he
didn't write any estrogen on the lab slip but maybe he can ask the dr. to do that. It makes
sense.
We have some weights and he's been using them all along too, but not consistently. I
guess he wants to get serious so that's why he's asking. Typically he's been the type who
just touches a weight and his muscles bulk up. All right, I may be embarrassing him and
I'll shut up now.
Our teenage boys like to use the weights also, so it's a family activity.
Again - thanks - you guys are great.
A total testosterone is the one test done in a basic protocol - such as the Endocrine Society's
Guidelines for Testosterone Replacement Therapy.
A basic set of follow up labs to help determine what is happening with testosterone replacement
includes:
Total Testosterone
Dihydrotestosterone
Estradiol
Free T3
Cortisol AM
DHEA-s
Fasting glucose
It's important to drink 0.5 to 0.75 liters (about 2 to 3 cups) of water prior to the lab test to avoid
getting artificially higher levels due to dehydration.
__________________
Re: Androgel now in use - how soon will effects be noted?
Quote:
Originally Posted by Andrew Androgen
Marianco, why do you say that a total testosterone test is the best one to carry out, when
SWALE says they are notoriously inaccurate? SWALE says that a free testosterone test is
best for determining testosterone status.
Actually, Dr. Crisler (A.K.A. SWALE) wrote that Free Testosterone is often inaccurate. The
reason being that it measures a very small amount of the total testosterone. Measuring small
amounts results in a higher risk for error.
He uses bioavailable testosterone (testosterone bound to albumin plus free testosterone) as the
measure for testosterone's activity - in addition to total testosterone.
Free Testosterone is not accurately measured by labs. It also does not measure all of
testosterone's effect on the body. Free testosterone is also not just a measure of testosterone but
is the sum effect of multiple hormones including thyroid, estrogens, progesterone, insulin, DHEA,
growth hormone, and testosterone, etc.
If total testosterone is low yet free testosterone is high, then there may be significant problems
with these other hormones for which treatment with testosterone is not a complete treatment.
Bioavailable testosterone is a better measure of testosterone's activity. The testosterone bound to
albumin is loosely bound and is active.
Total testosterone (I believe) is an even better measure because testosterone bound to SHBG is
still active. It is active on SHBG receptors, not testosterone receptors.
Re: Flomax-Iris-Adrenal fatigue test
Quote:
Originally Posted by JanSz
One of the tests for adrenal fatigue is to shine light on the side of the eye and observe if
iris closes under light and holds its position or opens and closes (fluctuate) due to low
cortisol.
Question, is this test still usefull for men that used Flomax or other alpha blockers when
dealing with their enlarged prostate.
Flomax affects iris behavior and requires modification to cataract surgery.
http://www.eyeworld.org/article.php?sid=3285
also:
=========================================
Men's Newsletter
September 18, 2006
In This Issue
• Prostate Drug Use May Mean Cataract Surgery Change
• First-Ever RNA Drug Targets Prostate Cancer
The quick answer is that it may be more difficult to see. Is it still useful? Yes.
The iris controls the amount of light entering the eye by controlling the size of the pupil (the hole
at the center of the iris).
The size of the pupil also controls the depth of field, hence contributes to control of focus,
particularly at small pupil diameters.
The iris has two rings of muscles which control dilation and contraction.
The Iris sphincter muscle contricts the pupil under stimulus from the parasympathetic nervous
system (via cranial nerve III, the oculomotor nerve).
The iris dilator muscle dilates the pupil under stimulus from the sympathetic nervous system (via
sympathetic nerves to the eye).
When one tests pupillary reflex to light, one is testing for several things including:
1. Intactness of the nervous system innervation to the eye (what most physicians do.)
2. Balance between sympathetic vs. parasympathetic nervous system tone.
3. Adequacy of energy supply to the sphincter and dilator muscles.
Points 2 and 3 are affected when one has adrenal fatigue.
During adrenal fatigue, one way to generate energy is through increasing sympathetic nervous
system tone. This makes it more likely for the pupil to dilate even when exposed to light since the
sympathetic nervous system tone may transiently override the control over pupillarly contraction.
The impairment in energy production in the body may also transiently weaken the pupillary
contraction in response to light, resulting in dilation.
Alpha-blockers work by blocking the alpha-type norepinephrine/epinephrine receptors. This
means they block signals from the sympathetic nervous system. In regard to the pupillary reflext
test, the pupils are more likely to be smaller and the reflex is harder to see.
__________________
Re: What is wrong with me? Please help
Quote:
Originally Posted by Caspian
Hello
I am new here. I was directed here from the stopthethyroidmadness forum. I’m pretty
desperate to find solutions and answers for my miserable condition and I would be very
grateful if someone could help or have an idea what to do next. My problem is very likely
hormonal because all my other blood tests are fine. I’m 31-year old. So here we go:
My symptoms:
*severe fatigue
*severe anxiety, nervousness, sometimes almost panic attacks
*cant handle ANY stress
*cant concentrate
*shaking, trembling
*often rapid pulse
*depression, lack of motivation, mood swings, crankiness
*gerenal weakness
*some muscle and joint pains/aches, tension in muscles
*cracking joints
*suddenly run out of energy
*feel unwell and ill most of the time
*low blood pressure
*lost a lot of weight
etc
Test results:
Thyroid labs:
free t4 12.2 (12-22)
free t4D 8.1 (8-21) – dialysis method
free t3 4.1 (2.8-7.1)
TSH 2.8
Saliva tests:
Cortisol
8 AM 0.19 depressed - range: 0.27-2.06
noon 0.61 normal - range 0.03-0.77
4 PM 0.16 low normal - range 0.03-0.56
11PM 0.06 low normal - range 0.03-0.5
DHEA
8 AM 408 elevated - range 14-277
DHEA/Cortisol 2147 elevated - range 35-435
Serum ACTH: 47 high (range: below 46)
Serum Testosterone 13 (10-33)
SHBG 35 (15-48) "sex hormone binding globuline"
Testo/SHBG*1000 (free androgen index) below the range 371 (410-1400)
(=biologically active testosterone?)
FSH 3.2 (1.5-12.4)
LH 5.7 (1.7-8.6)
Potassium 3.9 (3.3-4.8)
Sodium 143 (137-144)
I’m currently on 15 mg hydrocortisone daily but so far I havent noticed much
improvement. I started taking it a couple of weeks ago and gradually upped the dose. I’m
also using Paxil 10 mg for the depression but that hasnt helped much.
Thanks a lot for your comments!!
Adrenal treatment is a passive treatment. It requires time to work, along with minimizing stresses.
Serotonergic medications such as Paxil may help reduce stress. In worse case scenarios, such
as people who have severe posttraumatic stress disorder, it may take a year or two to see
improvement.
Once adrenal treatment is begun, when energy improvement is one of the primary targets of
treatment, then optimizing thyroid function is necessary. The adrenal glands need to be healthy
enough in order to tolerate thyroid hormone treatment. Thyroid hormone will also actively improve
adrenal gland function by increasing the number and size of mitochondria in every adrenal gland
cell.
Checking carbohydrate metabolism (e.g. chekcing for the presence of insulin resistance) is
important to improve energy level. Clues may be found from a fasting or postprandial glucose,
lipid panel, 3-hour glucose tolerance test, hemoglobin A1c.
Once adrenal and thyroid hormone functions are addressed, it may be important to optimize
testosterone level if low, to help improve mood.
There are other areas to examine should these measures not be fully effective for improving
mood, where the analysis becomes highly complex.
__________________
Lab Tests
Quote:
Originally Posted by CaesarWilliam
I am down in Latin America. I have never had labs done before. I have located a Blood
lab in a town near hear. I want to go get my levels checked. My question is, what test do I
have them run? Do I ask for a Hormone test (Testosterone, Estrogen Ect?) Or is there a
specific named test? Down here you don't need a doctor for test referals and health care
is cheap and very good. I just don't know what to ask for.
Look up sticy called TRT: A Recipe for Success for SWALE/Dr. Crisler's protocol including the
initial labs.
The labs need to be customized to the individual. A comprehensive set of labs for my patiens
would cost close to $5,000 or more. Not everyone can afford this, even with insurance, nor may it
be necessary or practical in order to address the most important problems, so I customize the lab
tests for the person.
A fairly comprehensive general initial lab work-up using standard blood and urine tests may
include:
REPRODUCTIVE:
Free and Total Testosterone Panel (this includes Total Testosterone, Free Testosterone,
Bioavailable Testosterone, and Sex Hormone Binding Globulin), Estradiol, Progesterone,
Luteinizing Hormone, Follicle Stimulating Hormone, Prolactin, Prostate Specific Antigen (in men)
THYROID:
Free T4 (Free Thyroxine), Free T3 (Free Liothyronine), Thyroid Stimulating Hormone,
antithyroglobulin antibody, antithyroid peroxidase antibody, thyroid stimulating immunoglobulin.
ADRENAL:
Cortisol AM, Cortisol PM, Cortisol-Binding Globulin, Adrenocorticotropic Hormone (ACTH),
Dehydroepiandrosterone Sulfate (DHEA-s),
CARBOHYDRATE METABOLISM:
fasting glucose (included in comprehensive metabolic panel when fasting), Hemoglobin A1c,
fasting insulin, 3-Hour Glucose Tolerance Test (samples of blood for measuring glucose and
insulin are taken at 0, 60, 120, and 180 minutes after ingesting a 1.75 g/kg glucose solution).
GROWTH HORMONE:
IGF-1 (Insulin-like growth factor I / Somatomedin-C), Growth Hormone Stimulation Test using
GHRH (growth hormone releasing hormone) plus Arginine (samples of blood for measuring
growth hormone are taken at 0, 30, 60, 90, and 120 minutes).
GENERAL:
Comprehensive Metabolic Panel (glucose, urea nitrogen, creatinine, calcium, sodium, potassium,
CO2, cholride, total protein, albumin, globulin, total bilirubin, alkaline phosphatase, AST, ALT)
CBC (complete blood count)
Lipid Profile (including total cholesterol, triglycerides, HDL cholesterol, VLDL cholesterol,
calculated LDL cholesterol)
Urinalysis
Magnesium
Vitamin D, 1, 25-Dihydroxy
Vitamin B12
Folate
Heavy Metal Screen (blood)
The tests are done in the morning after fasting overnight (no food or drink after dinner except for
water). The patient should drink 0.5 liters of water before the test to avoid dehydration. The
patient should avoid strenuous activity the day before, avoid restaurant food and stimulants such
as coffee, eat their regular meals, and avoid stressful situations for at least 2 days before the test.
Cortisol-PM is done in the afternoon between 4-6 PM on the same day as the morning test.
The 3-hour glucose tolerance test and growth hormone stimulation tests should be done on
different days.
ADDITIONAL SPECIALIZED TESTS:
A comprehensive 24-hour urine hormone panel (including DHEA, Androsterone, Etiocholanolone,
Pregnanetriol, Cortisone, Cortisol, Tetrahydrocortisone, Tetrahydrocortisol, Allotetrahydrocortisol, Aldosterone, Tetrahydrocorticosterone, Allo-tetrahydrocorticosterone, Estrone,
Estradiol, Estriol, Pregnanediol, Testosterone, Androsterone, 2-hydroxyestrogens, 16ahydroxyestrone, 4-hydroxyestrone, 2-methoxyestrone, 2-methoxyestradiol, 5a-androstanediol,
5b-androstanediol, 11b-hydroxyandrosterone, 11b-hydroxyetiocholanolone, Free T3, Free T4,
Sodium, Potassium, Calcium, Phosphorus, Magnesium).
24-hour urine growth hormone
Saliva test for Cortisol (4 samples in a day), DHEA-s (2 samples in a day).
Urine test for neurotransmitters (including sertonin, norepinephrine, dopamine, GABA, glutamate,
epinephrine)
MRI of Brain
Chest X-Ray
EKG
The follow up tests include a subset of these tests as well as other tests depending on the
situation.
__________________
Re: What lab test should i ask for?
Quote:
Originally Posted by pmgamer18
Wow I wish you were here in MI. I think I am moving to CA.
Other than the urine neurotransmitter tests, the other tests should be familiar to physicians
studying and practicing anti-aging medicine.
Each physician would then add their own tests based on their interests and specialty.
For example, in psychiatry, I may add a urine drug screen, testing for hepatitis, syphilis and other
sexually transmitted diseases, EEG, genetic tests, psychological testing, specific drug levels, etc.
depending on the person's circumstance.
__________________
Re: St John wort and dopamine hydroxylase
Quote:
Originally Posted by DAVID
St John wort is a natural anti-depressant; the principal mechanism is NA and 5 HT
reuptake and some MAO a inhibition.
But when you read study, you can see that millepertuis inhibe dopamine hydroxylase.
I'm not a expert of brain fonction but I understand that you increase dopamine in the
brain but you decrease in the same time brain noradrenaline.
Not so good for people who have noradrenergic depression and fatigue.
Actually, St. John's Wort has a very complex group of mechanisms of action, some of which are
not yet clear.
Here's an abstract:
Mechanism of action of St John's wort in depression : what is known?
by Butterweck V. CNS Drugs. 2003;17(8):539-62.
Extracts of Hypericum perforatum L. (St John's wort) are now successfully competing for status
as a standard antidepressant therapy. Because of this, great effort has been devoted to
identifying the active antidepressant compounds in the extract. From a phytochemical point of
view, St John's wort is one of the best-investigated medicinal plants. A series of bioactive
compounds has been detected in the crude material, namely flavonol derivatives, biflavones,
proanthocyanidines, xanthones, phloroglucinols and naphthodianthrones. Although St John's wort
has been subjected to extensive scientific studies in the last decade, there are still many open
questions about its pharmacology and mechanism of action. Initial biochemical studies reported
that St John's wort is only a weak inhibitor of monoamine oxidase-A and -B activity but that it
inhibits the synaptosomal uptake of serotonin, dopamine and noradrenaline (norepinephrine) with
approximately equal affinity. However, other in vitro binding assays carried out using St John's
wort extract demonstrated significant affinity for adenosine, GABA(A), GABA(B) and glutamate
receptors. In vivo St John's wort extract leads to a downregulation of beta-adrenergic receptors
and an upregulation of serotonin 5-HT(2) receptors in the rat frontal cortex and causes changes
in neurotransmitter concentrations in brain areas that are implicated in depression. In studies
using the rat forced swimming test, an animal model of depression, St John's wort extracts
induced a significant reduction of immobility. In other experimental models of depression,
including acute and chronic forms of escape deficit induced by stressors, St John's wort extract
was shown to protect rats from the consequences of unavoidable stress. Recent neuroendocrine
studies suggest that St John's wort is involved in the regulation of genes that control
hypothalamic-pituitary-adrenal axis function. With regard to the antidepressant effects of St
John's wort extract, many of the pharmacological activities appear to be attributable to the
naphthodianthrone hypericin, the phloroglucinol derivative hyperforin and several flavonoids. This
review integrates new findings of possible mechanisms that may underlie the antidepressant
action of St John's wort and its active constituents with a large body of existing literature.
A problem with St. John's Wort is that it stimulates activity of Cytochrome P450 3A4. This
potentially can weaken many medications simultaneously taken with St. John's Wort.
Increasing Dopamine while reducing Norepinephrine to treat depression is actually good when it
comes to reducing depression.
There is a pathway in the brain by which increased dopamine production can reduce output from
the Locus Ceruleus - which produces most of the brain's norepinephrine.
Norepinephrine is a stress signal in the brain produced by the sympathetic nervous system in
response to stress. Excessive and prolonged stress can cause adrenal fatigue - which can then
result in fatigue, depression, anxiety, and the inability to cope with stress.
One of the reasons stimulants and Bupropion fail to treat depression is that the increase in
norepinephrine level they promote can lead to adrenal fatigue and worsening of depressive
symptoms. They will only work if the overall dose is not too high, the patient's stresses are low to
moderate, and the adrenal glands are fairly healthy.
Increased dopamine is also good in that it stimulates testosterone production. Testosterone can
then limit excessive adrenal activity to help prevent adrenal fatigue.
I wonder if a "noradrenergic depression" is actually adrenal fatigue. In adrenal fatigue, sometimes
norepinephrine and epinephrine production is reduced.
Increasing norepinephrine is still very useful in reducing chronic pain, when combined with a
simultaneous increase in serotonin. Again, this treatment, however, is limited by the health of the
adrenal glands.
__________________
Re: St John wort and dopamine hydroxylase
Quote:
Originally Posted by pmgamer18
Some yrs. ago my Dr. tried stimulants to help with my fatigue they drove up my BP and
heart rate. So when Concerta came out he tried it I have been on 38mgs for some time
now. I am thinking maybe it would be a good Idea to get off this drug. Now that we know
I am Hypopituitary and low on cortisol and thyroid. Every time I read that meds like this
are hard on adrenals I can't help but think I would be better off not taking this anymore.
Yet I don't feel my cortisol levels are low to poor adrenals but the messages not that
strong from my pit. Still would it be better to get off Concerta.
If there is a dopamine deficit or dopamine resistance (where dopamine production is high to
compensate for receptors that are only partially sensitive to dopamine), then a person may have
a form of attention deficit/hyperactivity disorder for which continuing a stimulant is useful since
even testosterone optimization won't increase dopamine levels enough.
If the use of a stimulant is to improve energy level, then it would be far more useful to optimize
thyroid function, adrenal function and carbohydrate metabolism (e.g. reducing insulin resistance).
After such optimization, the use of a stimulant would be much less necessary, if at all.
Re: St John wort and dopamine hydroxylase
Quote:
Originally Posted by DAVID
Thank you so much - adrenal fatigue is like " atypical depression". You have adrenal
fatigue but a low catecholamine level too. SSRI make some people worse like me
Hydrocortisone and thyroid treament help for people who have a deficit. Sympathic
burnout is real. A lack of brain noradrenaline increase fatigue.
I remenber before my treatment of thyroid, I feel so great... you feel that brain are full in
energy like a maniac. (high NA Turnover or content)
But when I've beginning thyroid trearment for hypothyroidie, I've never feeling this
"brain good feeling" and begin to have lower mood.
I've tring myself tyrosine and moclobemide and coffee for a few year's with good result.
But at this time, this stuff doesn(t work anymore, because I've burning my adrenal).
After 3 year's of hydrocortisone, my adrenal test show again "low adrenal reserve.
Hydrocortisone help fatigue but my mood is low. You need quiet life. I've triing every
herbs, high vit C but nothing respond. I TOTALLY AGRY WHEN YOU SAID THAT
"again, this treament, however, is limited by the health of the adrenal gland"
In my country, many physicians doesn't known nothing about adrenal fatigue-very
difficult to have good advises in this condition. Psychiatre known only SSRI that make
you worse.
Anti-aging doctor give you hydrocortisone between 30 at 40 mg of hydrocortisone but
doesn't known about brain fonction/neurotransmetteurs/cytokines...
Mood has to be separated from energy as conceptual targets of treatment.
Improving energy level involves optimizing thyroid function, adrenal function, and carbohydrate
metabolism (e.g. reducing insulin resistance). The end organ targets of the involved hormones
must also be in good health. For example, the liver must be in good health so that
gluconeogenesis, thyroid hormone activation, etc. can occur.
Mood is a highly complex entity with numerous components. For example, mood is controlled by
a multitude of neurotransmitter, hormone, and cytokine activities, as well as the need for
adequate nutrient supplies (e.g. vitamins, fats, proteins, minerals, and other substances). Mood is
also controlled by psychological factors, other physical health factors, and environmental factors
that need to be evaluated and addressed as necessary. A complex coordinated treatment which
is customized to a person's condition may be necessary to improve mood.
Certainly the ability to produce norepinephrine is necessary to increase CRH, then ACTH
production that increases adrenal cortex hormone production and improves energy level.
Norepinephrine also triggers a signal through the peripheral sympathetic nerves that target the
adrenal medulla's activity. It is important to understand the pathway by which norepinephrine
increases energy level. It is primarily by acting on the adrenal gland. It is thus limited in
effectiveness if the adrenal gland is fatigued.
Developmentally the adrenal glands are part of the sympathetic nervous system (the medullary
cells primarily though there are also islands of sympathetic nervous system cells within the
cortex). The adrenal medulla is a sympathetic nervous system ganglion. Thus one can look at
"sympathetic burnout" as adrenal fatigue which also involves the adrenal medulla.
Adrenal fatigue treatments are generally passive - they usually don't directly improve the adrenal
glands ability to function. Rather they give the adrenal glands time to rest and recover.
Thyroid hormone optimization is one treatment which can actively improve adrenal function. It
does so by increasing the number and size of mitochondria in each of the adrenal gland's cells.
__________________
Re: What are symptoms of insulin resistance?
Quote:
Originally Posted by griffinannie
Does TRT affect it? Can you have normal blood glucose and insulin resistance?
Symptoms of Insulin Resistance depends on the cause. There are many causes.
Hypogonadism and hypothyroidism may result in insulin resistance, for example. The symptoms
would then be related to those conditions.
Common signs include darkening of the skin, skin tags, obesity and increased abdominal fat,
hypertension, high triglycerides, and high fasting blood glucose levels (though not to the point of
being officially diabetes).
Testosterone replacement may help reduce insulin resistance. In some people, however, high
levels of testosterone may instead increase insulin resistance.
A person can have normal blood glucose and insulin resistance if they have both insulin
resistance and adrenal fatigue (which lowers blood sugar).
Re: ED, Insulin and testing
Quote:
Originally Posted by griffinannie
Thanks Marianco. Could erectile dysfunction come into play also? How is insulin
resistance tested in the face of normal glucose?
Insulin resistance itself may cause testosterone deficiency.
Nerve signal conduction is impaired with Insulin resistance.
Erectile dysfunction may occur with insulin resistance.
Erectile dysfunction is very common in diabetics - with one reason being nerve
damage/neuropathy for diabetes.
Possibly useful tests include:
A postprandial (after meal) glucose and insulin level.
Finger-stick glucose 1 hour after meals, which is over 150 is suspicious for insulin resistance.
A 3-hour glucose tolerance test measuring both glucose and insulin levels - is a standard test for
insulin resistance.
A triglyceride to HDL cholesterol ratio over 3.5 is one clue.
__________________
Re: ED follow up
Quote:
Originally Posted by griffinannie
Marianco Thank you. One more question in the face of ed from nerve damage/
neuropathy what can be done to try to reverse?
That is a difficult condition to reverse.
Current thoughts on the matter:
It is of primary important to address insulin resistance by what means necessary (oral, insulin,
diet, exercise, etc.) to prevent further damage.
It is important to optimize thyroid hormone, testosterone, and adrenal hormone function (cortisol,
DHEA, progesterone) to help reduce inflammation and improve nerve cell function.
Sometimes Alpha Lipoic Acid, Acetyl-L-Carnitine, B6, and Vitamin E may help - but again it would
be clinical trial with no promise of improvement given the difficulty faced.
__________________
Re: What are symptoms of insulin resistance?
Quote:
Originally Posted by infoseeker
Marianco: This thread is very intersting - may I chime in with a question or two?
My husband is not fitting the profile listed above exactly:
Excellent low triglycerides (81)
PLA result quite low (45?)
Normal blood pressure (112/75)
total cholesterol low enough (145)
HDL barely off (38)
LDL in ideal range (91) BUT fractionated LDL slowing slightly elevated particle number
(1150), therefore his aggressive lipidologist has just put him on Tricor.
Metformin XR (1500 mg) is barely budging his weight (230, 6'1") and barely nudging the
blood glucose (typically 110-115 fasting AM and 170 at highest postprandial, many times
lower) down despite the best a person can do in the way of diet, exercise, as
acknowledged by the doctor and as testified by me, the observer. (A1C 6.1)
Because of total testosterone at an even 200 (he's 45), Androgel 10mg. per day has been
prescribed but not obtained yet due to funding problems; he's scrambling to obtain it,
though.
1. Is this (Androgel)safe enough re: cancer risk? (by the way, digital prostate exam
revealed no hypertrophy whatsoever.) I just literally watched my mother die from cancer
so understandably I have no stomach for risk
2. Another doctor friend we unofficially consulted said Androgel won't hurt but he
recommends letting the Metformin do its job (normalizing testosterone amongst other
thigns) and re-check T in December and supplement at that point if necessary - any
thoughts?
3. Could it be that the Androgel might be the potentiator to make this metformin do its job
(lower glucose closer to normal levels) and get the weight off? I testify that he's doing
everything right and the weight just sits there
4. Is ED and lack of libido in this case most likely due only to very low T and hopefully
not to nerve damage or blood vessel damage? I'm under the impression that the prettygood bloodwork shows no evidence of vessel blockage.
5. Cialis doens't do a whole lot (works some, but in my view doesn't improve the
inconsistent and definitely not "lost" but definitely not "normal" erectile function) which
leads me to believe the problem is not local (blood vessel) but rather all based in the low
T, which Cialis obviously doesn't do a danged thing for. The dr. we consulted unofficially
has said: "But please for now he needs to avoid any Viagra and related product, they do
not work on increasing the testosterone level but just
bringing more blood to the area, and with vascular issues it can be dangerous."
I've aked for clarification on that but none yet - I believe it has something to do with the
diabetes/pre-diabetes (there's already been very limited nerve damage to a toe, but it
seems to be reversible or at least not perceptible - feeling returning to feet was first thing
noted upon bringing A1C down.) We were under the impression that PDE-5 inhibitors
are safe and in fact benefiicial in the "use it or lose it" sense. Any comments, Marianco,
since this is obviously clear as mud to me? THANKS.
1. A systolic blood pressure of less than 118 could be regarded as low. Adrenal
fatigue/suboptimal adrenal function is one cause of low blood pressure. Adrenal fatigue can lead
to a lack of libido and erectile dysfunction, besides a lack of energy. Lack of energy can be
counteracted by increased sympathetic nervous system activity, which can increase one's stress
and anxiety.
2. A total cholesterol below 140 could be considered low. I don't advocate treatment excessively
low cholesterol since neurologic and endocrine system problems may result. The brain, for
example, has a very high choleterol content. Reducing cholesterol excessively may impair brain
function. Reproductive and adrenal cortex hormones are made from cholesterol - these would be
impaired in production by too low a cholesterol.
3. Weight loss from Metformin occurs when it impairs the absorption of carbohydrates from the
intestines. This is essentially a forced diet - which is not very pleasant for many people, given
diarrhea as a resulting problem.
4. Weight loss is difficult if metabolism is slow. The two systems that control metabolism are the
the thyroids and the adrenals. It is useful to assess both when contemplating weight loss. It is
difficult with hypothyroidism and adrenal fatigue to lose weight. The signals to essentially burn fat
are lost.
5. Androgel is very expensive. 10 grams a day runs about $450/month. If cost is an issue,
Testosterone cypionate or enanthate injections are much less expensive. Compounded higher
strength testosterone gels or creams are also less expensive.
6. When blood sugar is barely reduced with Metformin or other oral diabetes medication, diet, and
exercise, then multiple factors are in play to cause insulin resistance - including low thyroid
hormone activity, low testosterone, low DHEA (which occurs with adrenal fatigue), etc. It is useful
to examine these other factors. Addressing them may better help reduce blood sugar. Remember
that Metformin and other oral diabetes medications are essentially bandages to the underlying
problems which may be be causing insulin resistance, which still remain unaddressed, just as
antihypertensive medications are bandages, not direct treatments to the actual causes of
hypertension.
7. A blood sugar over 175 is toxic to pancreatic beta cells - which produce insulin. Prolonged
blood sugars over 175 can essentially convert a type-2 diabetic to a type-1 insulin-dependent
diabetic.
8. A testosterone level less than 300 ng/dl at age 45 may be difficult to optimize on Metformin
alone since multiple factors reducing the testosterone may be in play, including age-related
reductions in testosterone production, hypothyroidism, etc.
9. Optimizing thyroid hormone function can reduce insulin resistance and improve testosterone
production.
10. Testosterone optimization can improve libido and erectile dysfunction. An important
component of sexual function is having enough energy. For this, having optimum thyroid hormone
activity and adrenal function is highly important. Too often, many patients on TRT still have
sexual dysfunction despite having high testosterone levels. The answer is that there are other
problems besides testosterone that need to be searched for and addressed.
11. Excessively high testosterone levels may result in insulin resistance - the opposite of what is
desired, unless all the other hormones are also optimized. For example, high testosterone levels
can lead to high DHT levels, which then promotes an increase in abdominal fat, which then
increases the risk not only of high estrogen production but also functional hypothyroidism (from
increased thyroid binding globulin) and insulin resistance.
12. Cialis does not work when there is no drive or energy for sex. Drive in men is increased by
testosterone increasing dopamine levels in the brain. Energy is supplied by the thyroid glands
and adrenals. Other neurotransmitter/hormone/cytokine problems can also affect sex drive. For
example, high or low estradiol levels can cause a loss of sex drive.
13. Testosterone, from the data, does not cause prostate cancer. A theory about prostate cancer
is that prostate cancer cells start showing around the age of 25 y.o. in all men. The immune
system, however is strong enough, when young to kill the cells. As the immune system worsens
with age, it cannot keep up with the growth of cancer cells and prostate cancer develops.
Estrogen can promote prostate cancer when not balanced by testosterone. High testosterone
levels in young men may be protective from prostate cancer. The risk of prostate cancer can be
higher in men with low testosterone.
14. When prostate cancer exists, growth promoting hormones such as estrogens, testosterone,
growth hormone and insulin can accelerate the cancer's growth. It is important then to monitor for
prostate cancer then withdraw testosterone replacement when signs occur.
15. When a person is insulin resistant, the high insulin levels that result may be the greatest
factor in promoting prostate and other cancers.
16. Optimizing thyroid hormone activity is one way to promote reduction in the risk of cancer and
improve cardiovascular function - through its ability to reduce insulin resistance and reduce
inflammatory processes in the body and improving immune system function.
17. Inflammation is what promotes atherosclerotic changes in blood vessels. Medications such as
Lipitor, which reduce cholesterol, may have their most important effect by acting as antiinflammatory agents rather than by reducing cholesterol.
__________________
Adrenal fatigue
Quote:
Originally Posted by DAVID
great post- but can you explain when you mean adrenal fatigue and slow metabolism.
IF you take hydrocortisone for "adrenal fatigue" , do you known if your metabolism is
much higher ?
Please read the adrenal thread.
Some call the condition "adrenal fatigue" as "cortisol deficiency". It results in a lack of energy,
difficulty in utilizing fatty acids to create more glucose to use as an energy source for the brain,
muscle, and rest of the body.
It is more than a cortisol deficiency, however, since there usually results a deficiency in the
adrenal productions of other hormones such as aldosterone, DHEA, progesterone, testosterone
(and estrogen, particularly in women).
Cortisol is probably the most important hormone produced in the body. It is particularly important
in coping with stress. Without it, one may die in less than a day.
Re: What are symptoms of insulin resistance?
Quote:
Originally Posted by infoseeker
Marianco, my hat's off to you and I thank you very much for that thorough, detailed, and
very informative reply. I will read it again several times over and my husband will be
eager to read it, too. It does seem to jibe with the advice we've gotten from the dr.
treating him and another dr. acquaintance of ours (a cancer research dr.) Everyone has
had a slightly different take but basically come together on the same approach and
agreeing on the same principles.
I did ask his actual dr. today why thryoid was not checked and I'm waiting for a reply.
Thanks again, I'll read it again, much food for thought.
The tests for thyroid function are:
1. Free T3
2. Free T4
3. TSH
Of these, the Free T3 is the most important and the least often checked. It tells you how much
active thyroid hormone there is. If Free T3 is less than 310 (240-420), I would consider treating
the person for hypothyroidism.
If a person is showing signs and symptoms of hypothyroidism, I would consider treatment with
Armour Thyroid even if the tests were normal - since this can often occur. Signs and symptoms
are far more important indicators than labs when it comes to thyroid hormone treatment. Many
physicians, however, have forgotten how to examine a person for thyroid function - e.g. forgetting
the physical signs. They have come to rely on lab tests to make the decision.
Thyroid hormone is the most important hormone to consider optimizing. It affects every cell of the
body including the neurons in the brain. It improves every function. If I had only one hormone to
use, it would be thyroid hormone. As opposed to cortisol supplemention, thyroid hormone
replacement is an active treatment - directly changing and improving the function of every cell in
the body. With optimal thyroid function, the risks for heart disease, infection, mental illness,
diabetes, cancer, adrenal fatigue, hypertension, sexual dysfunction, inflammatory diseases, etc.
would be lower.
Re: What are symptoms of insulin resistance?
Quote:
Originally Posted by DAVID
I agree that thyroid treatment is great for very aspect of health but I disagree for armour
treatment only.
Let me explain : I known that T3 is the most important and Armour thyroid have T4 and
T3..
I known many people who take only armour have high T3 and low T4 depiste high dosage
of armour (up to 3 or 5 grains).
To get a good balance many hypothyroid people need to take with armour some synthetic
T4
I speak with the scientist Bauer by e-mail and he said that you need to have high T4 for a
good brain fonction. Serum levels of T4 are of paramount importance for the action of
thyroid hormones in the brain insofar as hardly any of the physiologically active
hormone T3 is taken up from the circulation, but derived from intracellular deiodination
of T4 (Crantz et al. 1982).
In fact the most important is : what do you feel and not blood test, for myself high
thyroxine work best.
Some people do respond better to T4 rather than a T4+T3 combination like Armour. So flexibility
is needed on part of the physician.
However, supplemental T3 is very active in the brain. There is a specific transporter protein for it
to allow absorption by brain cells. Augmentation with T3 for depression is much more effective
than augmentation with T4, arguing for T3's ability to reach and be absorbed by brain cells.
Moreover, more people respond better to the T4+T3 combinations, so it would be better to start
on Armour Thyroid than Synthroid/Levoxyl.
Usually Thyroid hormone levels in humans are about 90% T4, 10% T3. Armour Thyroid is 80%
T4, 20% T3. This disparity may cause problems with some people and an additional amount of
T4 may be needed to keep it in line with what the body makes.
There are people who cannot tolerate any T3 supplementation, however, because of anxiety or
other symptoms. T4 would be the best treatment when supplementation is indicated
Re: What are symptoms of insulin resistance?
Quote:
Originally Posted by infoseeker
I know just a little about thyroid (not all there is to know.) My daughter (only 3.5 years)
has trisomy 21 (and is doing quite well, good growth, phenomenal energy, remarkable
strength, she's bigger than 95% of her peers with t21 at the same age, rarely sits down,
she's so active,and hardly needs to sleep. Not hyperthyroid, that's not in question - she's
just healthy and active like kids should be - but we always watch for hypothyroid
developing.) You'd be shocked at the amount of inattention sometimes given, depending
on physician, of course, to wiped-out, ruined thryoids of people with t21, parents letting
their young kids' growth and development screech to a halt for one year or more while
the dr. says, "We'll recheck that TSH of 12 in one year, meanwhile, maybe she suddenly
can't get up off the floor to play and sleeps all day and has gained 7 lbs. just because of
her syndrome, that's the way all those Downs people are, constipated with dry skin, they
all sit around all day, their teeth hardly come in either and hair hardly grows, if they
don't gain a shoe size in two years, it's part of the syndrome, and don't you know they're
all exceedingly dull" - ahem.. Don't get me started. No constipation or dry skin here, and
she's energetic enough to scale the furniture and pour coffee in my musician husband's
best amplifier (no, no shock, don't worry.)
NOW, if you'll indulge me, I feel that it's always up to me to interpret her thyroid tests. I
was displeased by a recent rise in TSH. See if you have any comment for me. LIke I said,
clinical picture indicates anything but hypothyroidism. She is, however, only at the 25th
percentile for height (keep in mind her peers are at 3rd percentile, though, that is,
indeed, part and parcel of having an extra 21st chromosome, so she's doing better than
most) and on the syndrome-specific chart, she tracks at 95th percentile consistently (she's
ahead of 95% of girls her age with trisomy 21.) As I understand it, even in the face of
normal thyroid function, the short stature nearly universal with this chromosomal
condition is due to non-optimal reaction of cells to insulin-like growth factor, which is
not necessarily made better by growth hormone, which is appropriately supplemented in
some cases but not necessary or helpful in all. (I'm not even remotely considering it - that
was just an aside.) ANyway: (prior tests as good or better than first, with TSH around 1.6
or so)
At age 2 yr:
TSH 2.1 (range given is .46 - 8.1, but I have been told that's horsesh*t...?)
Thyroxine (T4) 6.7 (range given is 4.5-12)
t3 uptake 28% (range given is 24-36)
Free Thyroxine index 1.9 (range 1.2 - 4.9)
Triiodothyronine (T3) 158 (range 126 - 258)
At age 3 yr:
TSH 3.3 (all ranges given above are same for this test)
Thyroxine (T4) 7.8
T3 Uptake 29%
Free Thyroxine index 2.3
Triiodothyronine (T3) 194
To be honest, I'm lost. Could this be daily variation - and I assume children have
different values than adults, or could her thyroid be going "bad"? I'm sorry to veer offtopic, it's not "Men's Health," but if you have any comment, I'd love to hear it as I believe
the pediatrician, who is great in many respects, could be somewhat asleep at the wheel
here, so that I have to keep on top of this.
If TSH is all a person has to monitor thyroid hormone function, then a TSH > 3.0 is strongly
suspicious of being hypothyroid depending on the symptoms per endocrinologists. To me, a TSH
> 2.0 is strongly suspicious for hypothyroidism.
In populations where hypothyroidism is rare, the average TSH - i.e. - the norm for TSH may be
actually around 1.2
Still, it would be nice to see values for Free T3 and Free T4. Free T3 is not often done,
unfortunately. However, it is the most useful of the measures.
__________________
Re: What are symptoms of insulin resistance?
Quote:
Originally Posted by infoseeker
So do the two groups of results I posted not include either free T3 or free T4 (I don't
understand the lab's labeling of their tests.) Do the test results I posted look suspicious at
all? Like I said, the clinical picture looks fine, but it appears to me that all values could
be heading in the "wrong" direction.
The Free T3 and Free T4 are not among the lab tests.
A TSH of > 2.0 is highly suspicious for hypothyroidism.
Lack of thyroid hormone will impair growth and development. On the other hand, lack of thyroid
hormone can also cause excessive growth. Hypothyroidism can cause conditions at the
extremes. Many tall people may have hypothyroidism.
When a person has hypothyroidism, the brain make up for the loss of energy by increasing stress
signals that force the adrenal glands to work harder. A person with hypothyroidism can then look
like he or she has a lot of energy. Essentially, the sympathetic nervous system is more active in
such people in order to maintain energy level. This alternative generation of energy will work so
long as adrenal fatigue does not occur. Anxiety, tension, hypertension may be some symptoms of
an overactive sympathetic nervous system.
Since energy level, when the adrenal glands are functioning well, may not be a good indicator for
hypothyroidism, then using other physical signs may be useful. This includes dry cracked skin,
loss of eyebrow hair, thickening of the skin, puffiness of facial features, brittle fingernails,
generalized hair loss, low temperature, cold hands, etc.
Hypothyroidism can result in manic behavior from the compensatory overactivity of the
sympathetic nervous system - where energy level is excessive, there is reduced need for sleep,
and behavior is hyperactive or busy - the opposite of what is usually expected.
__________________
Re: What are symptoms of insulin resistance?
Quote:
Originally Posted by DAVID
[.
Great post - I known some hyperkinic people who have hypothyroidie but when you give
some thyroid tab like 1/4 of armour, this people lose weight ,feel tense and more
nervous.A ny suggestion for this people who have high sympathic nervous system ?
I see also many people wiht "loss of eyebrow hair" but the eyebrow hair never come back
with thyroid therapy T4 alone or T4 +T3 or T4+T3+ hydrocortisone.... May be this
people have thyroid resistance !!!
When patients cannot tolerate T3 because of anxiety, then using T4 can be useful.
Giving a serotonergic medication can also be useful to reduce sympathetic nervous system
activity. There are other options besides this if the serotonin route is not enough - such as using
GABA-ergic medications, Clonidine, and other psychotropic medications.
If low in testosterone, increasing testosterone can also help reduce anxiety - though not in some
people if testosterone replacement reduces thyroid hormone activity or excessive estrogen is
formed, testosterone limits adrenal function too much, or if other imbalances occur.
Progesterone may also help reduce anxiety through multiple mechanisms of action, though
excessive doses may risk side effects.
__________________
Re: What are symptoms of insulin resistance?
Quote:
Originally Posted by infoseeker
Obviously the test results I posted are not the most useful ones that could have been done.
But I was looking for input - and I don't expect anyone here to specialize in pediatrics but I thought I got the idea somewhere that values like TSH have a wider range of what
would not be considered alarming in young, growing children (excluding newborns, of
course - that's a whole 'nother story not worth going into for me, anyway.)
I was wondering if the values other than the TSH looked suspicious or normal enough, or
if possibly no one here can tell, if maybe the tests performed are useless enough that
there's not enough data. For example, I've heard that the TSH really should never be
looked at in isolation, because the T4 and other values are important to consider. But I
don't even understand what the T3 uptake even means or represents, nor any other of the
values I posted. Can anyone make a comment on whether they look decent or
problematic?
Observations as to hair, nails, temperature: All very normal. Great hair and nail growth,
no dryness of skin or nails, body weight neither fat nor skinny although tending toward
strong appetite and tendency to gain (only if given foods that encourage excessive weight
gain, though), warm body temperature including hands.
More important than lab tests are the physical signs and symptoms a person has.
If the signs and symptoms are not present, then perhaps a person does not have hypothyroidism.
If signs and symptoms are present, then perhaps a person has hypothyroidism, irrespective of the
lab test results.
__________________
Re: What are symptoms of insulin resistance?
Quote:
Originally Posted by DAVID
Marianco - You are a VERY VERY GOOD PHYSICIAN" better than all the anti-aging
physician than I known. Your ability to look the interaction about endocrinology,
psychiatry, metabolism is the correct way to understand people...
Thank you so much for your advises, it's very useful for my understanding
You are a psychiatre, do you take for anti-aging purpose or cognition , brain medication
and supplement like deprenyl, dilantin, omega 3...
If you don't answer it's not a problem- I respect your choice...
Best regards
Actually I am only scratching the surface of what is possible.
I am combining sociology, psychology, psychiatry, neurology, endocrinology, immunology,
nutrition science, sports medicine, general medicine into an integrated system for understanding
how the mind works, how the person works in their environment, and to develop more effective
treatments to improve functioning. For myself, the "mind" is the sum function of the nervous,
endocrine, and immune system. My focus is on behavior and mental health. Interestingly,
optimizing mental health happens to also optimize physical health. The mind and body are one.
As a psychiatrist, I am in a unique and advantageous position to realize this.
I respect the premier anti-aging physicians. They are at the forefront of understanding
endocrinology to a higher level than traditional endocrinologists.
I study anti-aging medicine. It is highly useful information for my purposes. One day, I may go for
"board certification" in anti-aging medicine. However, I am not an anti-aging physican so much as
an "aging-well" physician. My interest is not so much an escape from aging, but instead helping
others realize the highest expression of their individual spirits.
Certainly, one of my interests is in nootropic substances. However, optimizing endocrine function
and nutrition is one of the most potent and safe ways of improving intellectual functioning besides physical health - with clearer mechanisms of action than more artificial substances.
When artificial substances work, however, I am not dogmatic. Rather I maintain a flexible
position.
In regard to my own health, I practice what I preach.
Confidentiality is however necessary so I may more easily read the unconscious mind of others an allusion to the Freudian idea of the analyst as a blank wall.
__________________
Re: Marianco --depression ?????
Quote:
Originally Posted by taser
Marianco,
ever since i was 15 i have had bouts of depression but never knew what it actually was
until a few years ago.i was diagnosed with ADD about 5 years ago BUT STILL GET
BOUTS OF DEPRESSION. HOWEVER,IT USUALLY IS TRIGGERED BY
SOMETHING. FOR EXAMPLE,A NEGATIVE EXPERIENCE AT WORK,I AM IN THE
STOCK MARKET(LOSING SOME MONEY),will put me in a funk for 1-2 weeks.could
even be something small.like a negative experience at a social gathering.
when i was 15,i was hit in the head(temple) and suffered a concussion. was actually blind
for about an hour.had an mri a few years ago and everything is fine..could that head
injury have anything to do with it? when i feel depressed,i have the classic
symtoms,lonliness,sad,no energy,my muscles/joints hurt,wake up early,negative
attitude,talk slowly....i am married and am always around people but feel lonely,its very
strange.i ahve been to a doctor and he agree's that i have depression.. the fact that its
triggered by negative experience's(usually),is it still depression? thats the real
question..thank you Marianco...
An episode of depressed mood or loss of interest in activities which causes significant
dysfunction or distress is depression.
The real question is what is causing the depression - what are the factors which are contributing
to depression and what identified problems can be addressed in treatment.
To clearly answer the question would require a thorough evaluation taking into account the
functioning of the nervous system, endocrine system and possibly the immune system
Re: brain estrogen
Quote:
Originally Posted by DAVID
-------------------------------------------------------------------------------Some people feel exhausted after stress, ejaculation, to much exercise.
In fact some people have a low brain noradrenaline (genetic ?) or hormonal deficiency
(low thyroid or adrenal ).
Some tyrosine, B vit, help but not so much. When people take anti-aromatase, they feel
depress. Anti-aromatase increase MAOa, and lower noradrenaline and serotonine.
Brain estrogen is good for brain NA, but to much estrogen in the blood is bad for body
composition.
May be some people is this board have suggestion ?
I
It is important to have optimal activities of each endocrine hormone, neurotransmitter, and
immune system cytokine for optimal functioning.
When one has difficulty sorting out one's problems, then seeking help from others is useful.
When problems are complex and difficult to solve, then a physician who is familiar with anti-aging
protocols may be useful. Hopefully, one is nearby.
Brain estrogen, TRT, Hypothyroidism, Adrenal fatigue, etc.
Quote:
Originally Posted by DAVID
oestrogen is 54, is to much
testosterone is high normal
for adrenal fatigue = 30 mg each day
for thyroid = levothyrox 150 + 1 grain armour thyroid
to lower estrogen = arimidex, but exhausted the next day;
tyrosine, moclobemide, B vitamin have some help but so much. I think it's more difficicult
to increase the brain NA CONTENT than brain dopamine.
If you lower estrogen you increase MAOA very quickly and feel depress.
1. It is far easier to increase brain norepinephrine than it is to increase dopamine. Ritalin and
Amphetamine) increase norepinephrine and dopamine - often norepinephrine more than
dopamine. Wellbutrin (Bupropion) specifically increase norepinephrine. Strattera specifically
increases norepinrphine. Cymbalta increases norepinephrine and serotonin. Effexor increases
norepinephrine and serotonin. Stress increases norepinephrine. Caffeine increases
norepinephrine. Getting out of bed increases norepinephrine levels.
2. Increasing brain dopamine would give a person a sense of pleasure, reward, interest, intrinsic
motivation and drive that other neurotransmitters do not give. Other than with testosterone, there
is yet no clean way to increase brain dopamine levels without causing problems, i.e. there is no
happiness pill.
3. Estradiol and the other estrogens are MAOI inhibitors. MAOI inhibitors increase serotonin,
norepinephrine and dopamine - mostly in that order, which is one reason both low and high levels
pose problems. If estradiol is too low, for example, then depression may occur. For example, if
estradiol is too high - particularly if other factors such as thyroid hormone already raise serotonin
levels - then depression can worsen.
4. Estrogen and Thyroid hormone interact. When estradiol is too high, it competes with thyroid
hormone for thyroid hormone receptors, blocking the receptors. It also increase the production of
thyroid binding globulin, trapping thyroid hormone. This leads to a reduction in the effectiveness
of thyroid hormone, and fatigue.
5. Progesterone can counteract estrogen's effect on thyroid hormone. When a person has
adrenal fatigue, however, progesterone production is reduced - in favor of shifting production to
cortisol. Excessive progesterone can, on the other hand, can causes fatigue and sleepiness
because of its sedative properties on the brain.
6. Testosterone can stimulate thyroid hormone production. However, testosterone at too high a
level, independent of estrogen, can also reduce thyroid hormone production.
7. Testosterone helps protect the adrenal glands from fatigue by reducing ACTH production and
directly reducing adrenal activity. However, testosterone, particularly at too high a level, can
instead lead to worsening of adrenal fatigue.
8. 1 grain of Armour Thyroid (approximately 60 mg - but is actually 64.8 mg) is approximately
equivalent to 100 mcg of Levothyroxine.
9. Thyroid hormone increases brain serotonin production.
10. Excessive serotonin in the brain can lead to a reduction in dopamine production, resulting in
anxiety, depression, agitation, restlessness, insomnia - a condition of motor restlessness called
akathisia.
11. Without doing a lumbar puncture to get a cerebrospinal fluid sample from which one can
measure brain neurotransmitter content - at least indirectly - it is difficult to say that one has low
brain norepinephrine levels, or other neurotransmitter level.
12. Measuring urine neurotransmitter content can give us an idea of whole body neurotransmitter
content - which can roughly correlate with brain neurotransmitter content in many cases.
13. Increasing brain norepinephrine levels excessively can worsen adrenal fatigue. This is a
limitation of using stimulants and Wellbutrin. Stimulants and Wellbutrin will stop working once
adrenal fatigue is worsened. Increasing brain norepinephrine levels is useful since it increases
awakness, alertness, attention - but excessive amounts can cause anxiety, depression, and
adrenal fatigue.
14. High peak testosterone levels results in more aromatase conversion of testosterone to
estradiol. One solution when using depo-testosterone injections is to use smaller doses and more
frequent doses - such as twice a week doses rather than once a week doses.
15. In treating adrenal fatigue with cortisol/hydrocortisone at 30 mg a day, it is important to divide
the dose to prevent peak cortisol levels which may stop adrenal function.
16. Adrenal fatigue is one result of having had prolonged and excessively high levels of
norepinephrine in the brain.
17. Treatment of adrenal fatigue lowers brain norepinephrine levels. Cortisol feeds back to the
brain to reduce CRH. The reduction in CRH reduces norepinephrine production, essentially
calming the brain down, reducing stress.
18. Treatment with testosterone increases brain dopamine production. The higher dopamine
levels can reduce brain norepinephrine levels, thus reducing stress.
19. Treatment with thyroid hormone increases brain serotonin production. This can reduce
sympathetic nervous system activity and lower brain norepinephrine levels - thus reducing stress.
20. Treatment with serotonergic antidepressants reduce brain norepinephrine levels - thus
reducing stress. Serotonin is also necessary to produce thyroid hormone.
21. Mental illness such as depression makes hormone replacement therapy much more complex
since multiple neurotransmitters, hormones, and immune system cytokines are more intricately
involved - each has to be optimized to closer tolerances in order to achieve a sense of wellness.
Psychiatric medications may have to be used to help modify neurotransmitter levels to improve
functioning, particularly when the illness has a genetic basis affecting the brain itself rather than
just occurring from hormone imbalances.
22. Psychiatric medications have their own effects on hormones and cytokines. Knowledge of
how they work in these areas, outside of neurotransmitter control, is thus important to do fine
tuning of treatment.
23. Depression itself result in an increase in pro-inflammatory cytokine production.
24. Pro-inflammatory cytokines can reduce serotonin production, leading to depressive
symptoms.
25. Antidepressants and other psychiatric medications (such as some antipsychotics) reduce proinflammatory cytokine production as an effect independent of the neurotransmitter effects.
26. Estrogen can possibly increase pro-inflammatory cytokines, under certain circumstances.
27. Thyroid hormone and testosterone can generally reduce pro-inflammatory cytokine
production.
Given these highly interelated factors:
in a person with:
A. Testosterone deficiency - corrected with a depo-testosterone injection, but testosterone is high.
B. Adrenal fatigue - treated with cortisol 30 mg a day - hopefully in divided doses of 10 mg each,
or 15 mg in the morning, 10 mg at noon, and 5 mg dose later in the day.
C. Hypothyroidism - currently treated with the equivalent of 250 mcg of Levothyroxine a day - a
relatively high dose.
D. High estradiol level - which is causing side effects such as gynecomastia, perhaps depression
or anxiety - for which Arimidex blocks aromatase and reduces estradiol - but fatigue and
depression worsen.
E. Depression - which is partially treated through hormone replacement
Thoughts I have would be:
1. Why reduce estradiol with arimidex when estradiol can be reduced by reducing the dose of
depo-testosterone or by dividing the dose and giving more frequent injections - all to reduce high
testosterone levels which causes more conversion of testosterone to estradiol?
2. Reducing estradiol results in higher thyroid hormone activity. Higher thyroid hormone activity
can worsen adrenal fatigue (and depression and fatigue as a result), particularly when the
adrenal glands are not healthy enough to tolerate high thyroid hormone levels.
3. Should the testosterone dose be reduced given the conversion to estradiol and testosterone's
ability to worsen ongoing adrenal fatigue?
4. In a person with a complex problem, mental illness and high sensitivity to problems in
treatment, if I had to start treatment over, it would be in this order:
First treat adrenal fatigue. This would include a serotonergic medication to treat depression and
to reduce the perception of stress - thus protecting the adrenal glands from stress.
Second, after about a week of adrenal treatment, start treating hypothyroidism. Adjust thyroid
hormone until energy level is maximized. Give the adrenal glands time to improve - approximately
6 months. The additional thyroid hormone, itself, will help strengthen adrenal function. Do final
adjustments of thyroid hormone level. The person should have then normal or near normal
energy and a significant reduction in depression.
Third, start introducing testosterone treatment, while controlling estrogen if necessary. This would
then further improve mood and address sexual dysfunction. Sexual dysfunction itself may be
reduced once adrenal and thyroid function is optimized. The initial treatment of adrenal fatigue
and hypothyroidism sets the groundwork for testosterone treatment. It makes it easier also to use
lower doses of testosterone to achieve a sense of well-being, while minimizing side effects such
as from excessive estradiol levels.
Fourth, if depression is primarily a result of hormone imbalances, then an attempt to reduce the
serotonergic antidepressant may be considred. If depression involves brain dysfunction, then the
antidepressant treatment need to continue, though the dose might be reduced if possible without
recurrence of depression.
__________________
Re: Brain estrogen, TRT, Hypothyroidism, Adrenal fatigue, etc.
Quote:
Originally Posted by DAVID
[YES VERY GREAT POST )I take for HPA stabilisation 400 mg of phosphatydylserine. Some people take dilantin
What do you think about the book of Dreyfuss A remarkable medecine has been
overlooked ?
Phosphatidylserine (made from soy lecithin - not brain - to reduce the transmission of disease
such as mad cow disease) reduces adrenal gland activity.
When a person has adrenal fatigue, phosphatidylserine would worsen adrenal fatigue.
The adrenal glands provide energy on demand in response to stress. It is necessary to allow
them to work as well as they can so that a person can then respond to whatever stresses they
may face.
Thus far, the only reason to possibly take phosphatydylserine is in a condition where the adrenal
glands are enlarged and make too much cortisol. This, for example, can occur in a psychotic
depression.
The excess cortisol produced in such a depression is thought to cause the psychotic symptoms
(such as hallucinations and delusions). Medications (such as RU-486) which block glutocorticoid
receptors, which can then reduce the size of the adrenal glands and reduce cortisol production,
are useful to treat psychotic depressions. Of course, one cannot use such a medication forever
since the medication may cause adrenal fatigue.
Other than seizures and in a few exceptional cases to stabilize mood such as in a bipolar
disorder, I have not found any other use for Dilantin.
I am always interested in new ideas. What is Dreyfuss's full name and the title of the book?
__________________
Re: i am looking for low caloric diet forum
Quote:
Originally Posted by jann45
does low calories make lives longer? ar\tc? what do youy think?
Rats who were fed half of their usual calories lived about 50 to 100% longer than rats fed their
usual calories.
It is important to eat healthy foods and exercise. Unfortunately there are a lot of philosophies
regarding which foods and nutrients to eat.
Some anti-aging doctors promote a primitive diet as a more life-prolonging diet - where the foods
are easily digestible - what man may have eaten before the development of fire. This type of diet
avoids grains - which are indigestible unless cooked - unless the grains are sprouted - and are
thus a "living food". The diet encourages meats, healthy fats, etc.
One of the reasons caloric restriction can prolong life is that it reduces the production of insulin. In
many people, excessive insulin (as in insulin resistance and diabetes), promotes inflammation in
the body (leading to potentially fatal or disabling inflammation-related diseases such as heart
attacks, strokes, arthritis, infections, etc.), and promotes cancer.
__________________
Re: shut down - need advice
Quote:
Originally Posted by DFW Guy
i am 50 yo male in great health. a physian friend scripted Test Cyp for me after the
appropriate bloodwork. i was cycling 200mg every 15 days with good progress. i was
leaning nicely and had a great sex drive. recently he bumped me to 200mg a week for 8
weeks as i wanted to add about 10 pounds of mass. first two weeks were great but by the
end of the 3rd my sex drive crashed as well as my ability to get an erection. this is
obviously a problem. i thought that the additional Test would only further increase my
drive and the quality of my erections. need advice. thanks.
It's a fairly complex set of pathyways, but the bottom line is that more is not necessarily better.
You may get the opposite of what you expect, as other imbalances occur in the hormonal
cascade occurring from the supraphysiologic dose of testosterone. There may be imbalances, for
example, involving cortisol, thyroid hormones, growth hormone, estrogens, DHEA, dopamine,
serotonin, norepinephrine, among others. These all can individually affect sex drive and
erections.
Counter acting these imbalances to counteract a large imbalance of testosterone needs a
complex evaluation then treatment - where multiple hormones, medications, and nutritional
interventions may be needed in treatment.
For example, when watching a person such as Ron Coleman on stage, one is reminded that all
his hormones, neurotransmitters, and cytokines have been optimized to allow him to be in peak
shape. Not only does he have high androgen levels, but also no thyroid and adrenal problems,
among other things.
The question I would have would be: once testosterone levels are optimized in the physiologic
range, can one - like a young adult - gain 10 pounds fairly easily by hard work, good nutrition, and
rest?
Once on a steroid cycle - as one is on when going supraphysiologic - how much of the mass can
be kept once off the cycle? There has to be an excit strategy developed for that also.
Best wishes.
Saw Palmetto and TRT.
Quote:
Originally Posted by DFW Guy
seems saw palmetto is contraindicated with Test.
i stopped supplementing SP and i am back "online".
i am still planning to get bloodwork done mid-cycle.
thanks for the counsel. theis board is great.
Saw Palmetto is not necessarily contraindicated with Testosterone. It may be useful if TRT
promotes prostatic enlargement, for example.
Blocking the formation of Dihydrotestosterone (DHT) using Saw Palmetto or other 5-alphareductase inhibitor may in some men reduce sex drive and contribute to erectile dysfunction. It
does not cause this in the majority of men. However, some men are sensitive to their DHT levels
when it comes to sexual function
Re: Marianco- estrogen question
Quote:
Originally Posted by DAVID
Dear Marianco,
For sure to much estrogen is bad -many people have a good aromatisation in the central
nervous systeman brain. I think it's very good to have estrogen in the brain (more
serotonin and noradrenaline).
Estrogen is good too for memory in men and women too.
But too much estrogen is bad for prostate and body composition (more fat and water
retention), because estrogen increase angiotensin.
The problem with anti-aromatase is not so good for the brain. I like estrogen in my brain
but not for my body composition. May be an anti-aromatase that work only outside the
nervous system is more appropriate. But I don't find him.
In fact, many people like me when I take arimidex for decrease my high estradiol level(60
pg/ml ), feel depress very quickly. May be is a genetic factor or a low bordeline serotonin
and noradrenaline that push arimidex on depression.
Thank you for your advises about estrogen,brain and anti-aromatase.
Estrogen receptor gene expression in relation to neuropsychiatric disorders.Ostlund H,
Keller E, Hurd YL.
Department of Clinical Neuroscience, Psychiatry Section, Karolinska Institute,
Stockholm, Sweden.
Compelling evidence now exists for estrogen's involvement in the regulation of mood and
cognitive functions. Serum estrogen levels have been shown to play an important role in
the expression of psychiatric disorders such as depression and schizophrenia. We have
characterized the distribution of the estrogen receptors, ERalpha and ERbeta, in the
human brain and showed a preferential limbic-related expression pattern for these
transcripts. The ERalpha mRNA dominates in the amygdala and hypothalamus,
suggesting estrogen modulation of autonomic and neuroendocrine as well as emotional
functions. In contrast, the hippocampal formation, entorhinal cortex, and thalamus
appear to be ERbeta-dominant areas, suggesting a role for ERbeta in cognition, nonemotional memory, and motor functions. The role of estradiol can also be examined in
regard to its relationship to other neurotransmitter systems known to be linked to specific
psychiatric disorders. Estradiol has been shown to regulate the serotonin (5-HT) system,
which has been strongly implicated in affective disorders. We have studied a genetic
animal model of depression, and found altered 5-HT receptor mRNA levels in discrete
brain regions; many of the abnormalities are reversed by estradiol treatment, especially
for the 5-HT(2A) receptor subtype. The norepinephrine (NE) system is, similar to
serotonin, a target for antidepressant drugs, and projects to mesocorticolimbic structures
implicated in mood disorders. We have recently observed that NE neurons in the human
locus coeruleus (LC) express moderate levels of both ER transcripts. The possibility of
estrogen's regulating LC function has been documented in animal studies. Results from
our preliminary experiments have revealed that the ERbeta mRNA is decreased in
persons committing suicide, a cause of death that is highly linked to affective disorder.
Follow-up studies are currently under way with a much larger population to validate
these results. Overall, the discrete anatomical organization of the ER mRNAs in the
human brain provide evidence as to the specific neuronal populations in which the
actions of ERs could modulate mood and thus underlie the neuropathology of psychiatric
disorders such as depression.
The role of aromatization in testosterone supplementation
Effects on cognition in older men
M. M. Cherrier, PhD, A. M. Matsumoto, MD, J. K. Amory, MD, S. Ahmed, MD, W.
Bremner, MD, E. R. Peskind, MD, M. A. Raskind, MD, M. Johnson, BS and S. Craft, PhD
From the Department of Psychiatry and Behavioral Sciences (Drs. Cherrier, Peskind,
Raskind, and Craft, M. Johnson), Department of Medicine (Drs. Matsumoto, Amory, and
Bremner), and Division of Gerontology and Geriatric Medicine (Drs. Matsumoto and
Ahmed), University of Washington Medical School, Seattle; and Geriatric Research,
Education, and Clinical Center (Drs. Matsumoto, Peskind, Raskind, and Craft) and
Mental Illness Research, Education, and Clinical Center (Drs. Cherrier, Peskind, and
Raskind, M. Johnson), Veterans Administration Puget Sound Health Care System,
Seattle, WA.
Address correspondence and reprint requests to Dr. Monique M. Cherrier, S-116
MIRECC VAPSHCS, 1660 South Columbian Way, Seattle, WA 98108; e-mail:
[email protected]
Objective: To determine the contribution of conversion of testosterone (T) to estradiol on
cognitive processing in a population of healthy older men who received T
supplementation.
Methods: Sixty healthy, community-dwelling volunteers aged 50 to 90 years completed a
randomized, double-blind, placebo-controlled study. Participants were randomized to
receive weekly IM injections of 100 mg T enanthate plus daily oral placebo pill (T group,
n = 20), 100 mg testosterone enanthate plus 1 mg daily of anastrozole, an aromatase
inhibitor (oral pill), to block the conversion of T to estradiol (AT group, n = 19), or
saline injection and placebo pill (placebo group, n = 21) for 6 weeks. Cognitive
evaluations using a battery of neuropsychological tests were conducted at baseline, week
3 and week 6 of treatment, and after 6 weeks of washout.
Results: Circulating total T was increased from baseline an average of 238% in the T
and AT treatment groups. Estradiol increased an average of 81% in the T group and
decreased 50% in the AT group during treatment. Significant improvements in spatial
memory were evident in the AT and T treatment groups. However, only the group with
elevated estradiol levels (T group) demonstrated significant verbal memory improvement.
Conclusion: In healthy older men, improvement in verbal memory induced by
testosterone administration depends on aromatization of testosterone to estradiol,
whereas improvement in spatial memory occurs in the absence of increases in estradiol.
Estrogen has both good and bad properties.
It is important to have not too much but also not too little. There is a middle point for which
function is optimal.
One way to control estrogen without having to use an aromatase inhibitor is to use smaller and
more frequent doses of testosterone when injections are used.
For example, rather than a once a week injection, a twice a week injection with half the amount
each, will result in smaller peak blood levels of testosterone and less conversion in the body to
estrogens.
At the extreme is the use of implanted testosterone pellets, where testosterone is continuously
released in small amounts. In this case, estrogen is much less of a problem than with transdermal
and injected testosterone replacement.
__________________
Re: Marianco- estrogen question
Quote:
Originally Posted by DAVID
thank you- what do you think about DIM, Indole 3 carbinole , chrysin? May be to weak ?
I've reading in newsletter of life extension that 0.1 mg of arimidex (very low dose) is
effective for lower enough estrogen and anti-aging purpose. Do you agree with that ?
DIM and Indol-3-Carbinol are often used by some people to modify the metbolic pathways for
estrogens promoting the degradation of estrogens to the less anabolicly active estrogens - thus
reducing the risk of some cancers or negative effects of estrogens, while keeping the beneficial
effects - hopefully. It works for some people and may be useful to try.
I do not know if Chrysin actually works in clinical use - outside of its theoretical mechanism of
action. A question is - is it stable enough to work?
The dose of Arimidex depends on the person's circumstance. Some people are able use very
small doses. Some people need more. The usual psychiatric answer is "It depends
A testosterone over 500 ng/dl, lack of libido, depressed mood
Quote:
Originally Posted by Adub
Recently requested my doc for a T-level test. I'm a 37 y.o. in really good physical
condition. I just have no libido, depression and no results from a rigorous weight lifting
program and mountain bike racing.
Total 509 ref range 250 to 1100
percent free Test 0.83 ref range 1.0 to 3.1
free test 44.5 ref range 35-155
Do you think I can get a doc to help me?
What can I do on my own?
Thanks for your help
A testosterone over 500 ng/dl, low free testosterone, lack of libido, depressed mood indicates that
if there was a hormonal problem, it would be more likely due to suboptimal actitivity of hormones
other than testosterone. Common causes may be hypothyroidism and suboptimal adrenal
function. A clinical depression, itself, may be present. Low free testosterone indicates that
probably other hormones are influencing SHBG to reduce free testosterone.
I would think the large majority of physicians would not treat a total testosterone over 500 with
TRT. An anti-aging doctor may consider treatment with TRT since it follows from their philosophy
of optimizing hormone levels to the high side of normal. I would be hesistant to do so since 1) I
am not an anti-aging doctor though I am a member so I can gain access to their information for
my own education, 2) the depression and lack of libido are more likely due to other causes, which
should be evaluated first before considering TRT.
__________________
Re: Adrenal fatigue, hypothyroidism or something else?
Quote:
Originally Posted by CrashX
Hi!
I went to the doctor about a month and a half ago due to symptoms that have been getting
worse for the last few years. I can hardly get up in the morning, get going a bit, but
experience a huge crash in the afternoon, when I could just fall asleep in minutes. I also
experience general tiredness, have been putting on weight on roughly maintenance
calories, although this could be due to some bad food selections I´ve made. I am also
very weak, realative to my size, have dark circles under the eyes and erections, while not
bad, aren´t what they used to be. I have no motivation, bad concentration as thoughts
tend to wander off and don´t seem to want to do anything, not even the things I used to
enjoy. Social anxiety has also appeared, even though it never really was a big factor for
me before.
I got myself tested for TSH in the beginning of August and it came out at 3,338. Tested it
again on 9/11, along with T3 and T4 and the values came out as follows:
FT4 15,5 (12-22) pmol/l
FT3 5.0 (3,95-6,8)
S-TSH 2.3
This doesn´t look hypothyroid to me, so I´m suspecting adrenal fatigue, but as I live in
Europe, I´m not sure where to get a saliva test for it. My doctor is refusing the possibility
of AF as well as hypothyroidism and wants to put me on Prozac
.
Any thoughts on what could be going on? I´m 21, 230 lbs and over 20% body fat by now.
If a blood test is all one has, then labs for adrenal fatigue include:
Cortisol AM, Cortisol PM
DHEA-s
Progesterone
Sodium
Potassium
Fasting gllucose
Albumin
Total testosterone
In regard to hypothyroidism, some people have signs and symptoms of hypothyroidism even labs
are normal. One has to go by signs and symptoms in these cases to help decide on the course of
treatment.
__________________
Re: Low Free Testosterone
Quote:
Originally Posted by SteveJohn1965
I am 41 years old male and started having problem with libido and erection about two
years ago after quiting Paxil. I took Paxil for about 3 months for premature ejaculation,
1st month 10mg/day and then 5mg/day for another two months. I waited for side effect to
go away, but had extreme hangover and my sex drive went to zero. I stopped taking
Paxil, but my hangover and other side effect did not go away. That was two years ago.
Since then, I have seen many Drs and all sort of test, everything seems to be normal,
except the percentage of free testosterone. My Total T is about 600ng/dL and free T is
about 1.2ng/dL. The percentage is about 0.2%, the normal range is from 0.33% to
0.48%.
Many Drs felt my Testosterone were normal and did not put me on TRT. No one could
explain the role of Paxil. I was put on Antidepressant, Wellbutrin, for about 6 months
thinking this might be some sort of depression. Did not help with my ED.
Came of Wellbutrin, and after few months seeing a new Dr, he put me on Clomid. It
boosted my Total T to 980 and my free T to 2.3. I felt normal again and did not have to
use any medication for ED and my sex drive went back to normal.
After about two months, I felt loss of libido and problem with ED returned. I felt fatigue
and tired, and other symthom of low T. The blood test showed my Total T had gone up to
1120ng/dL, but my free T is back to 1.4. (percentage T less than 0.13% !!!). Somehow my
body is downregulating the amount of my free T.
Currently due to Clomid, my LH is high, 13.2. My SHBG is in normal range. Please
advise. Why my free T is falling. What other test I could do?
-SteveJohn
Premature ejaculation may occur when serotonin levels in the brain are not high enough to slow
down the sympathetic nervous system's triggering of orgasm.
Paxil may help to delay orgasm by increasing serotonin levels.
If excessive serotonin levels are present, sexual dysfunction with lack of libido and erectile
dysfunction occur. Factors include the high serotonin levels which cause subsequent lowered
dopamine levels in the brain.
Paxil is mostly out of the body by a week. Withdrawal effects generally last 2 weeks, sometimes
longer, but not two years. Other problems would be suspected.
Tests may be "normal" but that is up to interpretation. For example, most physicians order a TSH
and a Free T4 to determine thyroid function. But often these can be "normal" but a person suffers
from signs and symptoms of hypothyroidism. What most physicians do not order is the Free T3 which is a better indicator of thyroid hormone activity than the other two (those the Free T4 and
TSH are still valuable in the interpretation).
When a person has lack of energy, hypothyroidism and adrenal fatigue are the most important
conditions to evaluate for and treat. Insulin resistance is next. And low testosterone is fourth.
The neurotransmitters and hormones in the body have an extensive interaction - essentially a
three dimensional web of influences on each other. When one is changed, other changes in the
other chemical messengers occur in a cascade.
Testosterone is interesting in that it can both increase thyroid function and reduce thyroid
function, depending on the dose. It is possible for high doses to cause fatigue as a result.
Testosterone also can increase growth hormone production and slow adrenal function. Growth
hormone itself can slow adrenal function. These result in a loss of energy.
Thyroid hormone does numerous things. It increases brain serotonin production - thus having a
calming effect and possibly reducing premature ejaculation. It increases the number and size of
mitochondria in all cells of the body, thus increasing metabolism and improving the function of
every organ - including the adrenal glands. If adrenal fatigue is present, however, higher thyroid
hormone levels may worsen fatigue since thyroid hormone places a demand on adrenal function.
Thyroid hormone increases testicular steroid hormone production - increasing testosterone
production in the process. If there is one hormone that is most important premature ejactulation,
reduce depression, improve energy, and improve sexual function - it is thyroid hormone. Cortisol
(from the adrenals) and testosterone are second.
Wellbutrin increases norepinephrine levels to reduce depression. When used to treat erectile
dysfunction, it is important to use low doses. For this, regul****elease Wellbutrin works better - at
doses of around 37.5 to 75 mg a day. Higher doses risk causing adrenal fatigue - which would
then contribute to eretile dysfunction or sexual dysfunction, and loss of energy.
The body regulates free testosterone by the production of SHBG. Higher SHBG reduces free
testosterone. SHBG is reduced by testosterone and other androgens, insulin, and growth
hormone. SHBG is increased by estrogens, thyroid hormone, and progesterone. The balance of
these factors determines the total SHBG production. Testosterone can also be destroyed more
quickly if liver enzymes for it are stimulated in activity - such as in some drugs which induce
certain liver enzymes.
Free testosterone, however, is not that great an indicator of testosterone's function. One can
have normal or high free testosterone and still have multiple problems associated with low
testosterone levels and other hormone imbalances.
Total testosterone is better to gauge testosterone's level. If it is too low or too high, problems can
occur. If it is at a good level, then other hormone or neurotransmitter imbalances may be present
to cause the problems.
__________________
Free Testosterone as a measure
Quote:
Originally Posted by 1cc
If one was to measure Total testosterone only, then how would one know if a person's T is
too high or too low. Some people will have higher Free T with a lower Total T, or vice
versa. In the case of having a higher Free T with a lower Total T, increasing Total T
beyond that point may increase Free T too much, and/or increase E2 too much. It seems
that Free T is the gauge which indicates whether more or less supplementation is
required. What are your thoughts on this?
Free Testosterone will be determined by how much albumin is present to bind to testosterone
(weakly bound testosterone), and how much SHBG is present to bind to testosterone (strongly
bound testosterone). Albumin production is fairly stable and difficult to change without severe
illness present. The albumin concentration is primarily determined by hydration - with dehydration
increasing its level. SHBG is modified by multiple hormones: increased by thyroid, estrogens,
progesterone; lowered by testosterone, DHT, DHEA, growth hormone, insulin; and is modified up
or down by some medications, etc.
Is Free Testosterone a good measure of testosterone activity to determine whether nor not to
adjust the testosterone dose? Not really.
First, Free Testosterone not a reliable test.
Secondly, and more importantly, it is also determined by multiple factors. It is more a measure of
the sum of these factors than of testosterone activity itself.
For example, if there is too much estrogen, free testosterone can be lower since SHBG will be
higher. If there is too little thyroid hormone, free testosterone can be higher. If there is insulin
resistance (i.e. too much insulin), free testosterone will be higher. And so on. Thus, what is being
measured by free testosterone? Certainly much more than testosterone activity itself. Therefore,
it is difficult to say determine what needs to be adjusted to optimize function if free testosterone is
used as the primary measure.
If anything, high or low free testosterone indicates there is a good chance that other hormonal
imbalances (besides testosterone) are also occurring which need to be assessed and addressed
- e.g. hypothyroidism, insulin resistance, high estradiol levels, etc.
Testosterone activity is determined by the sum of free testosterone's activity, weakly bound
testosterone's activity (which has partial activity), and SHBG- bound testosterone activity
(testosterone has signaling activity to SHBG receptors when bound to SHBG). Thus, Total
testosterone comes closest to describing testosterone activity for clinical decision-making
purposes for testosterone dosing.
One can also add DHT's activity (as some practitioners do) but one has to be careful since DHT
can counteract testosterone's activity when DHT is too high.
How can one decide that the testosterone dose is too high or too low?
Using total testosterone, the TRT decisions become very simple:
1. The goal of TRT is getting the average total testosterone to at least 650 ng/dl (midrange on a
reference scale from 300-1000 ng/dl).
2. If any problems remain, then it is due to other neurotransmitter/hormone/cytokine imbalances
or excessive testosterone dose (i.e. supraphysiologic total testosterone).
These two constitute a rule of thumb - determined by the individual patient's circumstance - some
patients need a lower, some patients need a higher dose of testosterone. However, no matter
what the dose, realize that other imbalances in the body's information processing system (i.e. the
sum of the nervous system, endocrine system, and immune system activities) may be present
and need to be addressed.
Whether the total testosterone level over time is flat (as with pellets and usually alcohol-based
gels) or with peaks or valleys (e.g. with testosterone injections, oil-based creams) is determined
by the route of administration and the person's half-life for testosterone (and the ester if injections
are used). Whether a flat or peak/valley testosterone time-curve is preferred depends on what a
person best responds to.
Given how large an overlap there is between the symptoms of testosterone deficiency, thyroid
hormone deficiency, cortisol deficiency, insulin resistance/diabetes, etc., it is important to look at
the other hormones for a solution if total testosterone is at a good level.
How much estradiol (E2) is made depends a lot on how high total testosterone becomes and how
much aromatase activity is present.
HCG use increases the production of aromatase - increasing estradiol production.
High testosterone doses (such as injections given once every two weeks), results in long-lasting
supraphysiologic levels of estradiol. A solution in this case is to use smaller and more frequent
doses of testosterone (such as by going to a twice a week injection - rather than larger once a
week or once every two week injections). The lower peak testosterone levels resulting from more
frequent injections reduces the exposure to aromatase, resulting in smaller estradiol levels. At the
extreme, testosterone pellets usually have the least problems with estradiol. Of course, using
Arimidex can also reduce estradiol.
Re: Free Testosterone as a measure
Quote:
Originally Posted by Normandy
Marianco, any idea what's the mechanism of action of HCG increasing aromatase
production? Im not talking about increased aromatization due to increase T from HCG,
but I get the sense that HCG itself stimulates aromatase activity somehow. -- Normandy
Luteinizing Hormone (LH) stimulates the production of aromatase.
HCG works by acting like LH.
Re: Free Testosterone as a measure
Quote:
Originally Posted by 1cc
Would it be better to use Bioavailable Testosterone, since this is calculated taking
Albumin and SHBG into account, or does it also serve no purpose?
Bioavailable Testosterone (Free plus Albumin bound testosterone) is useful to obtain to help
interpret what is happening.
Free testosterone is useful to obtain (particularly if it is accurate) to help interpret what is
happening.
They do have a purpose - in interpretation of what balances or imbalances of other factors are
occurring.
When it comes to the determining the dose of testosterone, I still think total testosterone is the
single best and simplest measure.
For example,
Suppose a person has a total testosterone of 800 ng/dl. This is a level at the high end of the
reference range (300-1000 ng/dl), and is high even for young adult men. Suppose this person has
the symptoms associated with hypogonadism - low libido, lack of energy, concentration and
memory problems, anxiety or depression, etc.
Should this person receive testosterone supplementation?
I would say clearly "no". The total testosterone is already good. Most probably other factors are
contributing to the symptoms.
I would look for other neurotransmitter/hormone/cytokine imbalances that are causing his
problem. These are far more likely to be the problem than having a low testosterone level. The
common suspects would be hypothyroidism, suboptimal adrenal function, and depressive/anxiety
conditions. These and other problems that can cause similar symptoms to hypogonadism
Re: Update on Using Isocort.
Quote:
Originally Posted by pmgamer18
Just got back from the Dr.'s and my testis are great it looks like doing the Isocort has
made a big difference in my labs across the board. The only thing that stayed the same
was my low cortisol levels still between 9 to 10 doing a morning test.
My Dr. said he wants me to hold off taking anymore Armour he said my Thyroid test
came up from the last ones. I have only been the max dose of isocort for 12 days and the
blood test was 3 weeks ago so he feels things could be even better. Three office visits ago
he did not believe in Adrenal Fatigue now he is up on all of it this is what I like about
him. You show him something and if it is good like the book Adrenal Fatigue I showed
him. He will dig into this and come around.
I am shocked my Total and Free T levels only came down to what they were before
starting Isocort. Yet I am doing a lot less T. I have cut my dose from 64 mgs down to 41
mgs every 3 days. And my Total T came down from 1359 to 909 range 262 to 1598 ng/dl.
Free T came down from 33.5 to 25.7 range 8.8 to 27 pg/ml.
DHEA-SO4 is up from 302 to 492 range 80 to 560 ug/dl
Progesterone is 0.457 down from 0.73 range 0.27 to 0.90 ng/ml.
Pregnenolone is 21 was <20 range <20 to 150 ng/ml
IGF-1 is way up from 125 to 210 range 75 to 228 ng/ml.
Glucose fasting is up 107 from 65 range 65 to 140 mg/dl.
Thyroid Microsomal 10.2 range <35 Iu/ml.
Thyroglobulin <20 range <40 Iu/mL.
Alkaline Phosphatase is low 23 test was redone range 40 to 150 Iu/L not sure what this
means.
So I am to stop the 45 mgs of Armour and stay on the Isocort and keep my T and HCG
dose the same. In 60 days I go back in for testing.
DHEA will increase IGF-1.
This is why I would treat adrenal fatigue first - which increases DHEA production - before I would
consider growth hormone replacement therapy since the low IGF-1 level may instead represent
adrenal fatigue reather than growth hormone deficiency.
Hydrocortisone at sub-replacement doses (i.e. less than or equal to 20 mg oral hydrocortisone a
day in most people - some people need less) generally (with exceptions) has no side effects
when given multiple times a day, other than the effects increased stomach acidity, nausea,
diarrhea - while it is not yet absorbed. Some people need less than 20 mg a day.
Treatment of adrenal fatigue is a passive treatment. It takes time and the treatment to allow the
adrenals to rest and recuperate from stress.
When adrenal fatigue is successfully addressed - and low blood sugars come back to a normal
range - often insulin resistance/diabetes becomes uncovered. Insulin resistance/diabetes tends to
increase fasting blood sugars. I would suspect insulin resistance if the blood sugar is greater than
about 102.
Adequate thyroid hormone is necessary to allow HCG to increase testosterone production
maximally. Thyroid hormone stimulates testicular steroid hormone production - including
testosterone.
When a person becomes hypopituitary as a result of a head injury, the question I would have is
does the person have panhypopituitarism - i.e. have multiple hormone deficiencies - such as low
ACTH leading to low adrenal function, low TSH leading to hypothyrodism, low LH leading to
hypogonadism, etc. In this case, multiple hormone replacement therapy is needed.
DHEA helps reduce insulin resistance.
SHBG usually is low if there is insulin resistance. Low SHBG may result in high Free
Testosterone.
Free Testosterone is a tricky test to for making clinical decisions. Generally, the tests for free
testosterone are not reliable. Free Testosterone can also be normal even with hypogonadal total
testosterone. At this time, I prefer using total testosterone as the indicator for determining the
adequacy of testosterone replacement.
With thyroid hormone replacement, it is important to base the dose on the clinical response as
opposed to only lab testing. Improvement in hypothyroid symptoms, while avoiding the condition
of hyperthyroidism is the goal. Symptoms of hyperthyroidism are numerous including tachycardia,
anxiety, atrial fibrillation, sweating, insomnia, frequent bowel movements, etc.). There are people
who can tolerate only small amounts of thyroid hormone without going into hyperthyroidism.
Since some of the symptoms of hyperthyroidism are potentially lethal, care in treatment is
necessary. It is important to keep in consultation with one's physician.
__________________
Re: Update on Using Isocort.
Quote:
Originally Posted by Matt Muscle
Marianco, thankyou for the post.
In your experience, if sub replacement dosages of hydrocortisone are used to treat
Adrenal Fatigue, (thus giving the adrenal glands some time to recover), once this therapy
is withdrawn, (gradually of course) is there any chance that the glands will become
dependant on the external cortisol, or is this usually only the case when full replacement
dosages are used, which would cause the adrenals to shut down?
Generally, a sub-replacement dose results in the actual cortisol levels being the same with or
without the external cortisol. This means that when therapy is withdrawn once the adrenals are
fully functional, there is no withdrawal. The adrenals will have the full capacity to make the
amount of cortisol the brain wants at a moment's notice.
Generally, when full replacement doses (or higher) are used (this means a "medicinal" dose), the
adrenals shut down because the brain stops making ACTH to signal the adrenals to work. It can
be very difficult to restart the adrenals when such a dose is used for a long time. In some people,
it may take two years to get then restarted, if not longer. This makes the person dependent on
external cortisol or its equivalents (e.g. Prednisone).
Hypothyroidism and Adrenal Fatigue.
Quote:
Originally Posted by pmgamer18
This is why my Dr. will not let me use HC at any dose he feels the risk is to high. And he
said there is no way this can happen taking isocort. I don' t undrestand why my thyroid
went up on the Isocort. But even Dr. John looked at my Thyroid test the one before
Isocort and said this.
Quote:
Originally Posted by pmgamer18
I am not on Thyroid meds. yet people on the boards say I should be. Why is Free T4 so
low mine is this low.
TSH 2.929 range 0.4-4.7 uIU/mL
T4 Free 0.91 range 0.71-2.23 ng/dL
T3 Free 2.32 range 1/5-3.5 pg/mL
My morning Temp is before getting out of bed is 96.7 some say this is low Thyroid.
Phil
Your T4 is low normal, but it looks as though you are converting T4 to T3 well. Still, this
says nothing about the levels which are right for YOU.
I find the following useful as a starting point:
If a person HAS symptoms and signs of hypothyroidism,
then the following lab values confirm hypothyroidism:
1. TSH > 2.0 mIU/mL
2. Free T3 < 3.0 pg/mL
Free T3 is the more important value since TSH is the brain's opinion of how much thyroid
hormone there is. Unfortunately the brain is often wrong (e.g. with aging, with brain injuries, etc.,
the brain's ability to monitor thyroid hormone can go astray).
T4 has a secondary role in confirming hypothyroidism. It does have thyroid hormone activity itself.
But T3 is so much more potent in activity than T4, and is the hormone measured by the brain,
that it plays a larger role in thyroid function. Also, some people have difficulty in converting T4 to
T3, making it misleading to rely on the Free T4 alone.
If the Free T3 < 2.7 and adrenal fatigue is present, I would try to begin treatment with Armour
Thyroid at low doses (15 mg a day) a few days after starting adrenal fatigue treatment, backing
off only if it is intolerable (e.g. worsening of adrenal fatigue).
If the Free T3 > 2.7, then there is more freedom to either treat adrenal fatigue first or treat both
hypothyroidism and adrenal fatigue simultaneously - depending on the person's history and level
of health.
More fragile health or mentally ill patients have a difficult time tolerating any thyroid treatment until
the adrenals are strong enough, even with significant hypothyroidism (e.g. Free T3 < 2.0). Fairly
emotionally healthy patients can often tolerate starting both treatments simultaneously.
The key to the tolerability of thyroid hormone replacement when adrenal fatigue is present is the
person's level of mental health. The more severe the mental health symptoms - e.g. anxiety - the
less tolerated is thyroid hormone until the adrenals achieve a certain level of health.
It is a balancing act when both hypothyroidism and adrenal fatigue are present.
Unfortunately, hypothyroidism itself will impair recovery from adrenal fatigue when severe
enough.
Thyroid hormone controls how many mitochondria and the size of the mitochondria
the adrenal gland cells have - essentially controlling the ultimate health of the adrenals and their
ability to produce hormones.
This is why if the Free T3 is too low, it is important to at least try to add thyroid treatment
as soon as one can to accelerate the process of recovery - even if it is in small gradual changes
over time.
IsoCort contains hydrocortisone. It has the same risks as taking pharmaceutical grade
hydrocortisone. Hydrocortisone is less expensive and is often covered by health insurance.
IsoCort is useful when the patient prefers something "natural" or if it is useful to have the patient
be more independent of the physician. It is a significant out-of-pocket expense, however for most
people. Hydrocortisone is more likely to increase stomach acidity than IsoCort - thus should be
taken with food to avoid nausea, diarrhea or increased appetite as side effects.
The physician primarily has to monitor for symptoms and signs of excessive doses of
hydrocortisone to avoid adrenal shut down. These include:
1. manic symptoms - e.g. racing thoughts, excessive energy
2. worsening insomnia
3. weight gain
4. lower than baseline cortisol levels during treatment.
5. etc.
Each person does have a different point at which the hydrocortisone dose becomes
a replacement or medicinal dose. The rule of thumb of 20 mg a day total is a good
starting point. But there are people where the dose is lower. With experience and thought,
this is fairly easy to determine.
Re: Hypothyroidism and Adrenal Fatigue.
Quote:
Originally Posted by pmgamer18
When I first posted this thread I only had copys of my hormone tests Total and Free T
with E2. All I had was what my Dr. told me about the rest of the tests. He told me my
Thyroid went up on using the Isocort and my IGF-1 went way up. My wife picked up
more copys on her way home from work and when I looked at the copys all I could do
was shake my head. When I told him I had been taking 45 mgs of Armour just to see how
I felt he was not upset but told me my levels had come up and to stop taking it. I showed
him the Interview with John Dommisse, MD he read very little of it and told me again not
to do any more armour. I told him I feel better on it and he then to me doing the armour
will change my T levels and I will have to go back up on my T meds. I knew when he said
this that there was nothing I could say that would get him to let me do Armour.
Yesterday I stopped the 45 mgs. of Armour and felt ok until I went to bed I was up all
night could not sleep. This morning I had a lot fatigue and want to call my Dr. and tell
him so and that I am taking the armour anyway for the next 60 days to see how I feel and
if my levels change and I need more T meds I will stop using it. Well his office is not open
so I am going to take it now I am sick of feeling like this. I did so good last yr. and I feel
the longer I am laid up like this the worst it's gettting I am back up on the weight I lost
last yr. some 65lbs and this is killing me. I need my engery back so I can get some
exercise. I can't believe getting sick last winter with Bronchitius messed me up this bad.
And I still feel like I have it every morning I am coughing up chuncks of brown stuff that
gets stuck in my chest and makes me wheeze and it's hard to breathe I have one hell of a
time getting it up. Once I do then my breathing is better.
I don't have any more 90 mgs. of Armour to cut in half I do have some 120 mgs I think
this is 2 grains I am going to cut these in half and take them until I talk to my Dr.
monday.
Just to much out the that I have read says I would feel better on armour and I do.
Thanks for the Post Dr, marianco.
The lab values I wrote to confirm hypothyroidism are just a starting point. One has to still put a lot
of thought into what is going on.
When it comes to hypothyroidism, the most important information to make the diagnosis comes
from the history and exam of the patient - the presence of signs and symptoms of hypothyroidism.
Examining patients for the signs and symptoms of hypothyroidism seems to be a lost art as most
physicians rely excessively on the lab tests.
Many patients have frank signs and symptoms of hypothyroidism even with normal lab findings. A
trial of Armour Thyroid would be helpful. If the signs and symptoms go away, then the diagnosis
is confirmed.
Having frequent colds, infections, illness, is a symptom of hypothyroidism.
Treatment of adrenal fatigue can increase DHEA production. DHEA will then increase IGF-1.
Evaluation and treatment of adrenal fatigue should be done before considering growth hormone
treatment because the low IGF-1 used to justify growth hormone deficiency may instead reflect
low DHEA levels due to adrenal fatigue. This would save a lot of money as well as unnecessary
injections.
Re: Hypothyroidism and Adrenal Fatigue.
Quote:
Originally Posted by Legenden1999
Is the saliva test for free T3 precise enough, or should it be a blood test?
How about the saliva test for E2 and Testosterone?
Thanks,
JH
I think currently that other than DHEA and Cortisol, the best alternative tests for hormones are the
24-hour urine tests. Saliva tests can be used but there is more variability in the results.
With any test, however, it is very important to take them in optimal conditions to insure accuracy.
For blood tests:
- The stomach needs to be empty
- Dehydration (which raises blood levels) should be avoided by drinking 1/2 to 2/3 liter of water
(not ice cold or excessively warm) before the test
- Exercise or physical stress needs to be avoided before the lab test
- The person should be calm and not in stress (as reasonably feasible), since this raises or lowers
blood levels of hormones.
For 24-hour Urine tests:
- Avoid exercise or physical stress for two days before the testing
- Eat as normal but avoid restaurant and infrequently eaten foods
- Avoid taking medications if possible when obtaining a baseline
- The sample needs to be refrigerated
- Avoid excessive salt or too low a salt intake from normal
- Moderate fluid intake - avoiding diuretic drinks such as caffeinated beverages
__________________
Evaluating Growth Hormone
Quote:
Originally Posted by pmgamer18
Yes Marianco your a God Send to this group. I just remembered my Dr. is in today kids
started school so he is open till noon so I called and now I am waiting for his call back. I
did up my Dose of DHEA but the test that was done on the test befoer this one was IGF-1
and it was low normal 125. The test that my Dr. did on the last one is IGF-2 and IGF-3
so how does he know my IGF-1 went up or am I out of line here. And the IGF-3 was low
2.8 range 3.0 - 6.6 mg/l. The IFG-2 was 699 no range for my age 62 the range for age 51
to 60 is 414 - 1248 ng/ml. I have no Idea what this means. From what I have been
reading I don't want to do HGH if I don't have to.
Growth Hormone works primarily by raising liver production of IGF-1
IGF-1 is the actual hormone that does most of the work of Growth Hormone.
IGF-1 is the surrogate people use as an indirect measure Growth Hormone. It is the standard.
I think it is a mistake since IGF-1 is influenced by other factors including DHEA, testosterone, etc.
To determine if there is a Growth Hormone deficiency, the following tests should be done:
1. IGF-1
2. IGF-BP-3 - this is the major binding protein for growth hormone. A high level indicates low
availability of IGF-1. The ratio of IGF-1 to IGF-BP-3 gives one an idea of how much IGF-1 is
active.
3. Growth Hormone Plasma Level after Stimulation by GHRH (growth hormone releasing
hormone) and Arginine.
4. Growth Hormone in 24-Hour Urine - which is good for detecting overt deficiences and
excesses - though not mild deficiences.
I would not base growth hormone treatment solely on the IGF-1 level. One the lab tests are
obtained, it is also important to determine if there are symptoms not corrected by the other
hormones, which may be attributed to growth hormone deficiency - such as thinning lips,
looseness of the skin, etc. - which can serve as a target symptoms and signs to be followed for
improvement during the course of treatment. It is important to be able to measure and show
health improvement when being treated.
In any case, I think it is best to consider Growth Hormone replacement only after optimizing all
the other hormones because of growth hormones interactions with the other hormones and the
need to reevaluate the other hormones' statuses after initiating growth hormone treatment. For
example, when growth hormone treatment is started, patients often develop fatigue, depression,
anxiety, irritability or other symptoms of adrenal fatigue because growth hormone can reduce
adrenal output by up to 30 percent - which is significant. Growth Hormone treatment ends up
being complex because it can have good and bad interactions with the other hormones. And it is
important to keep in mind that it is IGF-1, not growth hormone, that does the heavy lifting for
growth hormone.
__________________
LH, FSH, Primary and Secondary Hypogonadism
Quote:
Originally Posted by pmgamer18
My first test my total t was 120 LH was 3.33 and FSH was 4.95 but at the time I was on
SSRI Anti-depressent meds. This could be why they said I was Primary. Have you tested
DHEA, Cortisol, IGF-1, Fasting Glucose and Free T3 and T4. I feel this was a big clue
to my being Hypopituitary because going back through the yrs. of test I have always been
low normal. Yet Free T3 and T4 were not tested. It is a dam shame Dr.'s don't know how
to read tests they just look and see your in the normal range and tell you they are good.
Hell my Dr. dose this maybe someone needs to make a PC program to flag problems on
tests at the lab and put on the test this shows there could be a problem with the Pituitary
or what every is wrong like adrenal problems to force Dr. to take a better look.
Results with ranges:
Total Testosterone 120 (300-1000 ng/dl)
LH 3.33 (1.5-9.3 IU/L)
FSH 4.95 (1.6-8.0 IU/L)
When a person has primary hypogonadism, I would expect the brain to be generating a high level
of LH and FSH to try to make the testes produce testosterone. The LH and FSH should be close
to the top of their reference range, while testosterone is low.
When a person has secondary hypogonadism, the pituitary is unable to generate enough LH and
FSH, resulting in low testosterone levels. The LH and FSH would be at the low end of the range.
It is possible to have both primary and secondary hypogonadism. The aging pituitary gland or
injured pituitary gland may not be able to make enough LH and FSH. The aging testes may not
be able to make enough testosterone in response to LH. In this case, a person may have low
testosterone and low or midrange values for LH and FSH.
__________________
Re: Update on Using Isocort.
Quote:
Originally Posted by pmgamer18
marianco thanks again I picked up my Armour yesterday and my Dr. gave me 15mgs. to
take once a day. I told him I had been taking so my wife had left over that was 1 grain 60
mgs. he told me this is to strong to start with. I know this maybe putting you on the spot
but what dose do you start with. I can't see doing this low a dose for 7 weeks then test to
see if I need more. I just feel to dam good to lower it.
We have lowed my T shots to .20 mls = 40mgs every 3 days down from 64 mgs. and
upped my HCG to 500 IU's the 2 days in between my T shots. My test before last was way
to high it looks like adding Isocort 4 pills in the morning and 2 at noon and dinner has
help my body to not us up so much of my T meds. Yet my test came back not going down
all that much. My total T went down from 1359 to 909 range for a young man 262 to
1593 ng/dl.
And my Free T went down form 33.5 to 25.7 range for a young man 8.8 to 27 pg/ml. So I
feel my testis are working dam good. Doing this with out HCG my levels are 550 total.
When my levels were higher I needed to take .5 mgs. of Arimidex everyday now I am only
taking
.25mgs every 3 days and still feel I am going to low. I am thinking of stoppeing the
arimidex and going back on the Indolplex/DIM this worked real good when my dose of T
was lower. I could take a half a tablet and stay at about 20 to 25 on my E2 test.
The dose range for Armour thyroid varies between 15 mg to 300 mg a day - generally in two
divided doses since T3 may last only 8 hours.
If a person has heart problems, then the usual top dose is 120 mg a day. There is a risk of atrial
fibrillation from high T3 levels when a person has heart problems such as having had a heart
attack. It is possible to go higher but one needs a lot of thinking and deliberation about the risks
involved and whether or not it is worth it. T3 does have some anti-arrhythmic property - reducing
the risk for ventricular tacchycardia - a frequently fatal irregular heart beat.
One can gauge the dosing by how much faster the heart beats compared to baseline. If the
resting heart beats more than 10 beats more per minute compared to baseline, than the increase
in dose may be too high and too fast. If the resting heartbeat goes past 100 beats per minute,
then the dose may be too high. If there is significant anxiety or if the heart rate is fast because
blood pressure is low, etc., then using the pulse as a gauge in treatment may be more difficult
and other signs and symptoms may be then used to measure response to treatment.
Ramping up too fast can exacerbate adrenal fatigue - which risks worsening the person's overall
condition. Then it is important to pull back on the dose, allowing time for the body to get use to a
dosage level (say about 2-4 weeks), before trying again to increase the dose.
Most people tolerate starting at 30 mg of Armour Thyroid a day (about 1/2 a grain). If in good
health otherwise, many tolerate starting at 60 mg a day. If the person is fragile in health or has
significant adrenal fatigue, then I may start at 15 mg a day. Then I may ramp up in dose by 15 mg
or 30 mg every 2 weeks as tolerated (i.e. so long as significant symptoms of hyperthyroidism do
not show up), to an initial plateau of 60 mg before getting lab tests, then if needed, gradually
increasing the dose every 2 weeks to 120 mg a day. If signs of excessive dose shows up, I have
the patient reduce the dose. If the person is fragile in health, a slower ramp up may be needed. If
reasonably safe and needed, ramping up to higher doses is done at a more gradual pace - e.g.
changes occurring once a month.
I try to be flexible about it, giving the patient some leeway to decide what is a tolerable and
effective dose for him or herself, while keeping in mind the boundaries of safety. I usually give
instructions and a flexible dose to allow this.
Patients can monitor their blood pressure and pulse to help determine the dosing of thyroid
hormone. Blood pressure may be reduced if hypothyroidism has contributed to hyperthyroidism.
Blood pressure may be low if adrenal fatigue is worsened. The pulse helps determine if a
hyperthyroid state is present.
It is more important to pay attention to the signs and symptoms of hypothyroidism (and of
hyperthyroidism if the dose is too high)during the dose adjustments than the lab tests. This is
particularly true when a person has hypothyroid signs and symptoms and has normal baseline
thyroid levels (e.g. mitochondrial disease).
The signs and symptoms of hypothyroidism - such as dry skin, lack of energy, cold intolerance,
etc. - should go away as an appropriate dose is reached.
Interactions with other neurotransmitters and hormones need to be attended to. For example,
thyroid hormone increases serotonin production. If the patient is on an SSRI, then signs of
excessive serotonin levels (such as restlessness or agitation) may occur. The SSRI may need to
be then reduced. If the patient loses weight, then thyroid levels may be reduced. The dose of
Armour Thyroid may then need to be increased. Should adrenal fatigue show up, then it should
be treated simultaneously with thyroid hormone treatment.
__________________
Re: Update on Using Isocort.
Quote:
Originally Posted by Naturdoc
I don't know how accurate the blood pressure and pupil reflex test are because everyone
I have tested is positive for adrenal fatigue. Someone should be normal.
pmgamer - where did you get Jeffries book, it is very expensive ($165) used
Adrenal fatigue is very, very common.
It is a stress-related condition. Modern society is very stressful.
I think almost everyone I met in New York City has it. This may be why many are so irritable and
rude.
It is so common, a physician I know, who is a known world expert on hormone replacement
therapy, often dismisses treating it, saying everyone has it. He, essentially, has made the mistake
that labs have made, of letting an illness state become the new normal state. Even many top antiaging doctors make the same mistake.
Orthostatic hypotension is a common sign of adrenal fatigue.
The pupil test is more difficult to do because just the shaking of one's hands can cause variation
in the light levels from a flashlight, resulting in changes in pupil size. There is no such thing as a
hand that does not shake (as camera makers can attest). Ideally, a holder for the light can be
used instead. Or to be more obsessive, an optometrists' slit-lamp stand. As it is, I would gauge
pupillary constriction by large changes as opposed to small changes which may occur with hand
shaking.
When adrenal fatigue is present, the sympathetic nervous system is activated to try and generate
energy. This may compensate for the pupillary reflex, making it more difficult to see.
It seems Jeffries book is out of print. Some people are trying to make a bundle selling it for high
price used. Hopefully Jeffries or the publisher can print more copies. However, Jeffries is getting
up there in age. I'd say, get the book while you can.
__________________
Hypothyroidism, Low Testosterone
Quote:
Originally Posted by fenstermaker
I am a 38 year old male that is post Graves. The treatment I received for Graves was
iodine radiation which in turn zapped my Thyroid completely. Currently on 175mcg of
synthroid. I have never felt "normal" since. That was about 6 years ago. I put on about
45 pounds and have never been able to lose the weight.
I insisted my Dr check more of my levels than my T3, T4 to see why I feel like crap all the
time.
My results came back a follows:
fsh=2.8 in range
LH=4.6 in range
IGF-II=1107 in range
GH= 1.7 in range
Test Total = 196 Low
Test Free %= 2.32
Test Free = 45
After this test result in the beginning of Aug 2006, My Dr put me on Androgel. 2.5 grams
daily.
That is when I started my research and found this site. Since my readings, I thought the
amount he started me on was very low for a guy my age and size. 38 6'3" 245lbs.
Included in my reading from you guys, you insisted that I make my Dr check my levels
again in approx four weeks.....I had to make my Dr agree to this and he did new results
are as follows:
Alkaline phosphatase 62
AST 15
ALT 17
Bilirubin total 0.9
Bilirubin Direct 0.2
Protein, Total 7.1
Albumin 4.5
Estrogens Total 96
Test, Total 176
Test % free 2.30
Test, free 40.5
DHT 36
So I recieved a note from my Dr with the test results to increase the Androgel to 5 grams
daily and run new tests in 3 months.
I am not thrilled by the new test numbers but I have you talk about the possibility of Test
dropping in the first stages. I am not convinced my Dr is completely ready for this
challenge that I am facing and he has not suggested that I seek another Dr.
So if anyone can give some input on the relationship of Post Graves to the low test
situation I am facing, or if there is no relationship between the two. Also if anyone can
suggest a good Doc in the Columbus, Ohio area.
Thanks for sharing you thoughts and time to post, for it has helped me get ready for this
TRT journey that I was not aware even existed. The personal situations that you all talk
about help relate for us new guys in this problem.
fenstermaker
Good thyroid hormone actilvity is necessary for testicular steroid hormone production - e.g.
testosterone production.
Low thyroid hormone activity often results in insulin resistance.
Insulin resistance is another factor that reduces testosterone production. It interferes with LH
production and may also directly reduce testicular testosterone production.
The bests tests for available thyroid hormone activity are:
Free T3, Free T4, and TSH.
The free T3 is the most important of the three since it measures the most active thyroid hormone.
T3 is about 4 to 10 times more active than T4. It is what the brain measures to determine how
much TSH to release.
Synthroid (T4) is not as effective in treating hypothyroidism as a combination of T4 and T3 such
as Armour Thyroid. In studies comparing T4 versus T4+T3, patients strongly preferred T4+T3
even if there were no difference in the lab levels. They simply felt better. Armour Thyroid is safer
to use versus the available T4+T3 combinations since the thyroid hormone in Armour Thyroid is
bound to thyroid binding globulin, and is then slowly released into the body when it is absorbed.
Thus Armour Thyroid is a long-acting version of thyroid hormone. This is in contrast to the other
T4+T3 combinations or T3 (Cytomel) itself. The problem is the sudden rise in T3 from these has a
higher risk of causing problems including cardiac arrhythmias. It is technically more difficult and
requires closer physician monitoring to use other T4+T3 combinations and T3 in treating
hypothyroidism.
A good starting point is that a person may often show signs and symptoms of hypothyroidism
when the free T3 is less than 310 pg/dL.
More important than blood levels of thyroid hormone is whether or not there are still signs and
symptoms of hypothyroidism with treatment. There are a large number of people with normal
thyroid hormone levels (normal free T3, free T4, TSH), yet who still have signs and symptoms of
hypothyroidism. These people have thyroid hormone resistance and need extra thyroid hormone
treatment.
When it comes to LH and FSH, the question is not whether or not the values are in range, but
whether or not the appropriate amount of testosterone is being made in response to the LH level.
This helps determine if one has a problem with the pituitary's production of LH (secondary
hypogonadism) or if the problem lies in testicular production (primary hypogonadism) or if there is
both primary and secondary hypogonadism.
Since there are multiple factors which can affect testosterone production both from the
hypothalamus-pituitary and testicular ends - such as other hormone imbalances - the LH and
FSH may not so much be useful except to determine if a pituitary tumor is present or if HCG can
be used as TRT (as with secondary hypogonadism).
Total testosterone is the best test for clinical purposes. The tests for free testosterone are not
uniformly accurate enough. Free testosterone can also be normal yet a person has all the signs
and symptoms of hypogonadism.
A good target for total testosterone during TRT is at least 650 ng/dl, measured at the midway
point between injections or at least four hours after applying transdermal testosterone, or any
time if pellets are implanted.
Its better to measure estradiol than total estrogens to get an idea of the total estrogen activity.
Estradiol level is in essence the total estrogen level but with greater weight placed on estradiol
itself and less weight placed on the other estrogens (which are much weaker than estradiol).
During testosterone replacement, the total testosterone is determined by how much testosterone
the testes make plus how much external testosterone is absorbed. There is a point where the
external testosterone dose is high enough to shut down testicular testosterone production but not
enough to make up the difference. In this case, the total testosterone actually is lower with TRT
than without. The solution is to increase the external testosterone dose to a point where it is high
enough to increase total testosterone rather than reduce it.
When it comes to Androgel, a dose of 5 grams of gel causes a substantial percentage of men to
worsen in hypogonadism (i.e. lower total testosterone). Many men do respond well and have
really good levels - e.g. 750 ng/dl and above. But to reduce the risk of worsening testosterone
levels, starting at 10 grams then lowering the dose if total testosterone, DHT, estradiol levels go
too high or of side effects occur, may be preferrable.
When a person has had hypothyroidism for a long time, absorption of transdermal testosterone
may be difficult. This is because there is a build-up of mucin (a glue-like substance) in the skin of
people with hypothyroidism, which causes the skin to become thick. This is called myxedema. It
can be subtle, not obvious to most physicians, who are not use to pinching the skin of their
patients to gauge the thickness of the skin. Myxedema impairs absorption of transdermal
testosterone - impairing treatment with transdermal testosterone.
When myxedema is present, it is better to go to testosterone injections for TRT
Re: Post Graves - Low Test - Need help
Quote:
Originally Posted by JanSz
I have a little theory here and would like confirmation from somebody who have a real
know how.
--------------------It would help if you had your Testosterone levels pre-radiation treatment, if not I assume
you testis were in good working order and you had a decent T level, then. In August 2006
you started correcting your T level using insufficient amount of Androgel, with mixed
success, so far. Per my theory, you should have started working on getting your thyroid
T's (T1,T2,T3, T4) plus adrenals, in order as first phase of treatment. And as a second
phase, work on correcting your testosterone. There is a good chance that all you are
really need is a Thyroid hormones lined up correctly, they also regulate Testosterone
production.
------------------As to immediate problem of shrinking testis, HCG is the way to go. Shrinking testis is not
only cosmetic problem, whatever else they produce, other than Testosterone, have an
effect on libido, ED and over-all feel of well being.
-----------------Good luck finding the right doctor.
Since you a fighting this battle for the last 6 years, one trip to Monterey, California, USA
to see Dr Marianco does not seem out of line, (how to contact him?? does anybody
know). I thing follow up can be made via phone or e-mail.
Good luck, bro, and keep us posted on your progress.
JanSz
Jan, you make great points.
In a person with hypothyroidism due to treatment of Graves Disease, the first order of business is
optimization of thyroid hormone activity.
If adrenal fatigue is simultaneously present, then it should be treated just before treatment with
thyroid hormone because adrenal fatigue makes it more difficult to tolerate additional thyroid
hormone. Treatment of adrenal fatigue can be started simultaneously or a few days before thyroid
hormone treatment is started.
Next, if still present, would be treatment of hypogonadism/testosterone deficiency.
It is possible to do all three at once and do fine tuning as time goes on. The follow up
appointments don't have to be so far apart. Transdermal testosterone reaches the plateau level
within 3 days. It can be adjusted in 1-2 weeks. Armour Thyroid can be adjusted every 2-6 weeks,
depending on a person's health - slower for more fragile persons. If injected testosterone is used,
then the plateau dose (steady state) is reached faster the more frequent the injections.
HCG is an option in treating hypogonadism. Shrinking testes indicates they still respond to LH,
which is reduced with testosterone replacement. The dose varies from 1000 to 5000 IU a week in
divided doses. Over time, as one ages, the testes may not respond well to LH, and one may need
to go to testosterone replacement. If the dose of HCG is too high, there is a risk of causing
resistance to HCG, ending the usefulness of HCG.
Testosterone replacement can be combined with very low dose HCG (e.g. 500 IU a week in
divided doses) to keep the functioning of the testes (this is Dr. John Crisler's/SWALE's protocol).
For contact info, send me a PM.
Re: when to get labs done
Quote:
Originally Posted by Musclehead21
I have been on androgel for 2 and 1/2 years. I am going to get my test and free test taken
in about a week. I was wondering when is the best time to get that done? The doctor told
me 2 hours after I apply the gel. Last time I had labs done I got them done 20 hours after
I applied the transdermal gel and my total testosterone was 224 ng which is 200ng lower
than where I started. What do you all think? I think me and the gel are done!
The best time to get labs when using an alcohol-based gel is just before applying the gel. This
gives you the lowest amount of testosterone, which can then be used to make decisions.
On average, the lab can be done at least after 4 hours of application of the testosterone gel. On
average, that is. It depends on the absorption and that particular person's half-life for
testosterone.
The problem with transdermal testosterone is that it has to be applied to the widest area of skin
possible to get the best absorption and to get the most consistent blood levels. If it is not spread
to a wide area, then the fat under the skin can get oversaturated with testosterone, causing the
testosterone to be absorbed directly into the blood stream. This causes the levels to not be
consistent - causing a larger peak and quick drop off of testosterone levels.
If a person is a good absorber of testosterone, a 5 gram pack of Androgel can get their levels up
to 750 ng/dl. But many people do not absorb it well and can instead get lower testosterone levels
than when they started.
A 10 gram pack of Androgel gives more consistently higher testosterone levels than the 5 gram
pack.
If the 10 gram pack is not well absorbed, one possible cause is thickened skin due to
hypothyroidism - called Myxedema. This may be suble particularly if the person is not obese. One
patient, for example, on a testosterone gel, dropped his total testosterone from 840 ng/dl to about
500 ng/dl once his thyroid hormone levels dropped. Low thyroid hormone may also cause insulin
resistance. Low thyroid hormone and insulin resistance (high insulin levels) both reduce SHBG.
This can reduce the half-life of testosterone and its subsequent blood levels.
Note that symptoms of hypothyroidism and adrenal fatigue can be the same as symptoms of low
testosterone. Hypothyroidism and adrenal fatigue may be each more common than
hypogonadism. Hypothyroidism can be genetic or environmentally induced. Adrenal fatigue is
most commonly induced by stress - of which there is a lot in modern society. When thyroid
function and adrenal function are optimal, sex drive can be maintained even at low levels of
testosterone (e.g. 250-300 ng/dl).
__________________
Fordyce spots on the penis
Quote:
Originally Posted by jann45
laser is good?maybe the tooth paste?please help
http://www.dermatlas.org/derm/IndexD...geID=569564079
i have much more then on the picture
Fordyce spots are essentially enlarged oil glands (sebaceous glands) on the skin. These have a
yellowish or white appearance. They can occur on the lips, the penis, the inside of the cheeks, or
the labia (in women). They are harmless, are not infectious and are not a sexually transmitted
disease. They are a cosmetic problem.
When on the lips, electrodessication or vaporization via laser treatment has been successful to
improve appearance.
Whether to resort to this treatment on the penis is a question for which I have no answer. The
person who has this problem has to discuss this with their physician or dermatologist. The skin of
the penis is fairly thin. I suppose the risk includes scarring, burns, disfigurement, nerve damage,
etc.
Dhea
Quote:
Originally Posted by dano79
At my last dr. apointment. My DHEA levels were tested, and they came back a little
below the test range. So my DHEA levels are below normal. My Dr. was not concerned.
Should I be? I'm 26.
Quote:
Originally Posted by pmgamer18
Yes I feel you should be a lot of Dr.'s don't care about low or below levels because they
can't give you a script for it. Most that have low DHEA need to test there Cortisol and
Thyroid. Do the cortisol test early in the morning and get Free T3 and Free T4 tested. I
take this for low DHEA and my wife just found out hers is low and her Dr. gave her the
same DHEA that I take so it must be good. I take one in the morning and one at noon
now my levels are 492.
Usually, I think if a doctor is not concerned about DHEA, it is because he/she does not know.
In the absence of other health problems or stress, DHEA is a marker for how old a person is
since DHEA levels go downhill over time.
In a young adult, low DHEA levels makes me suspicious for adrenal fatigue.
Low thyroid can also indirectly reduce DHEA by reducing adrenal hormone production, but not to
the extent that adrenal fatigue can reduce DHEA. Early on, the brain compensates for low thyroid
by increasing adrenal output - usually at the expense of feeling anxious, stressed, irritable.
Women generally cannot tolerate DHEA supplementation at high doses because it causes hair
loss or acne. Weight gain, fatigue, and oversedation are also possible side effects in women - the
opposite of what usually may occur. The female dose range is thus limited to about 5 mg - 12.5
mg a day.
__________________
Re: Serotonin deficiency and LH--Testosterone
Quote:
Originally Posted by chip douglas
I've been wondering why serotoninergics like for instance 5-HTP helps me libido wise. I
keep reding that serotonin has a negative impact on sex drive, but on the other hand 5HTP helps restoring a healthy sex drive in me. Now what automatically comes to mind is
depression--since 5-HTP helps with mood, it helps depression and depresssion is known
to adversely affect sex drive.
Since both my LH and FSH are low, and my prolactin high normal, I'm investigating the
possibility that serotonin may increase LH, which should increase T. My last Total T
reading was : 406 ng/dl at age 34--this lower than it should be--it should at least be midrange or in the upper end of the range.
Are you aware of anything that point to serotonin increasing testosterone levels in those
deficient in this last ? If so was the mechanism mentioned ?
Marc
Increasing serotonin production leads to a reduction in dopamine production. This leads to a
reduction in testosterone production. In most cases, the reduction would be mild since there are
other factors controlling testosterone production.
5-HTP - which is 5-hydroxytryptophan, a derivative of the amino acid, tryptophan - is converted
into serotonin (5-hydroxytryptamine) by the body. Almost all of this is used by the enteric nervous
system (the gastrointestinal nervous system) - and is thus wasted. But some goes into the brain
where it serves to increase serotonin levels.
Serotonin can inhibit sex drive and prevent orgasms.
But serotonin can in some people also increase sex drive.
Two common killers of sex drive are impaired thyroid function and impaired adrenal function hypothyroidism and adrenal fatigue.
Serotonin is necessary to produce thyroid hormone. Thyroid hormone increases serotonin
production.
Serotonin reduces the brain's perception of stress. This reduces norepinephrine and ACTH
production. This leads to a reduction of stress on the adrenal glands. This allows the adrenal
glands to recover from stress and recover in function - thus recovering from adrenal fatigue.
Anxiety and depression can also reduce sex drive. Increasing serotonin can help reduce anxiety
and depression, helping restore sex drive.
__________________
Re: New Lab Results...
Quote:
Originally Posted by DrmChld
TSH: 1.7 (Range .2-5.5)
Testosterone 398ng/dl (range 245 and up)
Lipids:
Total Cholesterone 142(no range given)
Triglycerides 57mg/dl (range <199)
HDL 59mg (range <40)
LDL 72mg (no range)
HGBA1c 5.5% (4.6-6)
Prolactin 10 (2-18)
Free T4 1.1 (0.8-1.7)
Sodium Serum 140 (133-145)
Since I moved the new Endo doesn't understand why I was put on Androderm 5mg a day
as my Testosterone levels were on the low end but still in the range. She says I am not
Secondary. She did said my gonads were smaller and softer than normal (said probably
due to athrophy, I told her that size was normal for me)
Since the Androderm 5mg daily I haven't felt any real increase in energy or feeling better
overall. Wife says my energy level has increased, but I believe that is just due to the extra
sleep I have been getting.
Whats the deal with these doctors?
I asked about an alternative on doing IM shots weekly with HCG. She said best would be
either 300mg every 2 weeks, or 400mg a month(1 shot) and that this is the normal
treatment. I showed her page 11 from the AllThingsMale PDF file. She basically said that
this was just Western/Alternative treatment. I also tried to discuss how the half-life of
Test-E/C was 7 days and a shot every 2 weeks/a month would just put me on a
rollercoaster of testosterone ranges and feelings. She said HCG was only needed if I was
trying to get my wife pregnant and had nothing to do with helping with my testes
producing Testosterone levels on their own.
I'd have to come into the hospitals shot clinic if I wanted to go the IM method. Doesn't
seem like they want to give it out for self-treatment.
I'm not sure whats up. Comment if you like. Just an update. I'm confused on what these
Endo's are taught and believe.
Thanks in advance for any input.
PS. short on time...no proof reading performed
The test data is too incomplete for clear assessment.
If on testosterone replacement therapy, the target for total testosterone is at least 650 ng/dl - per
the Endocrine Society guidelines. The dose needs to be increased if the level is lower than this.
When the problem is a lack of energy, the primary hormones to consider are the thyroid
hormones and adrenal hormones.
Some blood tests for the adrenal include: cortisol AM, cortisol PM, DHEA-s, progesterone,
sodium, potassium, aldosterone, fasting blood glucose, cortisol binding globulin, albumin,
chloride.
Some blood tests for thyroid include: Free T3, Free T4, TSH, thyroid binding globulin, and the
various antithyroid antibodies.
Testosterone can have a variable effect on energy. It can stimulate thyroid hormone production,
increasing energy. It may also reduce thyroid hormone production, reducing energy. It may
increase growth hormone production, which can then reduce adrenal hormone production, which
then reduces energy. It can cap adrenal hormone production, reducing one's ability to produce
energy. It can increase brain dopamine levels, leading to a reduction in serotonin, leading to a
reduction in thyroid hormone production, leading to a reduction in energy. It can counteract
estrogen's effects, leading to a reduction in thyroid binding globulin, leading to an increase in free
thyroid hormone, leading to an increase in energy. It can reduce abdominal fat, leading to a
reduction in estrogen and thyroid binding globulin, leading to an increase in thyroid hormone and
an increase in energy. High testosterone levels can increase estrogen production, leading
eventually to a decrease in energy. High testosterone levels can lead to high DHT, which can
then increase belly fat, which then eventually can lead to a decrease in energy. Depotestosterone injections reduce LH production, which then reduces the production of aromatase
enzyem, which then reduces the production of estradiol from testosterone, eventually leading to
an increase in energy. And so on. There are multiple pathways and hormone cascades by which
testosterone can either increase or decrease energy. Which one a person will experience
depends on the individual's response.
__________________
Re: New Lab Results...
Quote:
Originally Posted by DrmChld
Is this information available on a site that is affiliated with AACE and not one that is by a
"western" doctors, as my endo says. I told her I was interested in upping my Testosterone
levels to see if it would benefit me. She was not willing to try it, saying that anymore than
what I have now would just introduce a toxicity level.
I'd like to be able to be more closer to a mid to high range in my Testosterone levels.
Currently I have abnormally low LH and LSH levels also. I would have to check my
previous post regarding those other test results mentioned.
The Endocrine Society is the world's largest group of endocrinologists. It is a very conservative
group. It certainly is not engaged in alternative medicine. It publishes: The Journal of Clinical
Endocrinology and Metabolism, Endocrinology, Molecular Endocrinology, and Endocrine
Reviews. It was formed in 1916. The AACE is a smaller sister group of the Endocrine Society,
being formed in 1991, which does work with the Endocrine Society.
Their testosterone treatment guideline is downloadable at: http://www.endosociety.org/quickcon...line053006.pdf
__________________
Re: Lab Results, Help Please
Quote:
Originally Posted by austinsteviehend
Thanks for the input guys. Just for the record, i'm on NO test replacement therapy,
although I think my free test range seems to be very low for my age (21). I am on HGH
(human growth hormone) not HCG. Do you guys think Doc might prescribe HCG to try
to boost my free and total T levels a little bit. Basically I can't maintain an erection and
have hardly any energy. No random erections either. Just got tested for HIV and it came
up negative so thankfully not that. Sleeping like 10-12 hours daily and still tired.
Basically I noticed this overnite about 9-10 months back (right before Christmas) and I
don't know what else to do or try. ANY input or suggestions would be greatly appreciated
about what to do from this point.
Thanks,
Justin
Often a person on human growth hormone worsens in condition because the other hormones
were not first optimized then later adjusted after starting treatment with HGH. I think HGH is the
last hormone to be optimized after everything else is done to avoid problems given its interactions
with other hormones which can be good or bad.
Human growth hormone declines with age just as DHEA does. While DHEA has direct effects,
Human growth hormone works indirectly through IGF-1. IGF-1 is the active hormone. This is why
IGF-1 is what is measured. But IGF-1 is also controlled by other hormones including DHEA,
testosterone, thyroid hormone, etc. in addition to human growth hormone. This is why it is best to
optimize these other hormones first before considering HGH. It not only saves money and
additional injections, but it also avoids the problems that occur with HGH treatment.
When total testosterone is good, a person has lack of energy and has loss of libido or erectile
dysfunction, in the absence of mental or emotional problems, then frequently, the person has has
either suboptimal adrenal function or suboptimal thyroid function. I would look for corresponding
physical signs and other history then correlate it to the lab tests.
The thyroid and adrenal glands are far more important for health and functioning than growth
hormone in adults. Suboptimal thyroid function will determine, for example, when a person will
have their first heart attack or if they will survive congestive heart failure. Optimal thyroid function
can reduce the risk of heart attacks by up to 90 percent. This is far better than many other risk
factor.
Adrenal fatigue can come on suddenly. It occurs from an accumulation of mental and physical
stress. Once one's stress threshold is reached, fatigue, excessive sleep, lack of libido can occur
suddenly.
Thyroid hormone provides a constant level of energy. The adrenal glands provide energy on
demand. When energy level fluctuates, it is the adrenals that are most often involved.
__________________
Yes, you can test urine for levels of neurotransmitters.
A company called, Sanesco (sanesco.net), brought to the US FDA approved tests for the
neurotransmitters - serotonin, norepinephrine, dopamine, epinephrine, GABA, and glutamate. I
am evaluating their usefulness. A problem is in correlating the levels they givee to the patient's
clinical picture and ultimately the brain levels of the neurotransmitters. You, otherwise, cannot get
brain levels of neurotransmitters without a spinal tap. Even then, the level has to be determined
for each important localized and involved structure in the brain - not just whole brain levels - to be
clinically relevant. We shall see. The urine tests are fairly inexpensive.
You can do conventional tests for catecholamines such as dopamine, epinephrine,
norepinephrine, and the 5-HIAA metabolite of serotonin in urine and plasma. These are very
expensive - often needing a large volume of blood or a 24-hour urine catch - nothing to do on a
regular basis. They also do not work well for psychiatry since they are aimed primarily for other
illnesses such as neurotransmitter emitting cancers.
Besides, what is most important is the localization of neurotransmitter levels. For example, to
reduce psychotic symptoms, the newest antipsychotic medications increase dopamine levels in
the frontal lobes, while reducing dopamine levels in the limbic system part of the brain. A whole
brain measurement of dopamine may not be able to tell you a difference when the difference is
striking when localized.
__________________
Quote:
Originally Posted by TylerR
I was told that testing of neurotransmitters with urine wouldn't give an accurate picture
of how much each neurotransmitter is in the brain.
Is this something to be considered when testing neurotransmitters?
Whether or not urine neurotransmitter testing will correlate with brain levels of each
neurotransmitter is a good point. However, the only way to get brain levels is to do a spinal tap
repeatedly on a person - this is usually not an option.
Currently I would say that it is useful in some people to measure urine neurotransmitters. For
example, one finding I have is that often patients with attention deficit/hyperactivity disorder
(ADHD) have high levels of dopamine. This supports the theory that some people with ADHD
have either a dopamine-resistant condition or have a COMT enzyme that destroys dopamine 5
times faster than normal - leading to a relative dopamine deficient state despite the body
compensating by increasing dopamine production tremendously.
The ultimate utility of urine neurotransmitter testing remains to be seen. However for some
patients, it provides useful information on their mental illness. I would not use it all the time,
however.
__________________
Re: Testing for levels of neurotransmitters
Quote:
Originally Posted by MaFi0s0
Is it worth having a urine test for neurotransmitters before starting TRT?
I am turning 23, I have used recreational drugs in the past, I have anxiety and depression
etc, so was wondering how important it is for me to get this test?
How important it is to get neurotransmitter testing depends on what the physician is evaluating,
the affordability of testing, among other factors.
For the treatment of anxiety and depression, it is useful to get neurotransmitter testing in addition
to a comprehensive endocrine evaluation. This may help decide what treatment may be useful - if
the physician understands how to use the test.
I would not obtain a urine test for neurotransmitters if the physician involved in treatment does not
know how to interpret the test and determine treatment accordingly. That would be a waste.
__________________
Shbg!
The most common cause of low SHBG is excessive insulin - i.e. insulin resistance. Insulin
resistance in turn leads to a cascade of events which results other hormone imbalances such as
low testosterone production, suboptimal thyroid hormone activity, adrenal fatigue, etc.
Factors which together in a balance determine SHBG are:
1. Anabolic hormones generally reduce SHBG. These include testosterone, DHEA, insulin, DHT,
and growth hormone.
2. Thyroid hormone, Estrogens, and Progesterone (by increasing estrogen receptors/sensitivity),
increase SHBG.
In the absence of insulin resistance, the most common other cause of low SHBG is a very high
level of other anabolic hormones - most frequency high testosterone from TRT. Those who use
anabolic steroids at high doses often drive their SHBG to near zero.
When total testosterone is between 650 to 1000 ng/dl, and a person still has zero sex drive, I
would look for other causes for sexual dysfunction - e.g. other hormone, neurotransmitter, or
immune system problems.
Raising SHBG does not necessarily increase the risk for Alzheimer's disease. It is important to
keep in mind the factors which lead to the risk of Alzheimer's disease.
Insulin resistance (i.e. excessive insulin levels) causes low SHBG. It also greatly increases the
risk of Alzheimer's disease because it results in a higher level of inflammatory cytokine production
(Cytokines are the chemical messengers of the immune system). It is the inflammation which is
one of the underlying factors which leads to Alzheimer's disease.
SHBG level is most often a signal of the overall status of multiple hormone levels. The balance
may give an indication of whether one is in an pro-inflammatory state or anti-inflammatory state with inflammation leading to disease such as Alzheimer's disease, heart disease, strokes, cancer,
etc. Some hormones such as some estrogens and insulin can lead to inflammation leading to
illness. And other hormones such as the androgens (except DHT), growth hormone, and thyroid
hormone, can lead to an antiinflammatory state, reducing the risk for illness. The balance
determines the person's risk for illness.
What estradiol level is best for any individual often needs to be determined by trial and error. It is
unique for each individual. Most do best around 30 pg/ml. But some do best at lower and higher
levels. For example, I have a 65 y.o. patient with a total testosterone of 840 ng/dl and an estradiol
of 47 pg/ml. He's having the time of his life - able to make love numerous times each night - after
more than a decade of having no sex. The estradiol level works for him without side effects.
Some may do better with much loser levels of estradiol - the response is highly individualistic.
Even with low SHBG - which is difficult to correct since it depends on the balance of so many
hormones - when the other hormones and neurotransmitters are optimized, sex drive and the
ability to have an erection can often return.
When total testosterone is supraphysiologic - i.e. over 1000 ng/dl - problems with libido and
erections may occur. Testosterone increases dopamine in the brain in order to increase sex drive,
reduce depression, give pleasure to activities. The problem is that dopamine is a very fragile
neurotransmitter/hormone in its effects. Too high a dopamine level can cause tolerance to
dopamine. This is similar to how one can develop tolerance to drugs such as cocaine and
amphetamines which increase dopamine levels in the brain to cause their high. This can lead to
the loss of libido when high testosterone levels are maintained for long periods of time.
Conversely, when one is deprived of testosterone (and hence dopamine) for long periods of time
due to hypogonadism, one can get a high during the first few weeks of testosterone treatment
since the brain becomes supersensitive to dopamine when it has been deprived of it (e.g. making
more dopamine receptors to pick up the weaker dopamine signals). Unfortunately, as the brain
then gets use to the higher dopamine levels, it will develop some tolerance, and libido will drop off
- though we often wish that hopefully a good amount remains.
__________________
Growth Hormone and Fatigue
Growth hormone reduces adrenal activity. Some estimate this may be up to 30 percent. This
results in adrenal fatigue symptoms in susceptible persons. The lowered adrenal activity results in
an impaired stress response, which can show up as anxiety, irritability, anger problems, insomnia.
Growth hormone treatment necessitates also optimizing adrenal function.
It is also important to make sure thyroid function is optimal since thyroid hormone is necessary for
some of growth hormone's effects as well as in optimizaing adrenal function.
And it is important to reduce insulin resistance, since Growth hormone can increase insulin
resistance and worsen diabetes.
Growth hormone works primarily through increasing the hormone, IGF-1.
Since DHEA from the adrenals can also increase IGF-1, I think it is important and cheaper to first
optimize adrenal function (including the optimization of DHEA level) before starting growth
hormone treatment. IGF-1 levels may then in some cases return to normal - making it not
necessary to do growth hormone replacement.
It is also important to avoid alcohol use since even a glass of wine can negate any benefit from
the growth hormone injection that day.
One has to change one's diet to optimize the benefits from growth hormone replacement.
Growth hormone replacement is actually complex since growth hormone cannot often be given
alone without optimizing multiple other hormones and improving one's diet. Giving growth
hormone alone invites a lot of problems - such as adrenal fatigue, diabetes, etc. Growth hormone
would be the last hormone to optimize - after first optimizing the others - suche as insulin, the
adrenal hormones, thyroid, testosterone, estrogens, etc.
This is in contrast to thyroid hormone - where it can have a lot of benefit (unless a person has
significant adrenal fatigue - which then has to be addressed first) without having to adjust the
other hormones, since thyroid hormone optimization itself can possibly correct numerous other
hormone imbalances.
Re: TRT in men with low SHBG
TRT with Low SHBG is not simple to do because there are many other complicating factors such
as:
1. SHBG is reduced further by the increase in testosterone.
2. Insulin resistance. Low SHBG is one sign of insulin resistance/diabetes. Insulin resistance can
cause other hormone imbalances and impair nerve signal transmission.
3. Hypothyroidism. Low SHBG may be a sign of inadequate thyroid hormone levels.
Hypothyroidism is often present clinically though the lab tests are normal.
4. The duration action of testosterone is shortened by low SHBG - making one prone to a roller
coaster experiences.
5. Testosterone can reduce thyroid hormone activity - resulting in anxiety or depressive
symptoms depending on the severity of the reduction. There are multiple mechanisms of action
which can cause this.
6. Low SHBG may result in high free Testosterone. High Free testosterone is not necessarily
good. For example, if estradiol levels and progesterone levels are normal, the high free
testosterone may result in high blood pressure. Testosterone can either lower or raise blood
pressure depending on its relationship to the other hormones.
7. etc.
Testosterone functions depend on its relationship with other hormones, neurotransmitters, and
cytokines - these all are chemical messengers in the body. Low SHBG complicates matters but is
not an unsolvable problem in most people.
Re: what is the best time get blood test for testostorne levels?
Quote:
Originally Posted by the/rock
I am on 250mg enthante a week ..trt therapy.
On my second week so going for tests soon.
I was wanting to know when the best time to get
blood tests done for levels of test .I have looked on
the internet and what i have learnt is the test levels
peak at 24 to 48 hours after jab and are at there lowest
the day before next jab.I am going to ask the doctor if i can
test 48 hours after first test and on the morning of my jab.
(blood test are cheap in my counry).to get an adverage of
testostorne to see the difference and how much enthante
a week a will need to get me in a good range ,good energy
,increased libido,fat loss etc, with out side effects.I have a
great doctor!!
What do you think?
Obtaining a total testosterone Peak blood level and a Trough blood level is useful.
The Peak for Testosterone Enanthate is about 24-48 hours after the injection.
The Trough (lowest level) for Testosterone Enanthate is just before the next injection.
Obtaining both levels will give the range of testosterone one's body is exposed to.
This is helpful to see if a person is within a good therapeutic range.
The shorter the intervals between injections, the flatter the range will be.
Large variations between the peak and trough can be a problem because there can be large
changes in DHT and Estradiol levels - contributing to problems such as weight gain, acne, hair
loss, and hot flashes. Hot flashes occur when estradiol levels drop quickly - they are withdrawal
from estrogen.
Large peaks of testosterone may also result in large amounts of DHT and Estradiol being made.
When Estradiol is made from testosterone, its peak levels last much longer than testosterone
itself - resulting in a larger exposure to estradiol even as the levels of testosterone drop.
Testosterone Enanthate usually has a half-life of about 7-9 days. This results in a good total
testosterone level (e.g. 700-900) at a dose of 100 mg a week. The half-life varies though
depending on the person's ability to metabolize testosterone enanthate and testosterone.
In some men, the half-life of Testosterone Enanthate is much shorter. For example, in some men,
the half-life is around 4 days. To achieve a total testosterone of around 800, such a person would
need about 200 mg a week.
Given a Testosterone Enanthate dose of 200 mg every 2 weeks for an average hypogonadal
male, the total testosterone curve shows a peak of around 1250 ng/dl approximately 24-48 hours
after the injection, 1000 ng/dl around 4 days after the injection, 800 ng/dl 7 days after the
injection, 600 ng/dl 10 days after the injection, and baseline about 14 days after the injection.
A way to tell what the half-life would be is to give the person a 200 mg dose then measure the
total testosterone approximately 4 days or 7 days later. If the level is significantly lower than the
average male dose curve, then the half-life is going to be shorter.
For example, I have a patient with a level of about 600 ng/dl 4 days after the 200 mg injection.
This is about 40% less than the expected 1000 ng/dl seen in an average person. He has a very
short half-life for testosterone enanthate. One could argue that his half-life is about 3 days (since
600 ng/dl is about half of the peak of 1250 ng/dl 24 hours after the injection). His body quickly
destroys testosterone. He needed a 200 mg a week dose to achieve a trough blood level of about
800 ng/dl. It was best to dose this 100 mg twice a week to maintain an even blood level, avoiding
a roller coaster effect, given the very short half-life of testosterone and testosterone enanthate in
his body.
__________________
Re: what's going on doc? - ADHD and marijuana.
Quote:
Originally Posted by LifeSize
when I was young I was put on high doses of ritalin, at around 11 I decided I wouldn't
take them anymore and I quit cold turkey. the last few years I have been having problems
with focus, drive, motivation, memory.. how do I know if its still adhd or something else?
I feel more in focus when I smoke a joint.
Whether or not a person has ADHD or some other mental condition or illness is not clear until a
full evaluation and follow ups are done. There are too many conditions which can appear like
ADHD - e.g. bipolar disorder, adrenal fatigue, hypothyroidism, depression, anxiety, diabetes, etc.
Marijuana generally impairs one's ability to focus - even if the person feels their focus has
improved. It has a calming effect for some - just as alcohol has a calming effect on others. Some
people use marijuana for self-medication to reduce some symptoms which may impair their
functioning such as anxiety, agitation, etc. Unfortunately, dysfunction from chronic use often
occurs.
The appropriate treatment for a person will depend on what the condition is. ADHD is one of
several possibilities.
__________________
Re: what's going on doc?
Quote:
Originally Posted by LifeSize
marianco, thanks for yyour thoughts. I enjoy reading your posts on the board. looks like I
need to put the doobie out and see a doc. should I speak with my primary?
I was on 15-25mg of ritalin from the age of 5 to about 11. I'm going to do some research
now..
thanks for the advice folks...
The questions would be
1. What symptoms does one have.
2. What systems in the body may be involved in contributing to the symptoms - nervous,
endocrine, immune, cardiovascular, musculoskeletal, etc.
The answers would then guide the person to the specialist needed.
One can start with one's primary care provider. One can always get a referral or at least gain a
direction to go for answers from the primary care provider.
Each physician has a limitation in what they may know about a subject and how far he or she can
improve one's condition.
If one does not improve satisfactorily with the best treatment one gets from their particular
physician, then moving on to another may be helpful.
One's own research into the subject may be highly useful in determining what one needs.
Certainly search engines and the internet may highly be useful as well as help from various online
forums.
Thyroid Hormone
Thyroid hormone has numerous deep, f****anging effects on one's health. It has numerous
complex interactions with the nervous, endocrine, and immune systems.
For example, thyroid hormone is necessary to stimulate steroid hormone production in the testes
- resulting in an increase in testosterone production.
Thyroid hormone increases serotonin production in the brain - resulting in a reduction in stress. It
is commonly used in psychiatry to help stabilize mood or reduce depression. What is not realized
is that it can reduce anxiety.
Thyroid hormone stimulates activity in the adrenal glands. If the adrenal glands are not
excessively fatigued, this improves adrenal function.
Thyroid hormone increase the number and size of mitochondria in practically all cells of the body
- including the brain. This causes an increase in metabolism seen with treatment. It helps improve
brain function, heart function, etc. When people memory problems, it may be useful to give a trial
of thyroid hormone to see if it can improve function. In dementia, it may be a useful treatment.
Thyroid hormone reduces insulin resistance and its symptoms.
When adjusting thyroid hormone, it is important to give it time, to allow the body to adjust the the
higher levels. The inactive component of Armour Thyroid, T4, can take 4-6 weeks to ramp up to a
plateau in blood level - thus the need to go up slowly. Ramping up too fast may result in a
hyperthyroid state when the blood levels stabilize, with all the attendant problems including
cardiac arrhythmias.
Re: A Good Link on Thyroid.
Quote:
Originally Posted by pmgamer18
I printed this out and am giving it to my Dr. so I can get on some Armour.
http://www.thyroid-info.com/articles/dommisse.htm
Great link!
And he's a psychiatrist, like me, too! Love it!
From my point of view, it is far more important to examine a patient for signs and symptoms of
hypothyroidism than to rely solely on blood tests.
For example, there is a common condition involving genetically impaired mitochondrial function
which causes symptoms of hypothyroidism with fully normal blood tests. Symptoms include
myxedema, cold intolerance, lack of energy, low body temperature, frequent colds, etc. It is a
type of thyroid hormone resistance disease - though usually in thyroid hormone resistance, high
thyroid hormone levels are found.
There is no test for this mitochondrial illness. The diagnosis is obtained primarily from the history
and exam. The best treatment is thyroid hormone augmentation. A clinical trial of thyroid hormone
is then warranted given the signs and symptoms of hypothyroidism.
Overreliance on lab tests (such as by most physicians) wll cause one to completely miss the
diagnosis of hypothyroidism even if the physical signs are right in front of you. Unfortunately, the
overreliance on lab tests for thyroid function has caused many physicians (and endocrinologists)
to forget what signs of hypothyroidism are. For example, how do you diagnosis myxedema? The
textbook descriptions and pictures are not good or missing.
__________________
Testosterone Pellets
Low and more frequent doses of testosterone often result in lower DHT and Estradiol production
from testosterone.
This is one advantage of twice a week testosterone injections over once a week or less frequent
injections.
Testosterone pellets are essentially continuous, low dose infusions of testosterone and give the
best control of DHT and Estradiol, while avoiding the supraphysiologic peaks and the dips in
levels that come with injections, and avoiding the high DHT levels that occur with transdermals.
The main problem with testosterone pellets is that it is a surgical procedure. One is thus
dependent on the availability of the physician particularly if one has to get the pellets inserted
more than twice a year. Timing of the insertions becomes important to avoid needing the insertion
during important times such as vacations (both doctor and patient's) and holidays.
Some physicians view pellets as "primitive" given their surgical nature. But it can work well for
many men. Given the birth control rods that are inserted in women, pellets are an equivalent in
men. Injections and transdermals can likewise also be viewed as fairly primitive and inconvenient
methods for medication delivery. It depends on one's point of view and preference.
Some may view the pellets as a loss of control - since the entire procedure is highly dependent
on the physician involved. Injections and transdermals do allow less frequent doctor visits.
I have met men who have improved greatly with the pellets and have had no problems in years of
use.
If physician availability is good, then having to do the procedure only a few times a year can be
viewed as much more convenient than the more frequent injections or daily transdermal use.
Re: what is the best penis englarment method?
So far, I think penis exercises are the best method. But it must be done with attention to safely by
following detailed good instructions.
Penis enlargement is a very slow process.
For example, to go from 5.75 inches to 7.75 inches may take 3 years of 5 days a week of penis
exercises lasting up to an hour a day.
It requires much serious dedication. Having sex soon after penis exercising may be more difficult
that day. A rest period may be required to be able to have an erection.
The most active forum I've seen is at http://mens-network.com/forum/
__________________
Re: what is the best penis englarment method?
Quote:
Originally Posted by greyowl
Marianco, as a physician, who sort of lifts do you think would be most efficacious for
penis enlargement? Wrapping the penis around a dumbbell and performing a series of
hack squats? Or, would you recommend inducing an erection, securing the erect penis to
a cable with something like a wrist strap, and completing a set of seated rows? Also,
would you recommend training to failure?
Using weights on a penis is fairly dangerous and can lead to injury.
Working on improving one's grip and forearm strength, as well as improving upper arm and
shoulder strength are important since some of the penis exercises can tax the involved muscles
significantly. The squeeze movements, for example, can be very taxing for the thumb and
forefinger musculature. Exercising the PC-muscle is also important to maintain bloodflow in the
penis, while doing some of the exercises.
Examples of helpful lifting exercises include:
Grip exercises
Forearm Curls and reverse curls
Biceps curls
Triceps presses
Upright Rows
Deltoid raises
Pull ups
Rows
Bench presses
Exercising the pubococcygeal muscle (pc muscle for short) involves doing Kagel exercises. The
PC muscle supports the internal sex organs, running from the pubic bone to the tailbone, in a
figure-eight around the genitals. A well-toned PC muscle can enhance the experience of orgasm
and improve ejaculatory control, among other things. Some men and women also use specialized
bars to improve the grip strength of their PC muscle.
Re: HGH as an Anti-depressant
Unless a person has a deficiency of IGF-1 (not a low normal value), or a positive test on GHRHArginine Test, and unless treatment is monitored and treatment adjusted, there are significant
risks to Growth Hormone treatment.
Growth Hormone has significant adverse effects which need monitoring, including:
1. It can increase insulin resistance
2. It can reduce thyroid hormone activity
3. It can reduce adrenal cortex activity - essentially causing adrenal fatigue or insufficiency
These changes can themselves cause a chain-reaction and changes in other parts of the
neuroendocrine system - e.g. lower testosterone levels and other neurotransmitter and hormone
changes.
Other adverse effects include fluid retention, pins-and-needles and other sensory changes, joint
stiffness, muscle pains, carpal tunnel syndrome, edema, impaired eyesight (retinopathy),
accelerating tumor growth, etc.
Symptoms of excess growth hormone can include anxiety, insomnia, depressed mood, loss of
libido, lack of energy, mental clouding, weight gain, hypertension, heart disease, stroke,
osteoporosis, etc. These are opposite of what one hopes to obtain from treatment.
It is thus important to have more extensive monitoring and adjustment of the neuroendocrine
system, and growth hormone treatment be adjusted (i.e. lowered) when adverse effects occur.
Re: Self-administered TRT, startinng HCG
A total testosterone < 250 ng/dl is clearly hypogonadal when symptomatic - e.g. low libido, having
insulin resistance, etc.
The endocrine society - the world's largest group of endocrinologists - has published their new
guidelines - which are easy for a primary care provider to read and understand. The link to
download the guideline is http://www.endo-society.org/quickcon...line053006.pdf. It may be useful
to show this to one's physician.
Re: Estradiol = Estrogen = e2???
Estradiol (E2) is the most potent naturally occurring form of estrogen.
Measuring Estradiol alone will give you an idea of the total estrogen activity because it gives you
the total estradiol itself plus some of the activities of the rest of the estrogens.
To determine how much estrogen activity is only due to Estradiol alone, you have to do a
fractionated estrogens test. This will break down the estrogens into Estradiol, Estrone, Estriol,
and give you the total estrogen level.
For the purpose of hormone replacement therapy, a single measurement of Estradiol alone gives
a good idea of the total estrogen activity and is useful for making clinical decisions. It also can be
done very quickly as opposed to a fractionated estrogen test.
If there are complicating factors, if a patient is not responding as expected, it may then be useful
sometimes to order a fractionated estrogens test, to help figure out what is going wrong. The
Estradiol level obtained from a fractionated estrogens test will be different from the single
Estradiol test. They can't be compared since they are different tests.
__________________
Re: good news: TRT works!
Quote:
Originally Posted by The_Skeptic
How is your libido?
And have you ever experiminted with 125 mg of enanthate every five days as some of us
in the states have done with cypionate, going from 200 mg every 10-14 days to 100 mg
ever 5-7 days?
I used to be on the former, but now I'm on the latter protocal, but I'm thinking this does
not bring my levels up to how I used to get them. And even though it is said that I will
higher fluctuations on the former protocal, I am now supplementing my protocal with
HCG, so that might help when the T starts to drop in the second week.
Also, I just ordered some enanthate from Europe, so I will be using that instead of
cypionate.
I think, depending on the patient's response, the interval time between injections can vary
tremendously. Less frequent injections are more convenient and easier to schedule around one's
lifestyle. This is one factor in deciding on the schedule.
If a person wants very stable testosterone levels, two injections a week can accomplish this better
than less frequent injections. For example, an injection on Monday and Friday can be done.
Interestingly, as a patient loses weight - causing a reduction in aromatase enzyme activity - and
improves in health with testosterone replacement therapy - less frequent injections can be done
without too many side effects in many men depending on the health of the rest of the
neuroendocrine system.
For example, I have seen where a depo-testosterone injection given at a dose such as 300 mg
every 3 weeks or 400 mg every 4 weeks can be done with few problems. I use to worry about the
supraphysiologic levels at the beginning of the treatment cycle, but the men uniformly respond
well with very few side effects, both at the beginning and at the end of the cycle just before an
injection.
The key, I think, to the positive outcome, is paying attention to balancing the rest of the
neuroendocrine system using various supplements, hormones, and medications. This way,
testosterone optimization is not done in a vacuum from the rest of the system. When balancing
one neurotransmiter/hormone system, the rest will need attention as well, to allow optimization of
the person as a whole.
I am happy for Axl!
Re: For Mariano Insufficient Glucocorticoid Signaling or adrenal fatigue
Quote:
Originally Posted by DAVID
Thank you Doc for your great answer in te board of adrenal, many anti-aging physician
give hydrocortisone for patient who have CFS or adrenal fatigue
Previous theories of stress-related pathologies have privileged the pathological potential
of glucocorticoids. Herein we document that, in a number of instances, stress-related
neuropsychiatric disorders may be characterized by insufficient glucocorticoid signaling
as manifested by hypocortisolism or impaired glucocorticoid responsiveness associated
with evidence of immune activation/inflammation, increased SNS tone, and
hypersecretion of CRH. Hyperactivity of these stress-responsive systems, especially
inflammation, in turn, may contribute to the behavioral features of these disorders,
including depressed mood, anhedonia, fatigue, pain, and cognitive dysfunction, as well as
the neurobiological, metabolic, and immunologic consequences of stress.
glucocorticoid insufficiency contributes to unrestrained cytokine release, which in turn
further impairs glucocorticoid receptor functioning, leading to a feed-forward
inflammatory cascade
In addition to effects on the immune system, reduced glucocorticoid signaling (whether
achieved at the level of the hormone or its receptor) may also promote nervous system
states that benefit successful adaptation to chronically stressful situations.
My question is ARE YOU SURE THAT HYDROCORTISONE IS THE BEST
TREATMENT FOR THIS DISORDER ? may be anti-depressant is better option because
the impact of these drugs on second messenger pathways involved in glucocorticoid
receptor regulation, including activation of the cyclic adenosine monophosphate/protein
kinase A (cAMP/PKA) cascade is better option. Activation of both cAMP and PKA has
been shown, in turn, to enhance glucocorticoid receptor functioning
Thank your for your answer
Hydrocortisone is one treatment out of many treatments for adrenal fatigue and some forms of
chronic fatigue syndrome. Whether or not it is the best treatment for a particular individual will
depend on physician's the evaluation of the person's condition - including having an idea of the
pathophysiology of the person's condition.
Some forms of chronic fatigue syndrome, for example, result from hypersensitivity of the person's
brain to sensory input. For these people, hydrocortisone may not work at all. Some people have
normally low functioning adrenal glands. Hydrocortisone then may actually reduce adrenal
function excessively, worsening the person's ability to function. Some patients have extreme
chronic stress. For them, hydrocortisone may not work at all because hydrocortisone is a passive
treatment - meaning it does nothing by itself to directly improve functioning. It is up to the
person's adrenal gland to recover from stress, for which hydrocortisone provides some respite.
But under constant stress, that may never occur.
It is not really possible to say what is "best" as a treatment because a "best" treatment may not
apply for the individual patient. The treatment has to be customized for the individual patient. The
science also keeps moving forward and new treatment options are always being developed.
Luckily, there are numerous options available to try and help the large majority of people suffering
from adrenal fatigue or chronic fatigue. These options include various medications, herbal and
nutritional interventions, psychosocial and psychotherapeutic interventions, etc. However, there
will be some patients for whom the current technology cannot provide them with a satisfactory
answer.
__________________
Re: enanthate duration
In an average hypogonadal male, 200 mg of testosterone enanthate will keep testosterone level
above the original baseline for about 14 days. For example, if one has a total testosterone of 300
ng/dl, then gets an injection of 200 mg testosterone enanthate, then after 14 days, total
testosterone is back to 300 ng/dl. The total testosterone peaks around 1-2 days after injection.
The peak is often over 1000 ng/dl then drops off gradually the remaining days. There is variability
though depending on one's ability to metabolize testosterone enanthate and testosterone. For
example, the half-life of testosterone is highly variable from about 10-100 minutes. DHT and
estradiol have peaks that follow the total testosterone curve, though estradiol remains at higher
levels for more days than testosterone. Testing is needed to determine the appropriate dose and
frequency of injection.
Low libido may not be due to low testosterone (CNN article)
NEW YORK (Reuters) -- While there's a statistical link between men's sex drive and their
testosterone levels, in practice there's little meaningful difference in testosterone levels between
men with low libido and those with high libido, researchers report.
Dr. Thomas G. Travison, from the New England Research Institutes in Watertown,
Massachusetts, and his associates evaluated data from the Massachusetts Male Aging Study,
and report their findings in the Journal of Clinical Endocrinology and Metabolism.
Between 1987 and 1989, a total of 1,632 men ages 40 to 70 years were enrolled in the study.
They were assessed at the outset and two more times approximately 9 and 15 years later, when
922 and 623 men, respectively, were available.
At each time point, the men completed a self-administered questionnaire asking about the
frequency of sexual desire and of sexual thoughts and fantasies, and their hormone levels were
measured.
Men with scores of less than 7 points out of a total 14 were classified as having a low libido,
which included 19 percent of men at the start of the study, 23 percent after 9 years, and 28
percent at 15 years.
Travison's team reports that, overall, libido was significantly associated with testosterone levels.
However, the difference in testosterone levels between participants with low libido and those with
high libido was small and "inconsequential."
Looked at the other way, a low libido did not mean a man was particularly likely to have low levels
of testosterone.
Therefore, the researchers conclude that if a man complains of reduced libido, it cannot always
be interpreted as a sign of testosterone deficiency.
Copyright 2006 Reuters. All rights reserved.This material may not be published, broadcast,
rewritten, or redistributed.
http://www.cnn.com/2006/HEALTH/08/01...eut/index.html
Re: Low libido may not be due to low testosterone (CNN article)
Quote:
Originally Posted by The_Skeptic
NEW YORK (Reuters) -- While there's a statistical link between men's sex drive and their
testosterone levels, in practice there's little meaningful difference in testosterone levels
between men with low libido and those with high libido, researchers report.
Dr. Thomas G. Travison, from the New England Research Institutes in Watertown,
Massachusetts, and his associates evaluated data from the Massachusetts Male Aging
Study, and report their findings in the Journal of Clinical Endocrinology and
Metabolism.
Between 1987 and 1989, a total of 1,632 men ages 40 to 70 years were enrolled in the
study. They were assessed at the outset and two more times approximately 9 and 15 years
later, when 922 and 623 men, respectively, were available.
At each time point, the men completed a self-administered questionnaire asking about the
frequency of sexual desire and of sexual thoughts and fantasies, and their hormone levels
were measured.
Men with scores of less than 7 points out of a total 14 were classified as having a low
libido, which included 19 percent of men at the start of the study, 23 percent after 9
years, and 28 percent at 15 years.
Travison's team reports that, overall, libido was significantly associated with testosterone
levels. However, the difference in testosterone levels between participants with low libido
and those with high libido was small and "inconsequential."
Looked at the other way, a low libido did not mean a man was particularly likely to have
low levels of testosterone.
Therefore, the researchers conclude that if a man complains of reduced libido, it cannot
always be interpreted as a sign of testosterone deficiency.
Copyright 2006 Reuters. All rights reserved.This material may not be published,
broadcast, rewritten, or redistributed.
http://www.cnn.com/2006/HEALTH/08/01...eut/index.html
A problem in scientific studies is that they tend to focus on only one factor. In a condition as
complex as libido, where numerous factors are in play, incomplete answers are the outcome,
which can easily lead to misinterpretations.
The conclusion of the study is that low libido cannot be intepreted solely as a sign of testosterone
deficiency.
The misinterpretation that is easily made is that testosterone treatment should not be considered
when one has low libido.
I wish the researchers had measured more factors than just testosterone so that they could have
teased out the circumstances when low testosterone correlates with low libido out of the
confounding factors that were most likely present (e.g. low thyroid, adrenal fatigue,
atherosclerotic cardiovascular disease, diabetes, etc. etc.). These confounding factors
undoubtedly masked any correlation there was between low testosterone and low libido.
If anything, the researches could have at least stated the possible confounding factors and
weaknesses in their study - as good research generally does - rather than stand pat on a
conclusion which can be so easily misinterpreted and sensationalized.
__________________
Re: Lab Results are back
Quote:
Originally Posted by 021mk
I just got my lab results:
Total T = 307 (241-827)
LH = < 0.7 (1.5-9.3)
FSH = 0.9 (1.6-8)
I feel tired every day. I am on 5mg of androgel. I was thinking adrenal fatigue but I got
my results for a saliva test:
Cortisol 8 am = 0.61 (0.27-2.06)
cortsil 12am = 0.10 (0.03 - 0.50
DHEA 8am= 208 (14-277)
I spoke to the nurse about my feeliong tired, mildly depressed, a bit of mental fog etc. She
sdaid she will talk to Dr. but didnt sound like he is going to increase my androgel.
What does anyone make out of my results?
thanks
The doctor should have the Endocrine Society's 2006 guidelines to testosterone replacement
therapy: http://www.endo-society.org/quickcon...line053006.pdf. Giving the doctor a printed copy
would be useful.
Based on the lab test reference range, the target initial total testosterone level (using the
guidelines) should be 534 ng/dl (mid-range) (I prefer 650 ng/dl - using a reference range of 3001000 ng/dl). Thus a total testosterone of 307 ng/dl on testosterone replacement with androgel
means the treatment is seriously underdosed.
The Endocrine Society is the world's largest endocrinology organization. They are extremely
conservative. Their guideline won't solve problems for most men who don't have baseline
testosterone levels under 300 - rather it is more restrictive than their previous guidelines. But, the
protocol is so simply and clearly written that it is a highly useful guide for primary care providers
who don't know how to do testosterone replacement. It is a good starting point.
__________________
Re: DHEA and testo bloodtest
Quote:
Originally Posted by pmgamer18
I can't say if he uses it but he did say over 50mgs. will drive up E's.
DHEA supplementation is part of the treatment for Adrenal Fatigue.
The question I would have is: HOW does DHEA treatment drive up estrogens? That is not entirely
clear for every person. In many cases, it doesn't.
A complicating factor is that in a TRT protocol using HCG, HCG can drive up estrogen a lot
because it increases the production of aromatase, the enzyme that turns testosterone into
estrogens.
DHEA in high doses or levels, can conceivably drive SHBG down. Low SHBG can result in more
free estrogens. However, DHEA in high doses can also increase testosterone levels, albeit not by
a lot. I've seen cases where high DHEA levels results in lower estradiol level. Another
complicating factor is that many commercial DHEA tablets don't contain the labeled amount of
DHEA - the person is getting a lower dose than labeled.
I think one's mileage will vary. It would be best to do lab tests to verify the outcome of DHEA
replacement.
__________________
Re: think i may have a little addiction to gels
Quote:
Originally Posted by JanSz
AFAIK total testosterone is sort of not really important. Important is Free Testosterone.
You may need two gells to get it right.
I am using 2 Androgel packets myself. Before I started on Androgel my
T was 311 ng/dL (241-827)
FreeT 6pg/mL (2.6-64.8)
LU 5.7miU/mL (1.5-9.3)
Estradiol 24 pg/mL (0-52)
If I find the right doctor I am planning to add HCG as I think I was secondary and
possibly the HCG will reviwe my balls.
Only a blood test will really tell if the dose of testosterone replacement is enough - though
sometimes a person can get by by clinical effect since 2 packets of Androgel is a standard dose
that generally achieves good levels of testosterone in most men.
Total Testosterone is a more reliable measurement than Free Testosterone when it comes to
testosterone replacement. The problem of measuring free testosterone is that the lab tests
themselves for free testosterone are unreliable. The best test for free testosterone is by
equilibrium dialysis. However, only a few labs in the U.S. offer this test. For practical purposes,
the total testosterone level then is the better test. My initial target is achieving at least 650 ng/dl
for total testosterone.
Re: 800 out of 1400 range T levels good enough?
Quote:
Originally Posted by DrmChld
Hi,
Been on Androderm 5mg/day for about 5 months now. My last blood test had mny T
levels at 800. Is this good enough? I haven't noticed any real changes in libido, overall
mood, engery, anxiety levels. Would if be advisable for me to request a higher dosage
range to see how it makes me feel?
Thanks in advance
Trandermal testosterone treatment generally causes stable blood levels of testosterone.
A total testosterone level (after treatment) of 800 ng/dl is a good level.
If a person still has symptoms - e.g. lack of energy, lack of libido, depressed mood, anxiety,
insomnia or excessive sleep - I would look at problems with the other hormones and
neurotransmitters to fix. If these other areas are addressed and a person still is symptomatic,
then immune system cytokines would be another area to examine (however the science of doing
this is fairly in its infancy).
Aside from testosterone, other common chemical messengers (and their other associated lab
values) to examine include:
Estradiol and other estrogens
Dihydrotestosterone
Progesterone
Cortisol
DHEA
Insulin
Thyroid Hormone (Free T3, Free T4)
Dopamine
Norepinephrine
Epinephrine
Serotonin
GABA
Glutamate
Prolactin
SHBG
etc.
__________________
Re: HGH Therapy
Quote:
Originally Posted by austinsteviehend
Hi guys,
I went to Dr. Crisler a little while back and first off he's the best! But anyways, I had my
bloodtests run for all his major "labs I run". I don't have the numbers, but he said
everything was good except
1. Progestorone
2. IGF-1
He said with my IGF-1 low I could be warranted for HGH therapy. But i don't get it. I
still have slow facial hair growth, quite low libido and low energy. Could the HGH
therapy cure alot of these things? I can afford the therapy if it's worth the price. Also, i'm
a bodybuilder. Please don't get me wrong, i don't want "steriod like" hormones. I just
want what I should be at for a 21 year old healthy male so i have the ability to put on
muscle.
Thanks,
Justin
IGF-1 can be low also with low normal DHEA levels due to adrenal fatigue. Low progesterone
level, low energy, low libido are other signs of adrenal fatigue.
Before starting HGH therapy based solely on IGF-1 level, it would be useful to also measure 24hour growth hormone production, e.g. via urine assay, to see if it actually is low.
If adrenal fatigue is present, DHEA as a component of treatment can raise IGF-1 level.
Treatment of adrenal fatigue is much much less expensive than treatment of growth hormone
deficiency.
See adrenal thread.
__________________
Re: Question about SHBG and other blood levels
Quote:
Originally Posted by Winters1jm
Total Testosterone - 287. (241-827 NG/DL)
Testosterone, Free and Weakly Bound - 201. (84-402 NG/DL)
Testosterone, Free - 85. (34-194 PG/ML)
LH - 5.1 (1.5-9.3 MIU/ML)
Albumin - 5.2 (3.7-5.1 G/DL)
SHBG - 13. (7-44 NMOL/L)
Symptoms of testosterone deficiency are more common as the total testosterone level dips below
300 ng/dl.
Sex Hormone Binding Globulin (SHBG) binds testosterone and allows testosterone to have a
longer duration of action. SHBG also has its own receptors and transmits signals to cells with
these receptors when testosterone or estrogens are bound to it. The exact result of these signals
are not clear.
SHBG is increased by thyroid hormone and estrogens.
SHBG is lowered by insulin resistance (e.g. high insulin levels, diabetes), testosterone, DHEA,
growth hormone, other androgens.
With low SHBG and pure testosterone replacement therapy (e.g. gels or creams), one can get
large amounts of free testosterone temporarily, but as it is quickly destroyed, one gets lower than
expected testosterone levels. A roller coaster experience can result. Depo-testosterone injections
work better under this circumstance.
The initial target total testosterone level with testosterone replacement therapy (assuming a
normal range of 300-1000 ng/dl) is about 650 ng/dl - a mid-range level. This is recommended by
the Endocrine Society's new 2006 guidelines. I think it is a great conservative initial target
because I've seen too many practitioners who won't make adjustments because the initial
treatment (e.g. with androgel) caused the total testosterone to go over 300 - e.g. 400, into the
"normal range" - then declaring the treatment as adequate when the person still has symptoms of
hypogonadism.
__________________
The Endocrine Society's 2006 Guidelines for Testosterone Therapy
Here is the updated 2006 guideline from the Endocrine Society for Testosterone Therapy in Adult
Men with Androgen Deficiency Syndromes:
http://www.endo-society.org/quickcon...line053006.pdf
I like this guideline since it is written clearly.
The target testosterone level to achieve with replacement therapy was clarified to be at the
midpoint of the reference range. This means for a reference range of 300-1000 ng/dl, treatment
should achieve a testosterone level of 650.
The guideline is fairly simple, not including other options such as using HCG or considering other
factors such as DHT or estrogen levels. It is more rigid in requiring the testosterone level be
generally under 300 ng/dl. But it is a good starting point and is clear enough for family
practitioners to use. For example, I like the use of starting doses and monitoring guidelines for
labs. Practitioners who lack experience will feel more comfortable when given starting doses and
clear monitoring guidelines.
__________________
Superdrol
Superdrol, or Methasteron, is a designer anabolic steroid.
From http://www.muscletalk.co.uk/article-superdrol.asp:
Quote:
Superdrol (SD) is marketed as a 'pro-hormone' (PH) in the post-ban era of pro-hormones.
Following the ban of most pro-hormonal substances in the States, including the likes of
1-test, 1-AD, 4-AD, M1T, etc, Designer Supplements designed this 'pro-hormone' based
on the steroid Masteron, with an additional methyl group attached to the 17th carbon
position. It is described as a cross between anavar and masteron, with the virtual inability
for aromatisation to estrogen. It is highly anabolic (400-800% more so than methyl-test)
and a lot less androgenic (~20% of methyl-test). Superdrol has hence been given the
name Methasteron.
Despite being marketed as a supplement available legally and deemed another 'prohormone' or 'pro-steroid' by many, there is nothing very 'pro' about SD. In reality, SD is a
designer steroid, and that is what the reader must primarily understand. It is methylated,
so will cause stress on the liver, and it is an anabolic/androgenic steroid, thus it has the
potential to give side effects normally seen with such anabolic androgenic steroid (AAS)
use. It will shut your natural testosterone production down
Given the lack of safety information and studies, I would assume there may be some damage
which may be permanent or long-lasting. It would then be important to test multiple areas of one's
health (not just testosterone, LH, FSH) to determine where problems may lie. Liver damage, for
example, is one concern.
The lack of pharmacologic information is a concern - as is the case with many anabolic steroids.
How is SD eliminated, for example? Some substances (such as phencyclidine (PCP) or LSD) are
highly fat soluble and not easily eliminated. They can stay in the body for decades.
A steroid is generally highly fat soluble. A steroid which is not easily broken down in the liver or
other cells of the body may conceivably have very prolonged effects by staying in the body
months or years after taken - which is not good if the effects are harmful.
The body's own steroid hormones/neurotransmitters have very short lives. Testosterone, for
example, lasts only 10-100 minutes. The body has to attach testosterone to sex hormone binding
globulin and albumin to prolong its life. Testosterone is broken down by the body into substances
such as the estrogens or dihydrotestosterone, which are then broken down into other substances
which are more easily eliminated by the body.
The reason the body's own steroid hormones/neurotransmitters have short lives is that they are
used as signals. Communication is only useful if you can turn a signal on or off.
A designer steroid which is designed to avoid the body's natural elimination pathways in order to
be more potent is asking for a lot of trouble.
Dr. Crisler (allthingsmale.com) is one physician who has a lot of experience in treating former
users of anabolic steroids.
__________________
How long steroids stay in your system.
Quote:
Originally Posted by DLMCBBB
Yikes, relating its elimination on par with PCP & LSD is construed by me to be a scare
tactic. You do know that superdrol is purported to be a mix between Masteron and
Anadrol correct? And this user used it for 6 days, now he is prob scared out of his wits by
you telling him he may have perm damage.
Sorry, I wasn't intending to use a scare tactic, but an illustrative point (as a psychiatrist, PCP and
LSD are common examples of long-lasting substances).
I also answered azb777's question
Quote:
Anybody have any ideas why SD shut me down so badly??
Hopefully azb777 can continue to recover as his last posts may indicate.
It is food for thought if one chooses to use anabolic steroids. It is important to know as much as
possible about the risks involved.
Here's an interesting link which may illustrate my point of how long some anabolic steroids may
last: http://www.steroidtips.com/detection.htm.
Quote:
How long do steroids stay detectable in your system?
Steroids can remain detectable in a persons system anywhere from 1 week to over a year
after use. For the most popular substances like nandrolone (deca, testosterona), one year
is the usual time that they could actually be detected. For injectable testosterone, between
3-6 months is commonly sufficient.
Detection Times:
nandrolone decanoate - 18 months
nandrolone phenylpropionate - 12 months
boldenone undecyclate - 5 months
metehenolone enanthate - 5 months
trenbolone - 5 months
trenbolone acetate - 5 months
injectable methandienone - 5 months
testosterone-mix (Sustanon & Omnadren) - 3 months
testosterone enanthate - 3 months
testosterone cypionate - 3 months
oxymetholone - 2 months
fluoxymesterone - 2 months
injectabel stanozolol - 2 months
formebolone - 2 months
drostanolone propionate - 2 months
methandienone - 3 weeks
mesterolone - 3 weeks
ethylestrenole - 3 weeks
noretadrolone - 3 weeks
oxandrolone - 3 weeks
oral stanozolol - 3 weeks
testosterone propionate - 2 weeks
testosterone undecanoate - 1 week
clenbuterol - 4 days
Re: Dhea
Quote:
Originally Posted by youngBuilder
Im not hypogonadyl, but we all could use a little more test right?
More is not necessarily better. It can actually backfire on you and cause harm.
For example, excessive testosterone can cause polycythemia, which in turn can cause
congestive heart failure. Excessive testosterone in the presence of low estrogen and
progesterone may cause hypertension.
__________________
"I don't feel that combo is doing its job": What are the expectations of treatment? What
symptoms are suppose to be addressed by treatment?
I think any combination of antidepressants (and/or other medications) is fine so long as it
achieves the intended purpose, the benefits outweigh the risks of treatment, and the side
effects are tolerable and don't impair functioning.
Medications which increase serotonin (such as Celexa, Prozac, Effexor) can also reduce
dopamine. If the reduction in dopamine is too low, it may manifest as impaired memory,
increased weight, agitationed/restlessness, lethargy, anxiety, sexual dysfunction, among other
side effects. Serotonin, itself, can directly impair sexual function in excessively high doses for
the person.
Wellbutrin works by increasing norepinephrine. If the dose is too high, increased
norepinephrine can increase a person's stress level. The appropriate dose depends on the
person. The range of doses I use is between 37.5 mg to 500 mg a day. The risk of seizure at
600 mg a day is about 1 in 20. Wellbutrin can significantly inhibit cytochrome P450 2D6 - an
enzyme in the liver which metabolizes many medications, and is needed to convert thyroid
hormone T4 to the active version T3.
In general (which needs to be interpreted for every individual patient) Effexor works primarily
by increasing serotonin at doses from 1 to 150 mg a day. Above 150 mg a day, it also
increases norepinephrine significantly. Around 300 mg a day, it also increases dopamine
significantly. Thus its pharmacological effect will depend on the dose. My own maximum dose
is 575 mg a day - rarely needed, or tolerated (due to side effects).
When a patient does well on an antidepressant or combination of medications then the
medication or combination seems to stop working, it is the patient's illness or condition that
has changed, not the medication. The medications always work the same way - their
mechanisms of action do not change. But other factors in the patient's condition or health may
change the patient's response to treatment. These factors may include other neurotransmitterhormone changes and health related changes (hypothyroidism, further decreases in
testosterone, obesity, diabetes, stress and othe psychological factors, etc.) as well as the
addition of other medications with interactions.
Some practitioners believe in "SSRI Poop-out" - where it is thought that "tolerance" develops
to an SSRI (serotonin reuptake inhibitor - such as Prozac), which is why it will stop working. I
do not believe this generally happens. I think the patient's illness either changes in
characteristics or the diagnosis needs to be reassessed (e.g. bipolar disorder rather than
major depressive disorder may be present) or other complicating health factors contribute to
worsening of their symptoms.
The patient will have to continue working with his/her doctor to determine what factors have
changed.
__________________
Quote:
Originally Posted by HeadDoc
thanks Marianco for clarifying that last point. I never understood the "poop out".
Regarding the sexual s/e's of SSRI's, it would appear that you are less confident in
augmenting the SSRI with Wellbutrin. I have never seen it used, but would a small
amount of stimulant be a better choice.
Also have you used any secondary messengers for depression or anxiety, like inositol?
This is a reference that I have relied upon in the past. Any comments?
http://www.fpnotebook.com/PSY184.htm
The reference is good.
Like most psychiatric medications, your mileage will vary. In my experience, dating back to
when Wellbutrin was first introduced (1985), I have not seen it work often in improving sexual
function (but then I usually treat very severely ill people, thus the population itself may not
respond well because they have numerous physical and other co-morbid problems). Yes, it
may in some patients - thus making it worthwhile to prescribe first, given its relative safety. But
improvement in sexual function has been a rare occurrence. Realizing that Wellbutrin primarily
increases norepinephrine, this is then understandable. Dopamine has the much larger role in
sexual function. What is good about Wellbutrin as an antidepressant - when not used primarily
to improve sex drive - is that it does not interfere, by and large, with sexual function, unless
the dose gets too high.
The cleanest (i.e. with fewer side effect and other mechanisms of action) and best way I've
seen to improve Dopamine level is by optimizing testosterone activity for the individual, while
maintaining physiologic levels. I like this method because sex can then be spontaneous, in the
here-and-now. This is as opposed to having to prepare for it by taking Viagra or some other
medication, which removes spontaneity from sex. If you have to focus on a medication prior to
sex, sex isn't as fun. There tends to be too much anxiety about performance, whether the
medication will work or not. Being in the here-and-now and being spontaneous during sex is
very important to the pleasure of and loving experience for the woman/wife/girlfriend/partner.
A small amount of a stimulant (including pseudoephedrine, Dexedrine, Ritalin) is an option
when optimizing testosterone is not enough (given the multiple other factors that can affect
sex drive, arousal, the nervous system, physical illness etc.). I have prescribed Dexedrine or
Ritalin for patients in this regard. They tend to not prefer it over time, however. Stimulants
increase both norepinephrine and dopamine. The norepinephrine side tends to cause anxiety
and insomnia. They end up preferring a phosphodiesterase inhibitor such as Viagra. (As an
aside, cocaine, which I would not recommend using, is a strong multiple re-uptake inhibitor increasing dopamine, norepinephrine, and serotonin - not just a dopamine reuptake inhibitor
as is commonly thought.)
I like Cialis over the other phosphodiesterase inhibitors because its long half-life allows more
spontaneity in sex, and multiple sexual episodes - which is why it is called a "weekend" drug.
However some people are very sensitive to the flush reaction, headache, reddened eyes, and
nasal drip as side effects.
If possible, reducing the offending sexually-inhibiting drug to restore sexual function is
preferable to using another medication to address a side effect.
With the usual severe depressive and anxiety problems in patients I see, psychotherapy and
actual medications and hormones have the strongest effect. Supplements (like SAMe, Inositol,
etc.) are useful as adjuncts, but do not have a strong enough effect on depression and anxiety
to be used on their own. Some (like SAMe) would cost more than prescribed medications at
the doses useful to treat depression and anxiety.
In milder cases of depression and anxiety - such as would be treated by a primary care
provider, the supplements may be more useful since a small effect is all that may be needed,
when coupled with psychosocial interventions.
Supplements are much more useful in the patients I see, for the co-morbid conditions
accompanying, possibly contributing to depression and anxiety, and possibly caused by
depression and anxiety themselves - i.e. the psychosomatic illnesses. For example, if anxiety
and depression has a large component due to adrenal fatigue/insufficiency, then there is a
large contingent of supplements (including vitamins, minerals, etc.) which can be very useful
to help improve function and reduce symptoms of illness. If there is insulin resistance and
diabetes as a component of depression and anxiety, then there are supplements which can be
highly useful. If vascular insufficiency or neuropathy is a component of the illness, then there
are supplements which can be highly useful.
Paxil Alternatives
Quote:
Paxil Alternatives
That was quite a read on Testosterone and Neurotransmitters, Doc. My wife and I take
Paxil, 20 mg per day. I wonder if it causes akathisia because I toss and turn a lot, have
restless leg syndrome, and irritibility. Can I suggest an alternative to my M.D.? Like
what? The wife has tried alternatives because of increased appetite but they make her feel
awful. Any suggestions? Thanks
Akathisia is a motor movement disorder I hypothesize occurs when dopamine levels in the
brain become too low. Manifestations include fidgetiness, restlessness, tossing and turning in
bed, restless legs, irritability, anxiety, insomnia, agitation, anger outbursts, a feeling of wanting
to jump out of one's skin, a feeling of ants in one's pants. It can cause worsening of the illness
being treated. At the extreme, it can increase violent behavior, raise the likelihood of a suicide
attempt - as a way to escape extreme discomfort due to akathisia.
Akathisia is an important side effect to watch for with medications that raise serotonin levels
because raising serotonin will simultaneously reduce dopamine levels. I use it as the sign that
the serotonergic medication is at an excessively high dose. I instruct patients to automatically
reduce the dose of their medication if they think akathisia is occurring.
Reducing the dose often relieves the person of Akathisia. The lower dose is the optimal dose,
then, for that particular medication. If depression or whatever target symptoms still persists though reduced by the original medication - I will consider additional medications - which use
different mechanisms of action - to add to the treatment to try and achieve a fuller response such as a lower severity of depression.
When a partial response to an antidepressant occurs, I also consider if there are other,
undiagnosed underlying conditions which can be targetted in treatment, which contribute to
the development of the mental illness.
Paxil works by increasing serotonin levels in the brain.
Alternative medications that primarily raise serotonin levels include Prozac, Zoloft, Luvox,
Celexa, Lexapro, Effexor (at doses < 150 mg/day). Medications that increase serotonin and
norepinephrine include the tricyclic antidepressants (e.g. Elavil, Nortriptyline), Cymbalta,
Remeron.
__________________
Quote:
Originally Posted by Cryptochid
Ive been on every anti dep for over a 25 year period. The worse side effect is lack of
sexual arrousal and erectile dysfunction.
I found the sustanon shots left me with the equivelant of "that time of the month" issues
amongst women.
The adroderm for me was useless - depression was constant and my GP suggested anti
deps while on androderm, but when I started pallets, the depression completely resolved
itself. Have touched anti deps since last August, probably due the the "constant"
secretion of T.
I did notice when my free T dropped of after 4 months with pallets, depression started to
kick in. I only had the depression return for one week as another "insert" was done.
Testosterone Pellets generally would be third in line behind Depot-Testosterone injections and
Transdermal Testosterone because of the additional risks of a surgical procedure, and (for
myself) dependence on the physician (whereas with the other options, one can administer
testosterone to oneself).
However, when the first two options fail for various reason, the testosterone pellets may be a
good idea.
The improved level of Free Testosterone is an interesting finding - and possible benefit of the
pellets versus injections and transdermal route.
I wonder if an attempt to increase Free Testosterone when using injections or testosterone
cream/gel by using substances that reduce estrogen levels - which then reduces sex hormone
binding globulin - which is what binds testosterone, reducing free testosterone.
I wonder if a high enough dose of depo-testosterone or transdermal testosterone was used to
help increase Free Testosterone levels. Testosterone can be compounded at higher
concentrations (such as 10% Testoscreme) using absorption accelerants other than alcohol to
improve absorption and possibly effectiveness.
I wonder how depression correlates with dihydrotestosterone levels (DHT) in addition to Free
testosterone. If depression improves with higher DHT levels, then a testosterone cream can
be placed on scrotal skin to achieve higher DHT levels than at other locations.
__________________
Quote:
Originally Posted by Albert
The more I read about these drug and there use, the more I think our GP's and Primary
Care Physicians should not be handing these out like kids candy. Every time I see my
doctor and we end up not doing anything about my problems, the more they pushed antidepressants on me.
Antidepressants are highly useful. However, they do not solve every problem. They have a
difficult time treating depression when a different neuroendocrine imbalance not addressed by
the antidepressant is the cause (e.g. testosterone, estrogen, progesterone, cortisol
insufficiency). And, if the physician is not aware of all the profound effects antidepressants can
have, problems can arise.
__________________
Serotonin Reuptake Inhibitors (SSRIs) are very complex medications. The primary
mechanism of action is to block serotonin reuptake (causing an increase in serotonin).
However, they also block norepinephrine reuptake, block dopamine reuptake (increasing
dopamine), reduce dopamine production, act directly on serotonin 2C receptors, block
acetylcholine receptors, inhibit nitric oxide synthetase, block liver enzymes including 2D6, 3A4
or 1A2, etc. Each SSRI does these things to a varying extent. However, even if weak on one
mechanism, I do not discount it because I may and have met patient who were sensitive to a
mechanism of action, causing side effects, when the textbooks would say it should not.
Reducing dopamine levels or blocking acetylcholine can lead to memory problems. Each
SSRI has the potential to impair memory depending on the genetic response of the person
taking it.
In general, I prefer SSRIs which tend to have less weight gain as a problem. Obesity causes
so many neuroendocrine problems that impair treatment (e.g. excess estrogen activity, insulin
resistance, impaired self-esteem, etc.), that I prefer minimizing weight gain as a side effect.
Cosmetically, women and men prefer to avoid weight gain strongly. I use to have patient who
would gain 20-30 pounds while on an SSRI, and losing weight would be difficult. The ones
which are less likely to cause weight gain are Lexapro and it's "mother", Celexa. However, I
keep the other ones in mind, because depending on the person, he or she may respond better
to the other ones (Prozac, Paxil CR, Paxil, Zoloft, Luvox) for the intended purpose of
treatment.
Wellbutrin (regular, SR, XR), works primarily as a norepinephrine reuptake inhibitor (not
dopamine reuptake inhibitor). It is almost a pro-drug in that its metabolite is a much more
potent norepinephrine reuptake inhibitor than Wellbutrin itself, and is concentrated more in the
brain than Wellbutrin itself. Memory impairment, in my experience, is much less frequent with
Wellbutrin than the SSRIs. It may help improve attention - thus help improve memory - in
people with attentional problems. "Your mileage may vary" as the statement goes.
I have not heard of memory loss as a problem with Effexor. It is more potent than the SSRIs at
increasing dopamine levels, thus possibly compensating for the reduction in dopamine from
blocking serotonin reuptake. However, at about 150 mg a day and below, it primarily acts as a
serotonin reuptake inhibitor, and thus may have similar risks for memory problems depending on individual response to the treatment.
There is no perfect antidepressant. Depending on the severity of life stresses, a response to
any individual antidepressant can vary from 17-70 percent. Response means a 50% reduction
in symptoms of depression. Patients with severe stress respond most poorly to
antidepressants because the stress can overwhelm treatment. Often a multiple-medication
treatment is needed to adequately reduce the severity of symptoms.
Treatment has to be customized for the person - taking into account genetics, symptoms, the
nature of the illness, previous response to treatment, health problems, side effects and
interactions to avoid, etc. It is an art since we do not yet have specific testing for brain status
and function which partain specifically to mental illness. Since there is no perfect
antidepressant, I have to maintain an open mind about what may help a patient.
__________________
Quote:
Originally Posted by chap
Is there hope (or reason) to get a person off of ssri treatment, after they have been on for
years and are convinced they need it? Is it just wishful thinking on behalf of a loved one
to think there must be a better way?
If something is working for a person, why stop it?
Unless there definitely is a "better way", why stop what is currently working?
SSRIs are highly useful medications. They save lives.
Major depressive disorder or other mental illness can be devastating to a person.
The risk of death from major depressive disorder is approximately between 15 to 50%
depending on what other comorbid conditions there are. It is thus a high risk to stop treatment
that is working.
One's loved ones cannot know truly how it feels or what hell a person is experiencing unless
they themselves had a similar depression.
The prospect of returning to depression if one stops the solution - in this case an
antidepressant - is a good reason for many people to continue their medications.
Major depressive disorder - like many illnesses - once developed and recurrent (meaning it
has a tendency to return) - is a lifelong illness and needs to be treated in a lifelong way, just
as hypogonadism, once developed should be looked at with a lifelong perspective.
Unless there is a better answer (i.e. works better, definitely fewer side effects than the current
medication regimen), I would not attempt a switch.
__________________
Quote:
Originally Posted by Albert
Thank you marianco, you write so eloquently and express your opinion with the patients
interests in mind.
May I ask what are your thoughts on, when you're prescribing drugs, do you look at the
effects of the drugs verses the quality of life issues of the patient. Do you place quality of
life high on the list or are you just interested in what the drug does.
The reason I ask is, some of the drugs I have been give in recent times, either make me to
dopey to lead a normal life and/or total ED and etc. and my doctor is not interested in my
quality of life issues.
Thanks,
Albert.
Side effects are a quality of life issue.
I usually work from a patient's perspective - what they want to achieve. Individual criteria for
quality of life for the person is often high on the list of improvements and targets of treatment
desired.
Sometimes some side effects, though present, are acceptable to the patient because they
payoff for taking a medication is far more important to them - e.g. relieving symptoms of
depression may make sexual dysfunction acceptable as a consequence, when there are no
other options. Since I constantly look for options, unless I can offer a person something better,
treatment is a balancing act between the risks and benefits to the patient.
If a person feels his/her doctor is not listening to them, perhaps also this issue needs to be
discussed with the doctor. If a person feels his/her doctor continues to not listen to him/her,
perhaps a change in doctor is an option to be considered.
Note that due to side effects, many people stop taking their medications anyway. Helping a
patient adhere to treatment is an important task in medicine. Thus side effects automatically
become a treatment issue.
__________________
Antidepressant Mechanisms of Action
Quote:
Originally Posted by Novick
When you say that Wellbutrin primarily works as a norepineprhine re-uptake inhibitor, I
assume you mean as to its efficacy in depression?
I realize there is research that minimizes Wellbutrin's dopaminergic activity as being
relevant to depression (lack in correlation between DAT occupancy and response
[human], questioning the role of dopamine in the forced swim test [rat]). However, the
research does point to the idea that Wellbutrin (and its metabolites) can occupy the DAT
in humans, although not to the extent of say, ritalin.
I'd also think you'd agree that Wellbutrin is qualitatively different and possibly even
acutely more pleasant (not a rush, but pleasant) to take than a pure NRI like
desipramine, reboxetine, tomoxetine. Obviously there are people who have the "freak
out" response on Wellbutrin, as you've alluded to from hyperstimulaton. But anyway, the
properties of Wellbutrin's metabolite that make it dopaminergic without the cocaine-high
have been investigated by Volkow and Fowler.
My research is currently focused on investigating the role of dopamine in depressive
behavior (we work with a strain of rat that goes into learned helplessness very easily yet
is very responsive to drugs like desipramine, nomifensine and bupropion). From what I
gather from current psychiatric practice (and marianco, please correct me here), is that
drugs with dopamine activity can be very useful in depression, however "core"
antidepressant response for most comes from direct modulation of 5-HT and NE
pathways.
As far as I know, Wellbutrin primarily works as a norepinephrine reuptake inhibitor in humans in regard to any of its uses - depression, attention deficit/hyperactivity disorder, sexual
dysfunction, etc. In asking the manufacturer for a literature search and one of its
pharmacologist to write me a report about its mechanism of action - the literature bears this
out. Clinically, I also have not seen a dopamine-related mechanism of action and effect on
patients. If it, for example, can increase dopamine levels significantly, it should be able to treat
restless legs syndrome, treat dystonia, treat Parkinson-like symptoms, etc. Wellbutrin in rats
can block dopamine reuptake significantly - thus the disconnect between human and rat
effects. Wellbutrin’s other mechanisms of action are not clear. I think there should be more to
the story since Wellbutrin is a relatively weak norepinephrine reuptake inhibitor. Some of
Wellbutrin’s side effects resemble anticholinergic side effects (blurred vision, dry mouth,
constipation) but Wellbutrin isn’t known to significantly block acetylcholine receptors. Thus
remains the mystery, after all these years, of how Wellbutrin works.
The response to Wellbutrin that I see is different for each person, as is the response to other
“relatively selective” norepinephrine reuptake inhibitors (NRIs). It is abusable to a mild extent upon learning about how some prison inmates would crush their Wellbutrin pills and inhale the
powder. Some prison inmates, however, will try to abuse anything to feel better - given the
position they are in. Whether or not Wellbutrin is more pleasant in effect than other NRIs
depends on the person’s individual genetically-influenced response. Some patients get sharp
knife-like headaches or nightmares on Wellbutrin, for example. Overall, Wellbutrin tends to
have fewer side effects in clinical use than other antidepressants in most people. This makes
it useful as a first line antidepressant when one wants to primarily increase norepinephrine.
I have not yet seen a “pure” NRI (or "pure" anything for that matter). A problem I encounter is
that the manufacturer or textbook author will often minimize the other mechanisms of action of
a medication (e.g. using words such as “not significantly”) when such a mechanism of action
is clinically relevant - often contributing to adverse effects that are seen in real-life or other
positive uses for the medication. Simplifying the list of mechanisms of action makes the major
actions of a medication more understandable. But it leaves out the finer points which a good
physician can put to great use in helping understand what is happening to a person who
receives a medication.
Desipramine (the active metabolite of Imipramine) is a tricyclic antidepressant which primarily
blocks norepinephrine reuptake. However, it also blocks serotonin reuptake, blocks
muscarinic acetylcholine receptors, blocks histamine H1 receptors, and blocks norepinephrine
alpha-1 receptors.
Reboxetine (which was declined by the U.S. FDA) is primarily a norepinephrine reuptake
inhibitor. However, it also blocks serotonin reuptake; blocks cytochrome P450 enzyme 1A2,
2C9/19, 2D6, and 3A4; and blocks muscarinic acetylcholine receptors.
Tomoxetine (Strattera) is primariliy a norepinephrine reuptake inhibitor. However, it also
blocks serotonin reuptake and blocks dopamine reuptake, among its mechanisms of action.
These are not insignificant mechanisms since they may account for side effects from Strattera
such as nausea, and why Strattera may not work with some people - given how serotonin
reuptake if strong enough for that person may reduce dopamine production.
The primary lesson is to learn as much about what mechanisms of action a substance may
have. The words “not significantly” means someone is arbitrarily setting the definition of
significant - which may not be borne out by experience.
The primary mechanisms of action used to treat depression are to increase serotonin,
norepinephrine, and dopamine. All the antidepressants to a certain extent do all three but in
different proportions, some more selective for one than others. Effexor has variable effect on
serotonin, norepinephrine and dopamine depending on the dose used (with dopamine
reuptake inhibition becoming usually clinically relevant at the higher doses).
Interestingly, cocaine - which is primarily thought of in textbooks as a dopamine reuptake
inhibitor - is not. It fairly equally and strongly blocks reuptake of dopamine, serotonin, and
norepinephrine reuptake. It is not, however, an effective antidepressant, causing more
problems than not.
Another complicating factor in antidepressant treatment: Localization in the brain of receptors.
In general, serotonin reuptake inhibition causes a simultaneous reduction in dopamine
production - possibly (as far as I recall) by inhibiting tyrosine hydroxylase, the primarily limiting
enzyme in dopamine production. However, in some parts of the brain, the dopamine reuptake
transporter and the serotonin reuptake transporter lie very close together on the neuron cell
membrane. Serotonin, it turns out, can also be transported by the dopamine reuptake
transporter. Thus in these areas of the brain, the higher serotonin levels from reuptake
inhibition causes a competition for the dopamine reuptake transporter between serotonin and
dopamine. This effectively increases dopamine levels in that part of the brain. Interesting,
huh?
Increasing dopamine is highly useful in treating depression - being one of the big three
mechanisms. However, a limit to this mechanism is that with medications (other than pure
dopamine) it is often tied to other mechanisms of action - e.g. blocking acetylcholine receptors
(which can cause confusion and other adverse effects). Further, it is important to localize the
effect on the brain. Increasing dopamine in some areas, for example, can cause psychotic
symptoms (e.g. hallucinations, paranoia). Dopamine activity in the brain is further dependent
on so many other neurotransmitters (e.g. serotonin) that teasing it apart from other
mechanisms is very difficult. With Effexor, for example, you have to accept serotonin and
norepinephrine reuptake when you only want to increase dopamine.
Despite the “dirtiness” of present medications, however, while keeping an eye out for adverse
effects, the medications are still highly useful in treating patients with depression. There is a
lot of "art" to the treatment since there are many unknowns and we cannot specifically control
one mechanism action nor easily localize its effects to the desired parts of the brain.
__________________
Quote:
Originally Posted by androjello
I know huh? This guy is incredible! I can sit and read his writings/posts all day. Will be
interesting when I attend Med school next year after reading all the insights of Dr.
Marinaco.
Thank you.
Medical school for me is a distant but great memory. I was lucky enough to go to a medical
school which had no grades - just a pass/fail system. This incredibly improved the enjoyment
of medical school compared to schools which had grades. No grades means you have a class
of 120 friends (as opposed to the tension and the 120 potential enemies who may backstab
you or not share information as in schools which have grades). We worked as a team - the
entire class - in school. We shared old tests. We had several intermural sports teams such as
in basketball and ultimate frisbee. Most physicians hated their medical school experience. I
had a blast. It was a second childhood. Elementary school all over again.
One of the things I did was to "decelerate". This meant to take a year off from studies to do
whatever you want - while still being listed as a medica student. I took this time to self-study
computer science - after realizing classes were too slow - and helped start a medical software
company. And I traveled. The decelerated time is about the only time in one's life when
anyone can completely take off a year to do anything he or she wanted - while still being
under the umbrella of medical school. You can still live off student loans during this time. It
was a great time to "smell the roses". I helped convince a large number of classmates to do
the same. About a fourth of the class did so. Some went to other countries to study medicine.
One went into the desert to meditate. Some wanted to get to know their wives before
disappearing into residency (where you may not be home at all almost all the time). If this is
an option in your medical school, I would strongly look into it. The best time is after the second
year - prior to the 3rd year clinical rotations.
The most important skill to learn in medical school is to learn how to teach yourself. "To learn
how to learn" is the motto my residency program professors wanted to have. I shot them down
on that point - after which they chose a different nondescript motto. I told them a physician
should have learned that by medical school. By residency, physicians should be independent
thinkers and learners.
I do not believe you will get the information I write about in medical school. Medical school is
intense - the equivalent of a complete 4 unit 10-week course taught in one week. But medical
school is very basic. It has to be. To use an analogy: if medical school is analogous to
elementary school, and residency is analogous to high school, then what I do is at the Ph.D
level. Sadly, hardly any psychiatrist I meet, including residency professors, study molecular
pharmacology to the extent I do. And fewer still study neuroendocrinology.
Medicine itself is incredibly complex and data filled. And you forget 99 percent of what you
learn in medical school. What you hope to retain and develop is a saavy or street smarts
about how things work. This is the ability to understand something in a conceptual manner
rather than a rote memorized manner. This allows you do a lot with the material you retain. Its
similar to physics. If you conceptually understand college physics, for the medical school
admission test, all you would need to do well is to memorize a 3x5 inch card of basic
equations. From them you can derive all the others.
Most of the learning you will have about medicine is after your residency, when you truly have
to think for yourself. Its fun to watch how most young doctors mature. Coming out of
residency, the thought patterns reflect primarily book learning, has a rigidity to it. Over time,
they start exploring new things, add to their repertoire - forced to by the demands of real-life
patients. They learn to play jazz - so to speak - as they mature. They learn how to improvise
to form solutions (at least the good ones do). (A good jazz player has good solid
understanding of standard music as a base, from which they can improvise.)
__________________
Quote:
Originally Posted by Novick
Thanks Marianco for your reply. I agree that your insights are invaluable. I can
definitely appreciate the confounding issues of individual variance, receptor localization,
and neurotransmitter-neurotransmitter interactions when trying to tease out
antidepressant mechanism. I also agree that after all these years, wellbutrin in particular
is a bit mysterious.
I also applaud your willingness to accept the effects of psychotropics that most deem
"non significant", such as the receptor and CYP interactions that you've pointed out for
various drugs.
And I suppose that's why I'm going to attempt to convince you further of the
dopaminergic effects of wellbutrin. While therapeutic use of wellbutrin does not inhibit
the DAT to the >50% level that is seen with something like methylphenidate or cocaine,
the literature clearly does indicate that it blocks the DAT in humans (not just rats). The
value in the following studies usually shows values around 20% inhibition in the striatum
for bupropion treatment. One of the most interesting looked at just bupropion's main
metabolite (called radafaxine in the study), and also took into account its
pharmacokinetics. While this value might be "low" and very different from the action of
other DAT blockers (long lasting), it does seem to be a consistent effect of wellbutrin
treatment, something that isn't documented in humans with any other antidepressant (to
my knowledge), including zoloft and effexor (although the people at wyeth seem to be
pretty protective of letting any information out that would indict effexor as being habit
forming).
Thank you for the information. I'll keep it in mind - particularly in interpreting response of
patients. Note that I still haven't seen significant dopaminergic effects but I'll keep it in mind
and not discount it.
The ultimate test of any treatment I give, however, is the response from the patients I treat.
Their improvement in well-being is the measure of the effectiveness of any treatment I
consider. They are the only ones I ultimately have to account to.
Wellbutrin, itself, is a great antidepressant. It is very clean - meaning has relatively few
mechanisms of actions and relatively few side effects - compared to the others. Though in
concept, a multi-mechanism of action medication is potentially more effective than a single
mechanism medication, the main limitation is in one's ability to customize the treatment to the
patient. Every one is different. One or a few sizes do not fit all. Thus, a combination of
Wellbutrin and Lexapro, for example, may do better since you can then better control
norepinephrine reuptake and dopamine reuptake somewhat independently for each patient.
__________________
Quote:
Originally Posted by Novick
Marianco,
What are the dopaminergic effects you notice in your patients recieving high dose
effexor?
Obviously like you've expressed, effexor, like most antidepressants is going to have
consequences on the dopaminergic system (changes in levels and receptor density).
However, it's been my personal experience that wellbutrin "crosses over" much more
with something like ritalin or amphetamine compared to high dose effexor (>225mg). I've
noticed this in terms of motivation, concentration and sense of well being.
While I understand that clinical human respsonse is much more important than effects in
rats, an interesting observation about effexor is that it's documented to increase D3
receptor density in the exact same area of the brain (islands of cajella) that we notice
increased D3 expression in our HYPOdopaminergic rats. The D3 receptor is an autoreceptor that acts as a "brake" on dopamine release. When effexor is given along with a
D3 agonist, rats have trouble discriminating it from cocaine. One interpretation (though
far from the only one) is that the administration of the D3 agonist effectively
downregulates effexor's effect on D3 receptors, preventing their sensitization, allowing
for increased dopaminergic activity. Marianco, do you have any experience with
priampaxole used to augment antidepressants?
At high doses of Effexor, I would expect dopamine effects to take place - including improved
attention, organization on tasks, reduced depressive symptoms, reduced blood pressure
(negating the expected higher blood pressure from increasing norepinephrine).
Unfortunately, almost none of my patients have been able tolerate Effexor at high doses for
long. The one that did tolerate it (with no side effects) had inadequate reponse - continuing to
be depressed despite treatment at about 575 mg a day. Akathisia - from excessive serotonine
activity - is the primary limiting factor. But for the patients I treat, Effexor has not been very
tolerable. I keep it in mind, however, since some do respond to Effexor, particularly at doses
up to 225 mg a day.
Each clinician may have a different experience than I, since everyone's patient population is
different and may have different responses to medications. As the saying goes, "your mileage
may vary".
Note that dopamine activity regulates norepinephrine output in the brain through a tract from
the dopamine nuclei to the locus ceruleus, possibly contributing to some of dopamine's
somewhat paradoxical effects: increased calmness, sedation, and lowered blood pressure.
Pramipexole (Mirapex) is an interesting medication which has its use in psychiatry to treat
depression (besides its neurological use to treat Parkinson's Disease and Restless Legs
Syndrome; and its use in Fibromyalgia). As far as I know, it is a dopamine agonist on D2, D3
receptors, Alpha-2 Norepineprhine receptors (similar to clonidine); it increases Nurr 1 gene
expression (needed for survival of dopaminergic neurons); and is a potent anti-oxidant. Other
effects include reducing norepinephrine output (as described above), reduced thyroid
stimulating hormone (and thus reduce thyroid hormone levels), and increased growth
hormone level. As can be seen, the Mirapex story is not that simple.
As a dopamine agonist, it can potentially improve mood. As far as I know, it is primarily useful
as adjunctive treatment - alone, not strong enough for long-term treatment of depression.
Reducing norepinephrine activity and thyroid hormone levels, if significant enough in an
individual, can also increase depressive symptoms.
I have experience with it. Unfortunately, in the patient population I treat, no one has been able
to tolerate Mirapex. The most common reasons patients stop using it is anxiety,
dizziness/faintness, fatigue, oversedation and reduced alertness.
Some clinicians have more luck with it than I. It depends on the population of patients a
physician has (most of my patients, in general, are under constant, unrelenting, extreme
stress and have very severe, treatment, resistant illnesses - they are not the usual middle
class worried well). Thus, I keep it in mind as an option because it is a relatively clean
dopamine agonist, and may work in some patients where other medications don't.
Other effects to keep in mind: sudden unexpected, uncontrollable attacks of sleep can occur
(this increases the risk of patients getting into car accidents and of dying by accident - thus
one has to be very careful in informing patients about the risks). A patient can also develop
hallucinations and paranoid delusions (limiting its use in patients with psychosis), pupil
dilatation (not good when the patient is stopped by the police), increased heart rate.
__________________
Wellbutrin and Dopamine.
Quote:
Originally Posted by Novick
"At high doses of Effexor, I would expect dopamine effects to take place - including
improved attention, organization on tasks, reduced depressive symptoms, reduced blood
pressure (negating the expected higher blood pressure from increasing norepinephrine)."
So are you saying you don't see these effects with wellbutrin? I guess I'm still a little
unclear about how you're measuring the clinical effects of dopaminergic activity.
Measuring the clinical effects of dopaminergic activity is very difficult without doing a lumbar
puncture or an imaging study that can specifically pick out dopamine activity in the brain.
Dopamine itself can be measured via urine testing as can other neurotransmitters. But I
haven't found it to correlate well with how a person is doing.
Measuring the clinical effects of dopaminergic activity is primarily done from clinical
observation and history from the patient - and monitoring for effects expected from increasing
dopamine or reducing dopamine activity.
Other dopamine effects I would expect: the ability to give a person a sense of wellness and
contentment, the ability to reduce symptoms of Parkinsonism (tremor, stiffness, slowed
movement), the ability to increase testosterone levels, the ability to reduce norepinephrine
output, the ability to treat symptoms of akathisia or restless legs syndrome, the ability to
reduce anxiety and perceived stress, the ability to improve sleep, the ability to improve
memory, the ability to treat hyperprolactinemia.
No. I have not seen the clinical effects of increasing dopamine with Wellbutrin. I have seen
primarily its effect on increasing norepinephrine levels - including improving attention,
reducing depressive symptoms - but not clearly what is a dopamine effect. Wellbutrin clearly
raises blood pressure, not lower it. Higher doses of Wellbutrin increase stress levels greatly since norepinephrine is a signal for stress through the sympathetic nervous system - not
reduce stress as would be expected of a dopamine-increasing substance. Adrenal
insufficiency can occur from excessive doses of Wellbutrin. Adrenal insufficiency is much less
likely to occur if there was a significant increase of dopamine with Wellbutrin - dopamine being
protective at the brain level of adrenal function by reducing stress levels. Thus, Wellbutrin is
not a clinically useful way to increase dopamine in humans - so far in my experience, and in
the experience and research done by a neuroendocrinologist colleague I work with, who has
used Wellbutrin years before I did. I would say the that if it does raise dopamine levels, it does
it insignificantly - not enough to be a useful mechanism of action in the day-to-day treatment of
patients.
Perhaps the metabolites of Wellbutrin may have a more significant action on dopamine.
Maybe one day these will be used as antidepressants. We shall see.
Wellbutrin, despite its limitations on regard to dopamine, is still one of my favorite medications
for increasing norepinephrine levels relatively cleanly.
Deprenyl/Selegiline
Quote:
Originally Posted by Random987
marianco,
Have you ever used deprenyl in your practice?
I have used deprenyl/selegiline often in my practice, though less often recently. I am
reexamining its use - particularly when the selegiline patch comes out. The patch will bypass
intestinal monoamine oxidase, and thus reduce the risk of food and medication interactions
that limit monoamine oxidase inhibitors use.
Deprenyl/selegiline is a monoamine oxidase (MAO) inhibitor that is "specific" at "low" doses
(generally 10 mg/day or less) to the MAO-B type enzyme. This allows it to avoid blocking
MAO-A in the intestines which cause problems of excessive hypertension (and stroke, etc.) in
interactions with certain foods and medications (e.g. stimulants, decongestants, etc.).
MAO inhibitors are great antidepressants. Low blood pressure is one of the most common
side effects, not high blood pressure. I think they tend to be more effective than the other
antidepressants. The problem is that they have so many interactions with other medications
and have so many limits in what foods a person can eat (e.g. no pizza), that many people do
not want the lifestyle changes and many doctors are afraid of it and of others using it.
Hopefully, the MAO patch will at least reduce the intestinal food/medication interaction risks
and improve safety.
Deprenyl/selegiline is relatively safe at low doses. I say "relatively" because it depends on an
individual's susceptibility to side effects. Many people still have significant MAO-A inhibition no
matter how small a dose of Deprenyl is used - thus running the risk of death, etc.
Even at low doses, Deprenyl/selegiline, in general, cannot be used with another serotonergic
medication because of the risk of death from serotonin syndrome (excessive serotonin
activity). Unfortunately, since Deprenyl/selegiline is classified as a Antiparkinson medication,
many clinicians do not realize this and may inadvertently add a serotonergic medication
thinking it is safe - though it is not. I've seen this mistake happen and it was not pretty. If it was
classified as an MAO inhibitor, automatically this would be known. Adding Deprenyl/selegiline
even at 10 mg or less a day to Prozac or other serotonin reuptake inhibitor is very risky. It can
be done but one must be careful. Many medications increase serotonin and this has to be
taken into account. For example, the pain medication Tramadol/Ultram works as a serotonin
reuptake inhibitor, as one of its mechanisms.
The primary problem of oral Deprenyl/selegiline is that the doses needed to keep specificity
for MAO-B is too low for it to be effective in most cases as an antidepressant. At higher doses,
a person is just as well off using other MAOs with lower cost, such as Nardil. It is still
worthwhile considering as an alternative in treatment resistant cases.
MAO Inhibitors primarily increase serotonin levels as their main effect, though they also
significantly increase dopamine and norepinephrine. Given the risks of the use of MAO
inhibitors, and the primary mechanism of increasing serotonin levels, the serotonin reuptake
inhibitors largely replaced them in general use.
Deprenyl/Selegiline can be looked at as a "smart drug" or "nootropic" - and is used by some
practitioners as such. By its stimulant properties and antioxidant properties, it may improve
one's thinking capacity. Perhaps. I think your mileage may vary as with anything else. One still
has to be very careful about the potential for significant interactions and risks.
One using any MAO Inhibitor should carry a medical tag informing others of this so that in
emergencies, the paramedic, ER doctor, etc. does not accidentlly harm the patient by giving
the wrong medication. Simple things such as the over-the-counter decongestant,
pseudoephedrine are off-limits.
__________________
Quote:
Originally Posted by T Man
In your opinion what medications/substances can safely raise Dopamine levels? I want to
talk to my Doctors about this option. I am on Remeron 7.5mg nightly and Klonopin as
needed as I mentioned before (.25 or .5mg twice a week usually). I think I am getting
symptoms of Akastitia when we try to raise my Testosterone levels. I am not certain of
this, but the symptoms seem to be as you described. Anxiety, ants in the pants, burning or
tingling skin feeling. Maybe it is estrogen related as someone mentioned in another
thread. Also I do get restless legs for a short time after taking the Remeron. It goes away
within an hour or so and doesn't affect my sleep.
I also have a low sense of well being or contentment. I always felt content when on
testosterone replacement therapy in the past. I know that I must raise my Testosterone
levels back up to high normal again to feel good. I just can't seem to get this through my
Doctors head. I have been on TRT since 1989.
Once again my problem is that I can't seem to tolerate Testosterone levels above 400
ng/dl. I never had this problem before I went moronic and did a few cycles of high
Testosterone (400-500mg weekly for 10 weeks) and a few other Anabloic/androgenic
agents. I am tired of this anxiety and depression that comes and goes. Could higher levels
of Dopamine possibly help with my situation. The Doctors at a very good reasearch
University don't seem to know what to do or what medications I should take. They
suggested Buspar or Nardil. Or just stay on the Remeron and take Klonopin. Any
suggestions?
As far as I know, akathisia is difficult to create with testosterone alone. Akathisia (I speculate)
is a state created by lowered dopamine activity. But testosterone does the opposite - raising
dopamine activity.
Estradiol (or estrone) created from testosterone (via the aromatase enzyme) can cause
akathisia, agitation, anxiety. Estrogens raise serotonin levels. One mechanism by which this
occurs is that estrogens work in the brain as monoamine oxidase inhibitors (which primarily
raise serotonin). Raising serotonin reduces the production of dopamine - thus akathisia as a
side effect.
Estrogen is extremely potent compared to testosterone. I estimated that in regard to their
roles, estrogen is about 10,000 times more potent than testosterone. A small change in
estrogen level can make a huge difference.
If I was faced with akathisia as a side effect of testosterone treatment from the creation of
estrogen, I would first focus on reducing estrogen activity given how potent estrogen is. In
general, I prefer reducing the offending agent that is causing akathisia.
There are various ways to reduce estrogen activity including aromatase inhibitors,
Diindoylmethane, and Indole-3-carbinol. With any of them, care must be taken since
excessive reductions in estrogen has its own consequences (e.g. memory impairment,
osteoporosis, high cholesterol levels, no sex drive, etc.)
Treatments for akathisia - which can also manifest as restless legs syndrome - include
medications which raise dopamine or act like dopamine, and medications which reduce the
manifestations of akathisia - often primarily by sedation.
Medications used to reduce the manifestations of akathisia include norepinephrine betareceptor blockers (such as propranolol, atenolol), sedative/antianxiety GABA-enhancers (such
as Klonopin), histamine receptor blockers (antihistamines) which calm akathisia down
primarily by sedation (such as diphenhydramine, Remeron). Remeron often reduces akathisia.
I often use it as a treatment. But occasionally the increase in serotonin it causes can also
cause akathisia.
Buspar is worth a try for the treatment of anxiety. However, in clinical use, it rarely helps though it is worth a try because of its relative safety.
Monoamine oxidase inhibitors (MAOIs - such as Nardil) is an interesting call in regard to
reducing akathisia - apparently with the thought of increasing dopamine levels. However,
Monoamine oxidase inhibitors primarily increase serotonin, which may negate the increase in
dopamine if a person already is starting from a lowere dopamine state - such as of akathisia. I
haven't heard or read of its use in the treatment of akathisia. MAOIs are good antidepressant
medications - though are highly limited by the dangerous interactions they have with
numerous medications and foods and the life-style change they require as a result. MAOIs are
good, however in treating anxiety and depression.
Medications which act to raise dopamine or act like dopamine include essentially all the
medications used to treat Parkinson's Disease (an illness due to the lack of production of
dopamine). These medications are tricky to use since excessive doses can cause psychotic
symptoms and anxiety among other serious side effects. However they are useful when used
carefully. Mirapex, for example, is often used in psychiatry when a dopamine agonist is
desired.
Another class of medications which raise dopamine levels are the stimulants such as
methylphenidate, dexedrine. The limitation they have is stress and anxiety from increasing
norepinephrine, besides the taboo of abuse-potential in some patients. Theoretically they can
treat akathisia, but I have not used them so - preferring reducing the causative agent (e.g.
estrogen, antipsychotic, serotonergic medication) or by using one of the medications to reduce
manifestations of akathisia or a more pure dopamine agonist since akathisia at night cannot
usually be treated with a stimulant. Stimulants, however, are valuable adjuncts in treating
depression.
Aside from problems with estrogen or excessive dihydrotestosterone (which can be
addressed), the cleanest way to raise dopamine levels to improve one's sense of well-being is
by raising testosterone level. I have yet to see something cleaner or safer treatment than by
using testosterone. If it takes a high normal level to accomplish this for an individual, that is
what I would aim for. I would not advocate supraphysiologic doses, however. That would be
asking for health problems not wellness.
Unless I run out of options - which is difficult to do with the hundreds of medications available
in my toolkit - I usually would not settle for a partial response to treatment. I usually try for
remission of symptoms - something patients want and - ideally - doctors should strive for.
I am not familiar with the molecular pharmacology or neuroendocrinology of former steroid
abusers - and their post-abuse testosterone replacement problems. SWALE would be more
familiar of how to treat such patients, being part of his specialty. I would bow to his expertise
on this issue.
__________________
SSRIs and Sexual Side Effects
Quote:
Originally Posted by bullmastiff
It seems that ssris raise prolactin, reduce dopamine and ultimately reduce testosterone. Is
there any way of combining ssris with other medications to negate the side effects?Also
are there certain ssris that have less sexual side effects than others? I guess the higher
the dosage the greater the sexual side effects. So at low dosages do these medications not
have sexual side effects?
Serotonin-Reuptake Inhibitors (e.g. Paxil, Zoloft, Prozac, Celexa, Lexapro, Luvox, etc.)
primarily increase serotonin. But they also mildly increase norepinephrine, dopamine,
stimulate serotonin 2C receptors, block muscarinic acetylcholine receptors, interact with sigma
receptors, inhibit nitric oxide synthetase, block the enzymes cytochrome450 2D6, 3A4 or 1A2.
The overall effect of largely increasing serotonin can lead to a reduction in dopamine. This in
turn can lead to reduction in testosterone production and an increase in prolactin.
Actions of SSRIs which may lead to the sexual side effects (e.g. decreased sex drive,
decreased arousal, and/or impaired orgasms) include: the reduction in dopamine, the increase
in prolactin, the reduction in norepinephrine, the reduction in testosterone, the blockade of
muscarinic acetylcholine receptors, the inhibition of nitric oxide synthetase, and the increase
in serotonin.
The sexual side effects will depend factors including:
1. The individual's genetic susceptibility to each action
2. The dose used (the lower the dose, the less of an antidepressant effect a person may have,
however).
3. The particular SSRI used.
All the SSRIs can have sexual side effects - I don't have a preference for one or the other
when it comes to sexual side effects. One's mileage may vary a lot. It may be useful to try
several to see which one can reduce depression or anxiety best, at the lowest dose, with the
fewest side effects.
Counteracting the sexual side effects with other substances may or may not work because
there are multiple actions of SSRIs which lead to sexual side effects. Covering one or some
with one medication thus may or may not work - but is usually worth a try if one wants to keep
the SSRI.
1. Wellbutrin (Bupropion, Zyban) can be tried to reduce sexual side effects. Wellbutrin acts
primarily by increasing norepinephrine. The increase in norepinephrine may be enough to
recover sexual function. (Some believe it also may significantly increase dopamine).
If the dose of Wellbutrin is too high, however, then adrenal fatigue may occur (since
norepinephrine is also a signal for stress). Adrenal fatigue, itself, can lead to other
neuroendocrine changes which will impair sexual function. Wellbutrin, with its simpler
mechanism of action, tends to usually not result in sexual dysfunction. However, it can cause
sexual dysfunction in some people (I think primarily by worsening or causing adrenal fatigue).
From the prescribing information, as far as I recall, sexual dysfunction occurs in about 3percent of patients.
I tend to prefer low doses of Wellbutrin regul****elease (e.g. 37.5 to 75 mg a day) when trying
to counteract SSRI sexual side effects, because adrenal fatigue often is present. SSRIs,
themselves, by increasing serotonin, work to reduce depression and anxiety by reducing
perceived stress which is causing adrenal fatigue.
2. Another alternative to reduce SSRI sexual side effects is to use Viagra (Silfenadil), Cialis
(Tadalafil), or Levitra (Vardenafil). These inhibit the enzyme Phosphodiesterase type V.
Signals from the brain, through peripheral nerves to smooth muscle cells in the blood vessels
of the penis, trigger the production of nitric oxide. Nitric oxide then triggers the creation of
cycle GMP. Cyclic GMP then triggers and maintains an erection. Blocking Phosphodiesterase
type V with Viagra/Cialis/Levitra then prevents the destruction of cyclic GMP - allowing
erections to occur and be maintained.
In women, Viagra, Cialis, or Levitra, may help reduce anorgasmia from SSRIs through the
same mechanism that causes erections in men.
3. Another alternative to reduce SSRI sexual side effects is to use a low dose of a stimulant
(e.g. Ritalin, Dexedrine). Stimulants act by increasing dopamine and norepinephrine.
Increasing dopamine can reduce prolactin level. These stimulant actions directly counteract
three of the SSRI mechanisms of action.
Other alternatives to reduce SSRI sexual side effects (usually by counteracting some of the
SSRI actions) include:
4. Buspirone (Buspar)
5. Amantidine (which increases dopamine release)
6. Dopamine-like medications (dopamine receptor agonists such as Requip/Ropinirole,
Bromocriptine, Mirapex/Pramiprexole)
7. Ginkgo Biloba (which, by speculation, may work by increasing circulation in the genital area
- though there is a small risk of stroke)
8. Cyproheptidine (Periactin - an antihistamine which can block serotonin - which if dosed high
enough can cause sedation, and block the antidepressant effect of SSRIs)
9. Trazodone (though I would stay way from using this in men with normal to high testosterone
levels given the potential to kill the penis via priapism)
10. Yohimbe
11. Serotonin 3 Receptor blockers (antinausea agents such as Kytril/Granisetron,
Zofran/Ondansetron - though at too high of a dose can reduce the antidepressant effect of
SSRIs. They are extremely expensive too - Zofran can run $2000 for a month's supply. Kytril
can cost $50 a pill. These, however, can also be used as smart drugs/nootropics, albeit for the
very rich).
12. Testosterone (which also increases dopamine - particularly if it is not at a high enough
blood level - though estrogen levels need to be monitored and controlled).
13. Progesterone (which can lead to increased serotonin, norepinephrine, dopamine, GABA
levels, and may improve adrenal function since progesterone can be turned into cortisol by the
adrenals - particularly if the blood level is low - though if the dose is too high (e.g. men
produce about 10 mg a day, as far as I recall, thus replacement doses need to be less than
that), may cause gynecomastia by increasing sensitivity to estrogen through increased
estrogen receptor production).
14. DHEA (which is a mild androgen, which can lead to higher testosterone levels - 7-KetoDHEA may be an alternative (though untested) - since DHEA can lead to hair loss and acne).
Note that increasing norepinephrine can increase adrenal fatigue or precipitate mania.
Increasing dopamine excessively can cause mania or psychotic episodes. A doctor's
supervision is necessary in these treatments since serious adverse effects may occur.
__________________
Re: Antidepressants and Activation
Quote:
Originally Posted by T Man
Which of the SSRI's is the least activating? I am told that Prozac will hype you up the
most. I know that it was activating to me. Is Prozac known to be the biggest activator?
Which one is known to have the least activating effect? Prozac, Zoloft, Paxil, Luvox,
celexa, lexapro? I tried Paxil for a few days about 5 years ago and it seemed to make me
feel slightly sedated. But a Doc told me it is just as activating as all the rest. Not from
what I felt.
Also is Buspar an alternative to SSRI's? Does it have the same clinical effects on
depression/anxiety/panic/OCD that the main SSRI group has??? Someone told me that it
won't activate you or make you anxious as the SSRI's because it only raises certain
serotonin levels and not all. Whatever that means. Docs please.
The "activating" phenomenon of SSRIs may occur as a result of:
1. the increase in serotonin (which over time helps improve adrenal function - and energy), or
2. an increase in norepinephrine and dopamine (from norepinephrine reuptake inhibition and
dopamine reupatke inhibition), or
3. a reduction in dopamine (resulting from the increase in serotonin, which inhibits dopamine
production).
4. etc.
The reduction in dopamine may result in a condition called "akathisia". This is a psychomotor
disorder with varied symptoms including: agitation, anxiety, restlessness, fidgetiness,
insomnia, irritability, a feeling of ants in one's pants, a feeling of wanting to jump out of one's
skin, etc. Akathisia may contribute to behaviors including suicides that have resulted from
treatment with antidepressants.
The sum effect of any SSRI depends on the mechanisms of action of the SSRI, the person's
genetic predisposition to response to any and all of the SSRI's actions, the dose of the SSRI,
etc.
What will happen to any given individual cannot be fully determined until that person tries the
medication.
For example, for some people, Paxil causes "activation" or "akathisia" because it is the most
potent serotonin reuptake inhibitor. In others, Paxil's antihistamine action outweighs the other
effects and causes sedation.
Prozac may have the reputation as the most "activating" SSRI. But that cannot be applied to
the individual person. Some people would be sleepy on Prozac.
"Activation" depends highly on the dose used. Since Zoloft is the least potent SSRI (since a
higher dose is needed for the same effect as the other SSRIs), one can make a case that
Zoloft is the least activating when used at the same dose as the other SSRIs. Of course, that
dose of Zoloft may not be in its effective range. Zoloft is also usually not taken over 200 mg a
day since side effects may rapidly occur.
In clinical use, in regard to potency as a serotonin reuptake inhibitor (outside of the other
multiple mechanisms of action, and outside of the dose used), I would rank the SSRIs as
follows: Paxil > Lexapro > Prozac > Celexa > Zoloft > Luvox. Clinically, when treating an
individual, this ranking does not mean much since there are so many other variables to take
into consideration. These include: the person's prior experience with SSRIs, side effects,
interactions with other medications, etc.
In general, each person has to try each SSRI to find out which is more activating than the
others. The "activating" effect occurs very rapidly, depending on the dose. Thus one can tell
quickly whether or not they like a particular medication. One does not have to wait weeks to
find out.
Akathisia, as a side effect, usually does not go away. I use it as "the glass ceiling" - the dose
limit of an SSRI - meaning the dose is too high if it occurs. And I tell patients to automatically
reduce the dose if it occurs.
Buspar is usually not an effective antidepressant when used alone. It can help reduce anxiety
in some people. It is also used as an additive - help help an antidepressant work better.
Buspar's effects have been highly variable - often not working at all. But it is worthwhile to
keep in mind since some people respond to it well.
Re: Antidepressants and Activation
Quote:
Originally Posted by r100proof
Where would Effexor XR fall in the SSRI effect per dose of drug when compared to the
other SSRI's. I am making the change from 20mg's of Lexapro to 75mg of Effexor XR. It
was one week at 10mg Lexapro with 37.5mg's of Effexor to 2nd week 75mg Effexor with
no Lexapro. When the Lexapro was totally dropped 2 days ago....I am noticing less
energy and a lower mood. Does the dose just still have to be adjusted higher in your
experience?
It is difficult to compare Effexor with the SSRIs because individual response varies greatly.
However, as a ballpark approximation, 10 mg of Lexapro and 150 mg of Effexor are
approximately equivalent. At about 150 mg, Effexor is mostly an SSRI, with a mild increase in
norepinephrine reuptake (again depending a lot on individual response).
__________________
Re: Antidepressants
Quote:
Originally Posted by Dopamineloveaffair
Bringing iron levels up will also help with the RLS since it is a co-factor in dopamine
synthesis.
It is important to not take too much iron. Unless one is regularly bleeding - as in menopausalage women - supplemental iron stores can build up to the point of toxicity.
Blood Work and SWALE
1. Unfortunately, SWALE is no longer here.
In regard to sexual function and SWALE's protocol, some thoughts:
2. THYROID FUNCTION: I prefer Free T3, Free T4, TSH to best understand thyroid function.
Free T3 is the actual functioning thyroid hormone. TSH is the brain's opinion of how much
thyroid hormone is present. Unfortunately, it can be inaccurate.
3. INSULIN RESISTANCE OR DIABETES: clues include obesity, hypertension, high fasting
blood glucose, triglyceride to HDL ratio (>3.5), low SHBG, low testosterone level.
4. ADRENAL FATIGUE: useful labs include cortisol AM and PM, DHEA-s, fasting blood
glucose, progesterone, albumin, sodium, potassium. Adrenal fatigue is not a recognized
illness. It is often a component of other conditions such as anxiety, depression, sexual
dysfunction, chronic fatigue, irritable bowel syndrome, overtraining, "stress", obesity,
insomnia. If it isn't addressed, the person often has only partial response to treatment. See the
adrenal thread.
5. TESTOSTERONE: Low testosterone levels may not only lead to low sex drive but
osteoporosis, heart disease and stroke. Testosterone activity is tied to activities of other
factors including: estradiol, progesterone, sex hormone binding globulin, etc.
6. SHBG: Low SHBG may lead to transient high free testosterone but in the long-run it may
lead to low free testosterone since SHBG protects testosterone from destruction (free
testosterone lasts about 10-100 minutes before it is destroyed by the body). SHBG also has
its own receptors to which it triggers signals to cells when testosterone or estrogens are
bound to SHBG. SHBG is increased by estrogens, thyroid hormone. SHBG is lowered by
agents such as: testosterone, DHEA and other androgens, insulin (e.g. insulin
resistance/diabetes), growth hormone, and some liver enzyme inducers (such as certain
antiseizure medications).
7. CBC: excessive red blood cell production is one possible side effect of testosterone
replacement therapy. The CBC is usually monitored as a result.
8. MISSING VALUES FROM SWALE'S PROTOCOL: LH, FSH, Estradiol, Cortisol
Re: help with libido problem
Quote:
Originally Posted by marker
I am 36 and have never used steroids.About 1yr+ ago I noted that my libibo did not feel
normal. ... Although I would have days I thought I was improving,[slight libido increase]
90%+ of the time libido was abnormally low, and would revert back after a few days.
[january 06]
total test. - 765 ng/dL ref.[241-827]
free.test. - 17.7 pg/mL [8.7-25.1]
DHT - 44ng/dL [30-85]
DHEA - 681ng/dL [146-850]
estrogens, - 250pg/mL [40-115]
total
[june-06]
total test.- 714 ng/dL [241-827]
TSH - 2.29mIU/L [0.4-5.5]
prolactin - 6.3 ng/mL [2.0-18]
FSH - 8.5mIU/mL [1.6-8.0]
LH -9.2mIU/mL [1.5-9.3]
total estrogen -116pg/mL [<130]
estradiol -<32pg/mL [0-54]
The doctor felt the elevated FSH was the problem, and wanted to start me on injectable
teastoterone.
To give you an idea of my libido, I have been inactive since January-05 and on a purely
physical level do not even care. I have to push myself to even masturbate. I could even go
without that, but do every 1-2 weeks to try to keep some activity, and avoid any shutdown.
I still get overnite erections-probably 50-60% of nights that Im aware of. Even with
erections, there is minimal urge to ejaculate. The sensitivity of the genital region is low.
Having morning erections is a good sign. When total testosterone level is good, I would look at
other causes for lowered libido (a brain function).
Adding more testosterone by injection, long-term, seems unusual a solution. Depotestosterone tends to get stored in fat cells, increasing the production of estrogens. If high
estrogen activity is the problem, this may worsen the problem. Short-term use may be useful
to check the patency of negative feedback to the hypothalamus-pituitary.
Whether or not estrogen is a problem is not clear since the estradiol level is not clear -
estradiol being usually the most potent of the naturally occurring estrogens. Either a low
estradiol or a high estradiol may lead to low libido. The current estradiol level (<32 pg/ml) may
indicate that estradiol is too low (though having an accurate value would be helpful). Thus
taking an anti-estrogen would be expected to have no effect or worsen the problem of low
libido. Taking an aromatase-inhibitor may lower estradiol and estrone, but in some, it may also
lead to a higher total estrogen level - as other forms of estrogen are made.
More data appears needed - e.g. Free T3, Free T4 (TSH is not enough), progesterone,
cortisol (AM and PM), DHEA-s (not DHEA which varies rapidly), comprehensive metabolic
panel with a fasting glucose, insulin level, a sensitive estradiol level which is accurate (not a
vague <32 pg/ml), neurotransmitters tests, etc. More history is also needed - e.g. height,
weight, body fat, blood pressure, other health problems besides libido, energy level, level of
physical activity, appetite, diet, visual changes, sleep quality, mood, stress level, medications
and supplements, etc. There are numerous variables that determine libido.
__________________
Re: Doctors: Can HRT trigger severe hypogonadism?
Quote:
Originally Posted by pcgizzmo
Because of the HPTA when you introduce external testosterone there will be shut down.
At what levels and how long it takes for this shutdown to occur I don't think is known. It
seems to be different for each person. When Dr's first give Andro Gel the dose is often not
high enough to address the amount of T that is being produced as well as make up for the
HPTA shut down. Consequently the body stops making T and you are left w/a level that
us much lower than what you started with even being on replacement therapy. You are
often left feeling much worse than you did before the therapy.
I like Paul's explanation.
At certain doses, usually lower doses, TRT can result in lower testosterone levels than
baseline. It is evident in the prescribing guidlines for Androgel itself.
Transdermal testosterone can cause a large increase in Dihydrotestosterone (DHT). DHT can
cause fat accumulation - unlike Testosterone. It may give secondary sex characteristics and
helps libido, but excessive amounts has its downsides.
I would question the need for Testosterone pellets, testosterone cypionate, HCG, and Deca all
at once. I highly doubt that an anti-aging doctor would chose Deca. Be that as it may,
hopefully things turn out well.
__________________
Re: Reference Range question
Quote:
Originally Posted by Stonecutter
Just a question for you folks. You are probably aware that alot of labs use different
ranges for total and free testosterone among other things. My question is: do all the
different Testosterone reference ranges translate out to the same thing or do labs just use
different ranges?
For instance does 241-827ng/dl = the same thing as 210ng-1285ng/dl = the same thing
as 300-1000ng/dl. This is the assertion of one of my parents who is a lab tech. So
basically a score of say 300ng/dl could actually mean(237ng/dl, 382ng/dl etc) based on
which lab/ref range you used, even with the exact same amount of T in the blood. it
doesnt make sense but its supposed to be "common lab knowledge" or something.
Thanks for anyone who knows the answer of this!
The actual value obtained is what is important, along with an idea of margin of error.
The reference range can then be chosen by the physician depending on what the physician is
evaluating. The lab's reference range can be used as a starting point, but whether it is useful
depends on what the physician is trying to evaluate.
Unfortunately, labs don't publish their methadology for determining their reference range. To
me, this makes the absolute endpoints somewhat arbitrary given the high variability between
different labs for their reference range.
For testosterone, generally, in various guidelines, hypogonadism occurs frequently at a total
testosterone of under 300 ng/dl. However, hypogonadism also occurs at higher doses
depending on the clinical presentation.
The labs reference range can be used as a starting point for evaluation, however, it has to be
meshed with the physician's clinical experience, knowledge of the condition evaluated, and
the patient's history and exam.
__________________
Adrenal Fatigue
I believe that when you seek to balance one neurotransmitter/hormone system, you have to
also examine and balance the rest. They are all closely connected in their functions. From a
mental health point of view it is important to optimize functioning in the
neurotransmitter/hormone systems involved in reproduction (e.g. estrogens, testosterone,
progesterone), adrenals (e.g. cortisol, DHEA, norepinephrine, epinephrine, dopamine, etc.),
thyroid, pancreatic (e.g. insulin), besides the brain-involved neurotransmitter/hormone
systems.
For example, in order for the thyroid hormone activity to function, adequate serotonin is
necessary.
One of the important functions of testosterone is to limit adrenal activity - essentially to quell
the stress response so that it does not rage on uncontrollably. Testosterone both causes a
reduction of ACTH production from the pituitary, and directly reduces adrenal activity - both
reducing the production of cortisol. Testosterone, by also increasing brain dopamine
production, causes a reduction in norepinephrine production from the locus ceruleus.
Norepinephrine is a signal for stress.
A high cortisol is one indicator of the amount of stress a person is experiencing and is trying to
cope with - unless one is dealing with an adrenal disease state such as Cushing's Syndrome.
Another would be high norepinephrine levels.
If anything, I think the best ways to reduce such stress include: 1) behavioral and
environmental interventions to reduce stress, 2) increasing serotonin to help provide a buffer
against the perception of stress - i.e. things hurt emotionally less, 3) optimizing testosterone
level to control the adrenal stress response. When these don't work, other measures - often
other psychiatric medications - are used. Improving the brain's ability to produce GABA, for
example, is one of the alternatives - GABA being an inhibitory neurotransmitter than can help
induce calmness - which is modulated using anxiolytic and other medications.
I am not sure that limiting adrenal output is necessarily the best thing to do because that also
limits a person's ability to generate energy and get the body ready to respond to stress. The
adrenal glands are like a car's transmission, where the brain is the engine. If the transmission
is regulated, then the cars ability to accelerate when needed may be compromised. I think it
would be better to reduce the stresses that necessitate increased adrenal output in the first
place - before the adrenals fatigue.
Adrenal fatigue is a highly important condition to treat. It is a very common condition in our
highly stress-filled lives. Adrenal fatigue is like having a transmission that is broken or is stuck
in neutral. Pressing the accelerator pedal accomplishes nothing - which is what people with
adrenal fatigue feel - the inabilitiy to generate energy on-demand.
Adrenal fatigue is most easily determined using saliva tests of DHEA and Cortisol levels done
multiple times in one day. This is more sensitive than the blood tests. Adrenal fatigue can be
evidenced also by low DHEA, low Cortisol, low progesterone levels. Hypothyroidism often
occurs with Adrenal fatigue - possibly from the resulting impairment in production of
neurotransmitters necessary for thyroid function, such as serotonin.
__________________
Quote:
Originally Posted by SPE
As I understand it, the ACTH Stim is THE FINAL say wrt adrenal issues. It measures
how your body reacts under stress with cortisol. If the response is low, then your
response to stress is low. Individuals with cortisol levels in the normal range as identified
by a saliva test, could have very poor responses to stress and therefore feel bad. This is
also adrenal insufficiency.
The problem of using blood tests such as serum cortisol and ACTH-stimulation is in the
interpretation and design. The tests are often designed to look for extremes such as in
Addison's Disease and Cushing's Disease. It is more difficult to interpret for disorders that
involve small changes from the average.
As another example, often the "normal range" for TSH (thyroid stimulating hormone) is
between 2.0 to 5.0. The problem is that this norm was arrived at without excluding people with
hypothyroidism. Thus the numbers are skewed. Using the normal range, a TSH under 5.0
would be thought of as being normal and not hypothyroid. But that is not the case. If the Free
T3 and Free T4 are checked, often such a person would be hypothyroid. As a result, I use a
TSH of > 2.0 to determine hypothyroidism - verifying it wiht the Free T3 and Free T4. In other
words - the TSH is essentially useless in determining hypothyroidism. It would be best to just
check Free T3 and Free T4.
When it comes to hyperthyroidism, the TSH is also not very useful. It often a TSH near zero
stirs alarm when no alarm need be there. The TSH is the brain's idea of how much thyroid
hormone activity there is. It is not necessarily how much thyroid hormone is actually there -
because there can be a disconnect in disease states. A truer measurement of hyperthyroidism
is the Free T3 and Free T4.
__________________
Thyroid Hormone and Serotonin
Quote:
Originally Posted by SWALE
Mariqanco--Do SSRI's increase T4 to T3 conversion (outside of their ability to through
stated purpose of reducing stress for the patient)?
I corrected my note - removing that reference. Mea culpa - I shouldn't write when I'm tired.
Thyroid function and serotonin activity are highly linked. Both need to be addressed to
optimize function.
T3 (the active thyroid hormone created from T4 in the liver by the 2D6 enzyme) desensitizes
presynaptic serotonin autoreceptors - thus leading to an increase in serotonin production.
Giving T3 induces serotonin production. Similarly, in hypothyroidism, serotonin production is
reduced. T3 augments the effects of serotonin-increasing medications (such as the SSRIs) by
the additive effect both have on desensitizing presynaptic serotonin autoreceptors.
Serotonin stimulates hypothalamic TRH production, leading to an increase in TSH production
from the pituitary. Adequate serotonin production is necessary to maintain thyroid hormone
levels. Increasing serotonin levels with an SSRI may thus help improve thyroid hormone
production.
A caveat: Theoretically, an excess serotonin may lead to the opposite reaction. For example,
excess serotonin leads to reduction in dopamine production, which then leads to increased
norepinephrine production, leading to an increased stress response and cortisol production.
High levels of cortisol (which can also be caused by high stress levels, low testosterone, etc.)
can directly lead to suppression of pituitary TSH secretion, and impair conversion of T4 to T3,
and can impair serotonin function (by reducing serotonin receptor density, increasing
serotonin uptake via increase in serotonin transporter production, and by increasing
tryptophane oxygenase production in the liver - thus reducing tryptophan, the precursor to
serotonin).
It may be thus important to have an idea of serotonin levels (unless one has a good clinical
feel as to a patient's clinical response to assess serotonin levels - as a psychiatrist may have)
by measuring urine serotonin levels. This, somewhat, correlates with brain serotonin levels,
though I am still assessing this for clinical utility.
__________________
Adrenal Fatigue and Cortisol Levels
Quote:
Originally Posted by SWALE
If somneone cuts you off in traffic on the way to the draw point, that will falsely elevate
your cortidol level. So may the sight of the needle.
From my point of view, that is not a falsely elevated cortisol level. It is exactly what you want.
However, it is important to take into account the patient's psychological status and stress
during the day to help interpret the cortisol level - to help determine if an appropriate adrenal
response to stress is occurring.
Under stress, it is important that the cortisol level be elevated. If it is not, then that certainly
helps diagnose adrenal fatigue. If it is elevated, then one cannot for certain diagnosis adrenal
fatigue unless there are more data points - i.e. more tests done.
Adrenal gland output is not static - it varies from moment to moment. The adrenal glands
respond microsecond-to-microsecond to the signals received from the brain via the
sympathetic nervous system and the hypothalamus-pituitary gland. The adrenal glands then
produce the necessary neurotransmitters/hormones to rally the body's resources, to help the
brain respond to whatever stress the person experiences. The adrenal glands provide ondemand energy to help a person respond to stress.
Stress is anything that breaks homeostasis. It can be as little as lifting a pen, to extremes such
as repeated traumatic rapes in childhood (where the memory of which is indelible and is
constantly involuntariliy relived like a movie overlying one's present experience).
In adrenal fatigue, with constant exposure to stress signals, the adrenal glands become
unable to respond with enough of the neurotransmitters/hormones needed to help the brain
respond to stress. It sputters. There may be times, usually short, where it is adequate; and
frequent times when it is inadequate. There often is no on-demand energy generation.
The best test, then, for a sputtering adrenal gland, is continuous monitoring (such as with a
cardiac Holter monitor, or portable EEG device) which would allow the clinician to correlate
adrenal gland function with a person's psychological status and stresses during a day. This
can then be drawn on a chart as three curves with the time of the day as the horizontal axis.
However, we do not have this yet. What we have are single points on the graph. Often we
only have one point - the morning cortisol. That makes it difficult to determine what the
adrenal status is.
I like the saliva test in that
1. It is fairly low stress (essentially - chewing on a cotton wad to saturate it with saliva) and
thus itself does not interfere as much with the measurement process (The Heisenberg
Uncertainty Principal comes to mind).
2. It can be easily done multiple times a day - thus providing more data points to help
determine if adequate adrenal function is present.
3. It can be done where it matters most - where a person lives, works, etc. in whatever activity
the person is trying to accomplish (similarly to how it is important to measure blood pressure
at home, at work, and in whatever activities one has - to gain a better understanding of a
person's hypertensive response. When my patients see me, their blood pressures, which are
normal in their primary care provider's office, is high in mine - particularly since they have to
talk about highly stressful experiences when they see me that they do not have to recount with
their primary care provider).
With a patient journal of their activities and psychological status, one has a great correlation
between adrenal output and stress at multiple times in a day - multiple data points to give one
an idea of the adrenal response curve. Adrenal fatigue sticks out like a sore thumb when this
is done.
Contrast this with a blood test, where a person has to go to a lab, get poked with a needle,
and can probably only do this at most two times in a day. At least with a saliva test, you can
get four data points easily - eight or more if you want to be obsessive. The stress of the blood
stick is an artificial one and will vary depending on the person. With only one or two data
points, other labs are important to help obtain clues if there is adrenal fatigue - e.g. DHEA-s,
progesterone level, sodium, potassium, etc.
__________________
Saliva vs. Blood Test
Quote:
Originally Posted by 1cc
I had blood cortisol levels above the top of the range and yet when I did Saliva test it
showed that my cortisol levels were low (below normal).
When there is a divergence in a saliva vs. blood test, it may be necessary to obtain additional
information.
A single series of low saliva cortisols, however, does give strong evidence of adrenal fatigue since one is trying to find at least a single instance of inadequate adrenal output in response
to stress - particularly when correlated with the history. When adrenal fatigue is severe
enough, it may show up in all indicators.
A high test in one does not exclude a low test in another - they are not mutually exclusive. The
results depends on additional factors.
Additional helpful information for the interpretation:
1. What is the person's psychological state at the time of the tests?
2. What is the stress faced at the time of the tests?
3. What are the additional test results: DHEA-S, progesterone, sodium, potassium level,
urinary serotonin level, thyroid hormone level, etc.
Testing a quickly changing value to find an abnormal result can be difficult. For example,
testing for the presence of seizures by EEG is often hit or miss. If a person is not actively
seizing, no abnormality may be found. This does not exclude the diagnosis of a seizure
disorder - however. Sometimes, some deep seizures need special techniques - such as
probes inserted deep into one's nose - to catch the seizure - when normal EEGs show
nothing. The diagnosis of a seizure disorder is thus often made by history alone.
A sputtering adrenal gland can show up normal or high in cortisol output under some stressful
situations. It reminds me of one patient who had four cortisols and two DHEA levels in one
day. The DHEAs were normal. The morning, afternoon and midnight cortisols were low. The
dinnertime cortisol was sky high - correlating with the high stress dinner he had due to family
arguments. The presence of low cortisols - e.g. the low morning cortisol- and his history and
exam (e.g. pupillary constrictor strength fluctuations in response to oblique light) - supported
adrenal fatigue as the diagnosis.
__________________
Albumin and TRT and Adrenal Fatigue
Quote:
Originally Posted by zadok
My FT level will not raise above the bare minimum, TRT, or no TRT. TT can be v high,
but FT is always v low. It is not Estrogens causing the prob cause i have eliminated that.
SHBG is v.v low also. Scientifically, the test must be going somewhere, or binding to
something else, which must be high. My question is what else does test bind to? My
Albumin is high normal 46nmol/l (35-50), however i dont think that would be causing this
problem, what else could it be?
Total testosterone consists of:
1. Testosterone strongly bound to Sex Hormone Binding Globulin - inactive
2. Testosterone weakly bound to Albumin - potentially active
3. Testosterone which is free - fully active
Measuring Bioavailable Testosterone (free and weakly bound) is important when questioning
the effectiveness of TRT, if free T is low.
Albumin makes up about 70% of the circulating protein in the blood. It is highly important to
maintain blood pressure and to transport other substances.
By weakly binding Testosterone, Albumin protects Testosterone from being destroyed in the
liver. Free Testosterone itself may last only about 70 minutes before being destroyed.
Testosterone bound to Albumin may be considered the body's way to create a natural
extended-release form of testosterone - just as medications often come in an extendedrelease version.
High albumin level is primarily associated with dehydration.
Dehydration and high albumin level is one possible clue that adrenal fatigue or insufficiency is
occurring. In adrenal fatigue or insufficiency, besides cortisol and DHEA, not enough
aldosterone is produced. Aldosterone is important in maintaining sodium level, fluid and salt
balance in the body, maintaining blood pressure.
Adrenal fatigue or insufficiency may contribute to sexual dysfunction (and other conditions)
and can lower testosterone production.
__________________
Frustration and Adrenal Fatigue
Quote:
Originally Posted by zadok
No doctors can get my FT to raise above v.v low levels. My TT can be very high, but FT
will not go up. (SHBG is vv low as well) Actually the higher TT goes, the lower FT goes. I
had E2, Estrone and Estriol tested and they are all low normal. I am so frustrated, I have
been like this for 1.5 years, no sign of getting better.
When bioavailable testosterone levels and total testosterone levels and estrogen levels are
good but sexual dysfunction/depression/anxiety/frustration/etc. persists, then the most
important step I've found is to check for adrenal fatigue.
When many of my patients describe feeling "frustrated", "desperate", "crabby", "grouchy",
"moody", "snappy", "touchy" - when they are irritable, have frequent mood swings, have
frequent panic - I look for adrenal fatigue.
Whenever a patient repeatedly calls me in a crisis, I look for adrenal fatigue.
The inability to maintain a stable temper or mood often indicates that one's ability to adapt to
stress is overwhelmed or impaired.
The adrenal glands - which are specialized components of the peripheral nervous system like
the hypothalamus is a specialized component of the central nervous system - are one of the
main components of our body which allows us to adapt to stress.
When the adrenal glands are well-functioning, but stress is very high, the excessively high
cortisol levels produced can cause depression, mood instability, and psychosis. The high
cortisol levels can cause insulin resistance, which then lower testosterone production and
cause sexual dysfunction.
When the adrenal glands are worn down by chronic stress, the low cortisol levels produced
(as well as low levels of the about 150 different neurotransmitters and hormones produced),
lead to mood instability, depression, anxiety, low testosterone production - and sexual
dysfunction.
__________________
Adrenal Fatigue and Stimulants
Quote:
Originally Posted by mxim
are you saying a longer acting stimulant would protect me from potential adrenal fatigue
? is it only seen with short acting drugs like ritalin? can using these drugs cause
PERMANANT damade to the adrenal glands?
Would you please point to the post where you came to your conclusion? Thanks.
All stimulants (both short and long-acting) demand more output from the adrenal glands. One
metaphoric way of looking at this issue is that the adrenal glands are like the engine of a car.
Using a stimulant is like pressing the accelerator pedal of the car.
All stimulants can eventually wear down the adrenal glands causing adrenal fatigue. Longeracting stimulants can also cause adrenal fatigue. However, because the peak blood levels are
lower, there is a lower risk of doing so. However the higher dose dose, the higher the risk of
adrenal fatigue.
I do not know if they can cause permanent damage to the adrenal glands. I have yet to see a
case of that in my more than 15 years of practice.
Total failure of the adrenal glands - an Addison's Disease crisis - quickly causes death (in
about a day) since cortisol is absolutely necessary for life.
I haven't seen cases of Addison's disease (severe adrenal insufficiency) in patients treated
appropriately with stimulants.
__________________
Adrenal Fatigue and Cortisol Levels
Quote:
Originally Posted by zadok
Cortisol is low normal, so it cant be that....
When a person has a low normal blood cortisol level, Adrenal Fatigue may be suspected.
The problem of using blood tests to determine the presence of Adrenal Fatigue is that the
tests are designed for determining the extremes of adrenal function - such as Addison's
Disease (where there is near zero cortisol produced) or Cushing's Disease (where there is
excessive cortisol produced).
Adrenal fatigue is a deviation from the mean which is not recognized by endocrinologists as
an illness because it is not extreme, but which can cause devastating behavioral symptoms
and impairment, nonetheless. The signs of Adrenal fatigue are not far from normal - thus a
primary care physician may not find anything wrong.
Blood test findings may include (not all may be abnormal - its the pattern that clues us in):
1. low normal cortisol
2. low to low normal DHEA
3. low to low normal progesterone
4. low potassium
5. low sodium
6. low normal blood sugar
7. low normal hemoglobin A1c - with a low normal mean blood sugar
The best test I've found so far is doing a saliva test at least four times in a day for cortisol and
DHEA. The saliva test is more sensitive than the blood test for deviations near the mean.
Here, adrenal fatigue sticks out like a sore thumb.
In adrenal fatigue, the adrenal glands have not failed - like in Addison's Disease. Rather, then
"sputter" - unless severe - where they may sometimes work, and sometimes not.
Other clues to adrenal fatigue (without other illnesses such as diabetes or hypertension):
1. low normal blood pressure (for which a person would receive praise and told they will live
long - with the primary care physician totally missing the presence of adrenal fatigue by not
doing further investigation).
2. sugar cravings
3. salt cravings
4. fatigue or sleepiness in the late afternoon
5. insomnia
6. occasionally feeling lightheaded when changing position
7. feeling cold often; low body temperature
8. a tendency to tremble, particularly under pressure
9. feeling better after a meal (unless severe)
10. low libido
11. lack of energy - in the morning making it difficult to get out of bed.
12. wanting to sleep in late
13. feeling better when stress is reduced - such as by going on vacation
14. needing coffee or stimulants to function
15. frequent colds
16. PMS symptoms in women
17. depressed or anxious mood, irritability, difficulty handling strress
18. irritable bowel symptoms
19. asthma-like symptoms
20. difficulty in concentrating, impaired memory
Many symptoms of adrenal fatigue are similar to the symptoms of having low testosterone e.g. low sex drive, depression, fatigue, poor concentration, anxiety, irritability, etc.
One of testosterone's roles is to prevent overdriving the adrenals. It limits the stress response
so that stress is not chronic. It reduces pituitary ACTH secretion, which reduces cortisol
production. It also directly reduces adrenal gland output, independent of ACTH.
Thus, when a person develops low testosterone (or low progesterone for women), such as
with age, he is also susceptible to developing adrenal fatigue.
__________________
Hormone replacement priority
Quote:
Originally Posted by SPE
Looking at these, many progressive doctors would say I have secondary hypogonadism.
BUT, my cortisol and DHEA are both low. Which brings me to treatment. Upon going on
testosterone and getting my levels into the UPPER 3/4's, I still felt blah. It wasn't until the
addition of armour, then isocort that I really began to feel better. In a case such as this,
WHY ARE TESTOSTERONE LEVELS TREATED WITH TESTOSTERONE? Isn't this
treating the secondary effect and NOT the cause? Would treating testosterone with an LH
analog be more appropriate? I have now doubt that improving both cortisol and thyroid
will improve the above testosterone number. Adding in something like HCG, Selegiline,
or tamox/clomid would address part of the cause, wouldn't it? Maybe I'm just rambling.
Having one hormonal deficiency does not exclude having others.
It is possible to have low testosterone and reproductive hormone imbalances, adrenal fatigue,
insulin resistance, low thyroid, etc. all at the same time.
Low testosterone due to low LH means either there is a pituitary tumor or the pituitary gland is
aging, among other causes.
The choice of testosterone replacement therapy is really up to the doctor and the patient.
Each type of replacement therapy has benefits, risks, advantages, and disadvantages. The
treatment has to be individualized.
Direct exogenous testosterone replacement via injection or transdermal solutions have one
advantage of being easy to do, directly replacing what is missing. The primary disadvantage
being shutting down testicular production.
Human Chorionic Gonadotropin injections may also work. But as the testes age, they may not
respond as well over time to HCG. HCG is also very fragile and sometimes is in short supply.
When it works, it does have the advantage of having nearly full function of the testes - with the
production testosterone and other hormones, sperm production, etc.
Selegiline increases dopamine, which can increase testosterone production. The problem is
that it also may increase serotonin and norepinephrine, has interactions with other
medications and foods, which complicates treatment. It is not as clean as simply adding back
testosterone.
Tamoxifen/Clomid work for some men, by blocking estrogen receptors at the hypothalamus,
increasing production of LH. The question with an aging pituitary is if the LH can be increased
enough. Can the testes produce enough testosterone. Tamoxifen and Clomid are both weak
estrogens, and thus pose risks of excessive estrogen activity including blood clots.
Arimidex and other aromatase inhibitors can increase testosterone, while minimizing estrogen.
Is the increase enough - is one question. Does the low estrogen activity pose a risk (e.g. high
cholesterol, osteoporosis, etc.) - is another question.
In regard to balancing hormones, there is a priority in treatment to consider. For example:
1. Diabetes - when insulin resistance is severe enough to be type-2 diabetes. Diabetes is as
serious neuroendocrine condition. It impairs other neuroendocrine balances - e.g. contributes
to low testosterone. It impairs neuron signal transmission - impairing psychiatric and hormonal
treatment.
2. Adrenal Fatigue. Adrenal dysfunction causes more severe mental illness and physical
impairment than testosterone deficiency. One cannot feel well when receiving testosterone
replacement when adrenal fatigue is present. Increasing DHEA can help reduce insulin
resistance. In women, adding progesterone can also address adrenal fatigue. Addressing
adrenal fatigue with a serotonergic medication when depression and anxiety are present also
helps improve thyroid hormone activity.
3. Thyroid hormone. I would usually not add thyroid hormone until after addresing Adrenal
fatigue, unless thyroid hormone levels are extremely low (e.g. TSH >30-50 - due to risk of
delirium, psychosis with extremely low thyroid hormone). Thyroid hormone demands an
increase in adrenal production. If there is adrenal fatigue, thyroid hormone can cause a
person to crash by worsening adrenal fatigue.
4. Reproductive hormones - i.e. adjusting testosterone, progesterone. Improving testosterone
activity can reduce insulin resistance, partially help reduce adrenal fatigue. Addressing low
progesterone in women can help reduce adrenal fatigue and improve thyroid hormone
effectiveness.
5. Adding estrogen (in women). Given estrogen's risk for clots, heart attacks and stroke, I
would replace estrogen last. The addition first of testosterone and progesterone reduces the
risk for these problems.
__________________
Adrenal Fatigue and Salt balance
Quote:
Originally Posted by love_en
Isn't high potassium the indicator for adrenal insufficiency? I was under the impression
that a lack of corticosteroids caused loss of sodium and retention of potassium.
Remember that the body tries to maintain balance when something is out of balance.
In adrenal fatigue, there is an initial loss of sodium due to the lack of production of
aldosterone. This can result in low blood pressure and feeling faint.
The body eventually compensates by retaining sodium by sacrificing potassium. This results
in the low potassium level I most often see in long term adrenal fatigue, compared to low
sodium, high potassium seen in early stages.
When some clinicians see the low potassium, they try to compensate by increasing the
patient's potassium intake. This only worsens the problem. The patient with adrenal fatigue
actually needs sodium more.
__________________
Adrenal Fatigue and self-treatment.
A word of concern about self-treatment without physician monitoring:
Unlike some of the other treatments for adrenal fatigue, taking hydrocortisone (including
Isocort or adrenal extracts) can be dangerous.
Taking excessive amounts can shut down the adrenal glands, giving the person essentially
Addison's disease - which can be fatal if left untreated. It is like running a car engine's battery
down until it is dead.
Unfortunately, it may take at least 2 years repair and restart the adrenal glands once this
happens. And sometimes, it can't be restarted at all - leaving the person with a permanent
disability.
Some people's tendency to think that if something works, more is better. This would be
dangerous when it comes to treating the adrenal glands. More is clearly not better.
Florinef (fludrocortisone)
Quote:
Originally Posted by 1cc
What is your opinion of using fludrocortisone to help maintain salt in the body. I have
read some place that fludrocortisone does not work well in adults. Is this true?
Fludrocortisone (Florinef) is used to treat Addison's Disease. It is a highly potent medication
with properties of both cortisol and aldosterone. It acts on the kidney to conserve sodium and
excrete potassium. It can be highly dangerous to use unless closely monitored by a physician.
Note that Adrenal fatigue is not Addison's Disease.
Treatment with "big guns" like Prednisone or Florinef may be a lot more than required,
entailing more risk. It would be similar to using anabolic steriods for testosterone replacement.
Adrenal Fatigue and hair loss
Quote:
Originally Posted by Vforcer2
I worked my way up to 20 mg a day of Isocort, a