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Nutritional & Metabolic (Tele)Medicine
John Vlok Dommisse, MBChB(S.Africa/CapeTown),
MD(USA/Canada), FRCP(Canada/Toronto, recognized in AZ and other states)
US citizen; medically licensed in AZ (active),
CT, VA, ONT/Canada, and SouthAfrica (inactive)
1840 E River Rd, Ste 210, Tucson, AZ 85718-5892
Ph.: 520-577-1940 Fax: -1743
E-mail: [email protected]
Fed. Tax ID No. 68-6136057
Website (URL): http://www.galaxymall.com/health/Nutrnl_Mtblc
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The Natural Medicine Newsletter, #7
Volume 4, Number 1, September 1999:
Announcements of New Developments;
A Clever Article about Food; A Brief Case-Report:
Severe arthritis, loss of appetite & hair, fatigue, anxiety, and allergic symptoms,
reversed by the correction of ‘sub-subclinical’ hypothyroidism, a ‘totally normal’
Vitamin-B12 level, severe manganese, sex- and growth-hormonal and amino-acid
deficiencies, with macrocytosis, delayed food-allergies to 4 foods, and copper excess;
and the Text of the Paper I Just Presented in Amsterdam
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This is my 7th semi-annual Newsletter, and the 3rd one written since my website has
gone up. It therefore straddles both the old paper-based ‘snail’-mail and electronic-based e-mail
worlds of publishing communication, but now with e-mail being the primary means of
distribution. This issue focuses on some of the physical effects of nutritional and metabolic
abnormalities, sensitively detected in the blood and optimally corrected.
Announcements of New NMT Developments
(1) Office affiliation with a new laboratory: Ever since Quest Diagnostics’
Arizona operations were bought by Sonora Labs in June 1998, Sonora Quest has been in a ‘freefall’ or ‘melt-down’ process as far as its organization, specimen-drawing, etc., are concerned. I
was familiar with the other labs that have a strong presence in Tucson and wanted to try for
something better for my practice, which relies so heavily on accurate, efficient blood-testing.
After scouring the Internet, I settled on Specialty Labs, of Santa Monica, CA, which does all or
most of the ‘unusual’ tests that I order, in-house. This enables them to give me lower prices for
my patients, vs. SQ, which was having to rely increasingly on sending specimens outside of their
own system in AZ and, therefore, on increasing its prices to my patients. ‘Specialty’ will also
provide blood-drawing in all 50 states, for despatch to their facility in Santa Monica. They will
probably provide a phlebotomist in my office full-time, who will also co-ordinate and ‘troubleshoot’ draws in other states, thus relieving my Tucson patients of having to go to another location
to get their blood drawn, and relieving my staff and myself of the time-consuming job of coordinating and ‘trouble-shooting’ blood-draws.
(2) All new approaches and products are working out well: As detailed in
the previous NsLtr, these include: Eden-GH1, the new oral growth hormone (spray).
Amino-acid secretagogues, with attention to amino-acid blood-levels (a
modification that is my own and which has made a huge difference in the growth hormone
response). The amino-acid blood panel is the test that I will be saving patients the largest
amount of money on by switching from Sonora Quest ($509.00) to Specialty Labs ($153.00!). I
will probably be recommending a fantastic new multi-amino-acid product with immunoglobulins
(antibodies) from Metagenics, Inc., in the near future, for those needing general protein support.
Biomune OSF Plus capsules for general bodily immunity, and Biomune OSF
Nasal Spray for overcoming and resisting nasal, throat and ear infections. In the testing for
natural killer cell function (not just numbers), patients will again save hugely with Specialty (+
$107.00) vs. Sonora Quest Labs ($382.00!).
‘Vitalaxin’, the connection-to-fibromyalgia discoverer’s brand of relaxin
hormone, has already made a huge difference in most of my fibromyalgia patients who were still
having significant pain after I’d applied my previous approaches.
Cetyl Myrist-Oleate: I discovered the availability of this newly-discovered natural
fatty-acid substance since my last NsLtr was published. It is claimed by its developer, Dr Chuck
Cochran, that it increases the total-success rate of glucosamine sulphate in osteoarthritis from
64% to 88%, and the partial-success rate to include all the remaining patients. It has already
helped several people in my practice, including one whose rheumatoid arthritis pain has
disappeared altogether.
(3) All patients whose case-histories were posted in all previous
NewsLetters are all still doing outstandingly well.
ARE YOU EATING OBESE VEGETABLES?
by Mary Ann Tilford
Let'
s start out with a gruesome but useful analogy: Suppose that humans are being raised
to sell by the pound, just as they reach young adulthood. What will the most valuable humans
look like? They will be as large and heavy as possible, because their worth will be measured by
the pound. What will we feed these humans that we want to be as large as possible? Anything
that makes them big and fat. You won'
t bother with too much in the way of vitamins and
minerals, because your humans don'
t have to function as anything except market items. You don'
t
care about how healthy they are, just what they weigh and what you can sell them for. You'
ll get
away with the cheapest method of getting them as fat as possible, to get the best market return on
your investment in feeding them.
Based on your experience, what do the healthiest humans look like? According to the
weight charts, if smokers are eliminated from the data, the thinnest humans live the longest and
have the least incidence of disease.
Let'
s cross over to plant foods now. Suppose, instead of growing humans to sell by the
pound, you are growing fruits and vegetables, which ARE sold by the pound. What will you feed
your fruits and vegetables? Anything that will make them big and fat. Will you bother with
feeding them trace minerals that used to be in the soil, but which don'
t make them big and fat?
No way! You'
ll feed them with the cheapest, most effective fertilizer for getting your return on
your investment. You'
ll do your very best to grow obese vegetables.
When was the last time you tasted a tiny, wild strawberry? Remember the wonderful,
intense flavor? Have you tried one of those huge grocery-store strawberries that are sold by the
pound? Did you notice the lack of taste? Did you realize you were eating an obese strawberry?
Since those vegetables were grown with technology designed to make them big and fat, as
opposed to technology designed to make them healthy for you to eat, you are eating food that has
a low nutritional density, food that has a size way out of proportion to the nutrition you are
getting from eating it. Either you will have to eat enough to make YOU big and fat, or you will
be deficient in important nutrients that were not cost-effective in growing the plants big and fat.
You may become so deficient in important minerals that were not included in the fertilizer, that
you develop mental or physical symptoms of deficiency. Many, many of the vague and not-sovague symptoms that people go to their doctors for, are caused by mineral deficiencies, due to
eating foods with a lack of nutrition in them, that is, obese foods. It has become impossible to
get proper nutrition from diet alone, because of the depletion of the soils caused by intensive
farming methods that only replenish those nutrients that cause plants to become big and fat.
Is there a solution to all this? In a market economy, change is difficult, but consumers do
have some power. The lack of nutritional density is one of the factors behind the organic foods
movement; another factor is pesticide use, but I won'
t go into that here. Organically grown
vegetables that meet the California standard are grown without commercial fertilizers that will
produce obese plants. For that reason, organically grown plants are smaller than plants grown
with commercial fertilizers, and they are more nutritionally dense. They also often taste
different, having enormously more taste than their obese cousins. Many organic farmers make
an effort to rotate crops and allow fields to lie fallow, as in the old days before commercial
fertilizers made it possible to continue to grow profitable crops on depleted soils.
You may have figured out by now, that I am making a case for eating organic plants
instead of commercially fertilized plants. A nutritionally denser food source, that allows you to
absorb more nutrients from less weight, will also allow you to weigh less and be healthier, with
fewer nutritional deficiencies. You might also live longer. If enough people stop buying
commercially fertilized foods and start buying organically grown foods that meet the California
standard, we can change the food system in this country and all become more healthy.
Just remember all this the next time you bite into an obese strawberry.
Copyright 1999, Mary Ann Tilford.
All rights reserved.
A Brief Case-Report:
Severe arthritis, loss of appetite & hair, fatigue, anxiety, and allergic symptoms,
reversed by the correction of ‘sub-subclinical’ hypothyroidism, a ‘totally normal’
Vitamin B12 level, severe manganese, sex-hormonal and amino-acid deficiencies,
with macrocytosis, delayed food-allergies to 4 foods, and copper excess.
(1) In her own words: [email protected], 12 Oct. 1998: Dear John,
I have been your patient since my husband met you (while explaining your medical
approaches on a cable-TV station, about 2 years ago) and recommended I consult you about my
chronic ill-health.
My health has improved amazingly since you started treating me. I have a better appetite
and my hair-growth is improved. I used to be exhausted after a single shopping trip but I can
now stay out all day shopping, playing bridge ane even sometimes taking in a movie without
falling asleep. I am more relaxed and my allergies seem to be diminished. The best news is that
my arthritis has been in remission for many months.
This summer, I was able to fly to England to attend my granddaughter’s wedding. I had a
splendid, busy vacation without being limited at all by health problems. Best wishes and many
thanks for enabling me to enjoy life again.
(Audrey Hewitt)
(2) My Commentary: (a) Manganese is known to be very important for the integrity
of joints. It is likely that the correction of her severe deficiency of it was as much responsible for
her dramatic recovery from osteoarthritis as the glucosamine sulphate and omega-3 oils were, in
her case. Manganese would not have helped if she were not deficient. A manganese blood-level
is hardly ever obtained, in any medical practice.
(b) Loss of hair, fatigue, anxiety and aggravation of allergies are all known to be
possible symptoms of hypothyroidism but most physicians would say that Audrey’s blood-tests
for this condition were negative and they would not have treated her with thyroid hormone; nor
would they have used a combination of both T3 and T4 thyroid hormones; and they would not
have optimized the blood-levels of both these hormones in order to achieve the degree of
response that I did here, partly because of a largely-unfounded fear of promoting osteoporosis.
[My patients who have both hypothyroidism and osteoporosis see their bone mineral density xray scans not only not deteriorate every year but even improve, some by as much as 30
percentage-points, even with high-normal free-T3 levels, which is where I like to keep most
patients’ levels.]
(c) Fatigue/exhaustion and loss of appetite are known, by some physicians, to be
caused, in some cases, by vitamin-B12 deficiency. Her level was not deficient but only just
normal, by my standards, and I find that patients do even better when that level is optimized,
rather than just being allowed to hover in the low end of the normal range.
(d) The food-allergy blood-tests that I order (IgG4 antibodies, by the ELISA
method, not the RAST method) are scorned by most allergists and other physicians as not
yielding valuable information or providing the rationale for avoiding certain foods (although
there is a significant literature supporting their efficacy). Yet, almost always, when I get the
patient to avoid the foods causing the highest antibody titers, and only eat the ones causing the
moderate elevations once in every four days, they see dramatic reductions in their allergic
symptoms of their skin, sinuses, irritable bowel, and asthma.
(e) Most physicians doing hormone replacement therapy in post-menopausal
women who have had a hysterectomy use synthetic estradiol only, thinking that, since uterine
cancer doesn’t need to be prevented in them, progesterone-type hormones are unnecessary. I
disagree with this, both from reading the papers of Drs John R Lee and Jonathan Wright and
from my experience with always optimizing estriol, estradiol, progesterone and testosterone
blood-levels in every female patient.
(f) Copper excess in the blood has been reported to cause severe fatigue,
depression, anxiety and other symptoms (Nolan, 1984), and the mechanism for this has been
explained as being the inhibition of the formation of methyl-B12 from vitamin-B12; the methyl
version is the only one that gets through the blood-brain barrier and feeds the brain
(VanTiggelen, 1984).
A presentation at the ‘Advanced Clinical Nutrition 1999'conference
of the European Laboratory for Nutrients, based in Utrecht, Holland,
and Vitamin Diagnostics, of New Jersey, USA,
at the Grand Hotel Krasnapolsky in Amsterdam, 20-22 August,
by John V DOMmisse, MBChB(CapeTown), FRCP(Canada)
Preventing and Reversing Severe Depression, Early Dementia, Fatigue,
Cardiovascular Disease, Osteoporosis, and Peripheral Neuropathy
by Sensitive Blood-Analysis and Optimal Correction of
Vitamin B12, B6 and Folic Acid, Both-Thyroid, Sex- and Growth-Hormone Deficiencies:
Introduction and Summary (Preprinted and included in program)
There are already thousands of papers in the medical literature outlining the effects of
these deficiencies on these conditions. The main reason why these conditions are not muchmore-often treated by the correction of these deficiencies is that the political economy of
medicine and its teaching and research has shifted very strongly toward pharmaceutical
approaches. It takes a special commitment in a practising physician to take the time out of his
busy schedule to read enough of the published nutritional-metabolic literature to apply this in his
practice, esp. when there are numerous punishments for such practising, in matters of his medical
licence, health insurance reimbursement for his work, criticism from colleagues about having
turned into a '
quack'
, etc.. However, if he is persistent, such a physician will in due course
receive rewards that will far-outweigh the penalties, not the least of which will be the satisfaction
of seeing the superior outcomes that he will be able to achieve with his patients. Probably the
second greatest benefit will be that he will be so sought-after by the public that he will be able to
practise independently of the health insurance companies and managed-care organizations that
now dominate the medical landscape in some countries, such as mine.
In my particular case, the reading of thousands of nutritional-metabolic articles in the
'
mainline'medical literature started in 1977, about 2 years after completion of a psychiatric
residency at the U of Toronto in Canada. I was director of out-patient services at a community
mental health center in Portsmouth, VA, when I came across several articles about the purported
mechanism of the depression in women taking the oral contraceptive pill. Although as residents
we had been taught about the mechanism of the action of the tricyclic antidepressants on the
neurotransmitters in the median forebrain bundle, we had never been told the food-substances
from which those neurotransmitters had been formed in the first place, under the catalytic
influence of yet other nutrients! Since I had been very interested in nutrition in medical school at
the U of CapeTown, it shocked me to now realize how, and to what extent, the teaching of
medicine (or psychiatry, in this case) had been hijacked by the pharmaceutical industry.
So I read every article I could find, through literature searches, on the depressive and
other effects of vitamin B6/ pyridoxal phosphate deficiency. Then I read all the articles I could
find on the effects of a deficiency of folic acid; then all those on vitamin B12 deficiency; then I
went through the effects of several mineral deficiencies. As I learned about these subjects, which
blood-tests could be ordered to ascertain the deficiencies, and how best to supplement the
patient'
s diet in order to completely correct the deficiency, I then applied this knowledge in a
practical way in my practice, which had moved into the private sphere, still in Portsmouth, in late
1978. In 1987, 10 years after starting to order these blood-tests in my patients, I ordered them on
myself and my family. It blew my mind to discover grade-2 hypothyroidism in myself, and
numerous nutrient deficiencies in my whole family, despite my attention to diet and nutrition in
the meals prepared by my wife, who had completed nursing-training at Groote Schuur Hospital in
CapeTown; and despite several consultations with physicians in the past.
One of the interesting facts I learned from my extensive reading of the nutritionalmetabolic literature is that the deleterious effects of the deficiencies of these substances were
proven to occur quite often, even when the blood-level of the nutrient or hormone in question
would be in the lower part of the laboratory'
s so-called '
normal range'for that substance. In such
cases, I then immediately revised the normal ranges for the substance in question, in my own
mind, and wrote the corrected normal range, by hand, in the appropriate places on the lab-reports
- and aggressively treated such deficiencies with enough supplementation to not only put the
blood-level into the revised normal range but to keep it at an optimal, high-normal level on an
indefinite time-basis. Within a few weeks or months of so doing in each patient, I observed that
patients who had been chronically depressed, or who appeared to be sliding into a seeminglyinevitable dementia/ Alzheimer'
s condition, or who had been diagnosed with chronic fatigue
syndrome (despite the universally poor prognosis for patients with this condition), suddenly
improved way beyond the state that I had previously been able to achieve with the use of
antidepressant medication, brain stimulants and '
revascularizers'
, ginseng, ginkgo biloba, and the
standard unoptimized intake of vitamins, minerals, hormones, etc..
Applying the principle of optimizing blood-levels to both serum free-thyroid hormone
levels; to all the pertinent reproductive hormones in peri- and post-menopausal women and
middle- and old-aged men; and to insulin-like growth factor No.1 (IGF-1), the marker for
growth hormone, in middle- and old-aged adults, has likewise produced dramatic improvements
in the health and quality-of-life of these fortunate patients. They rejoice at finding a physician
who doesn'
t only find that "all the blood-tests are normal, you must be depressed - here, let me
write you a prescription for Prozac". They have found a physician who has done his job and
found the biochemical abnormalities that have greatly depressed, cognitively-impaired and
fatigued them, and produced the hyperlipidemic cardiovascular disease, osteoporosis, peripheral
neuropathy and numerous other chronic conditions from which they had come to believe that
their only possibility of relief was their death. They can now start living abundantly again.
So a plea is made here for the '
normal ranges'of many of these substances to be revised
upward quite drastically (downward in the case of the thyroid-stimulating hormone), as indicated
by the '
low-normal'blood- and CSF-levels, and high-normal TSH levels, already recorded to
have caused these conditions. By applying sensitive blood-analysis and diagnostic criteria,
combined with aggressive sustained, monitored, optimal treatment of these deficiencies, it is
virtually assured, as night follows day, that an impressive track-record of reversing these serious,
often-intractable, sometimes-fatal conditions can be accumulated.
Scores of references. Key words: Superior patient outcomes in chronic physical
disorders; chronic mental disorders; vitamin B12, other nutrient and hormonal deficiencies;
grade-3 primary hypothyroidism; central and non-thyroidal hypothyroidism; sensitive bloodanalysis; upgraded '
normal ranges'
; optimal treatment.]
Introduction to Oral Presentation
Ladies and Gentlemen, I want to thank the European Laboratory for Nutrient
Measurement (Dr Vogelaar) and Vitamin Diagnostics of New Jersey (Prof. Herman
Baker) for their organizations’ kind sponsorship of my trip over here from Tucson,
Arizona, giving me the opportunity to present the most cogent aspects of my nutritionalmetabolic practice of the past 22 years. In return, I am doing you the honor of wearing a
jacket and tie, something I hardly ever do - and only when really necessary. But I must
quote to you a feminist columnist in the US, who had this to say about the wearing of
neck-ties: “If men can run the world, why can'
t they stop wearing neckties? How
intelligent is it to start the day by tying a little noose around your neck?”
-- Linda Ellerbee
I look forward to the discussions that will follow this lecture and take place on the
program tomorrow.
What are the main strategies that I have adopted that have improved patient-outcomes in
my practice? Although I was for one year at the University of Toronto as a practicing
psychiatrist on the staff there, I have never been in a university or research setting since starting
to undertake my nutritional-metabolic work, 22 years ago. So what I have to say is simply the (Ihope)-intelligent application of thousands of ‘mainline’ medical and psychiatric journal articles
on nutritional and metabolic medicine to my private solo practice. At first this was as a
Canadian-board-certified general psychiatrist in Virginia but, as I have added more and more of
the nutritional and metabolic aspects to my practice, these have now become my first and second
areas of practice, and psychiatry is only 3rd in the hierarchy, in terms of time spent on each area.
Let me now take, in turn, each of the diagnostic conditions that I have chosen for this
presentation, and tell you what I believe to be the most important value-added features of my
work that have greatly-improved my outcomes, compared to my psychiatric outcomes when I
was a ‘straight’ drugs-and-psychotherapy psychiatrist, and compared to the generally-accepted
medical outcomes of ‘straight’ medically-oriented practitioners. In all the diagnoses above,
except osteoporosis (in which it is hard to tell what has done more than other factors in reversing
this condition by all-natural means), vit.B12 has possibly had the most dramatic overall effects.
In fatigue, hyperlipidemic cardiovascular disease, and peripheral neuropathy, optimizing the freeT4 and free-T3 thyroid hormone levels, even in the mildest grade of hypothyroidism (grade-3)
and even if it meant so-called ‘over-suppressing’ the TSH, has had the most beneficial effects. In
osteoporosis, the optimization of natural testosterone in men and all 3 natural sex-hormones in
women, as well as the optimization of growth hormone status (as measured by the insulin-like
growth factor no.1 (IFG-1), or somatomedin-C, serum level) in both sexes, have had definite
reversal effects, sometimes by as much as 30-point improvements in the percentage of bone
mineral density in a single year. Of course, calcium, vit.D, B12 (see Melton & Kochman; and
Carmel has also written about B12 in osteoblast formation) and several other minerals will have
played their part as well, but all the latter do not achieve as much improvement when the patient
is not on the hormones.
Reference
Melton ME, Kochman ML: Reversal of severe osteoporosis with vitamin B12 and editronate therapy
in a patient with pernicious anemia. METABOLISM 43; 4(Apr):468-9, 1994.
Vitamin B12 (Cobalamin) Deficiency
Diagnosis: This deficiency, because of its association with pernicious anemia, is often
still associated more with anemia and macrocytosis than with affective disorders, dementia,
paranoid psychosis, or violent behavior (Zucker et al, 1981). This is unfortunate because the
diagnosis of pernicious anemia is easily made and easily treated, whereas the B12-deficient
etiology of the affective disorder, the dementia, paranoid psychosis or violent behavior often
remains unsuspected, undetected, and therefore also untreated.
This is tragic because the deficiency can be fairly-easily reversed if diagnosed early
enough and treated vigorously enough. Since the classic paper of Langdon in the J Am Med
Assoc in 1905 (see references, below), there have been numerous successor-papers detailing the
fact that the affective disorders, dementia and other neuropsychiatric conditions resulting from
this deficiency, including peripheral neuropathy (Lindenbaum et al; Perold), can occur in the
absence of any anemia or megaloblastosis. Yet, to this day, a large percentage of physicians,
possibly a majority, will not consider a diagnosis of cobalamin deficiency unless the patient is
anemic and/or macrocytic!
The diagnostic significance of macrocytosis has been all but lost because pathologists
have gradually increased the upper figure of the normal range of the mean (red cell) corpuscular
volume (MCV) to such an extent that now only macrocytosis of >100 fl MCV is recognized as
such. I find that, when my patients have all their nutrient and thyroid hormone and liver enzyme
blood-levels optimized, it is rare to see an MCV above 93 fl. It is a pity that this clue to B12 and
other deficiencies has been rendered much less useful by the extension of the normal range.
Even Breedveld, Bieger and Wermeskerken, at the Bronovo Hospital in Den Haag (The Hague),
in an otherwise informative paper in 1981, accepted an MCV of up to 105 fl as normal.
What is even less known is that this deficiency can be the cause of both bipolar and
bipolar-2 disorders, according to papers by Goggans, Phillips & Kahaner, Verbanck & LeBon,
Reading, Lindenbaum et al, Newbold, and Bell et al. Psychotic depression is particularly likely
to be due to this deficiency, according to Levitt& Joffe, in the Br J Psychi in 1988. The affective
disorders include major depression, w or w/o psychosis; bipolar disorder; bipolar-2
(cyclothymic) disorder; atypical depression; and chronic depression or dysthymic disorder. I
have seen all of them improved or eliminated by the optimal correction of even so-called mild
deficiencies of cobalamin.
Then there is also a whole series of papers drawing a strong connection between this
deficiency and dementia - at serum levels up to 200 points above the low end of the laboratory
normal range for this vitamin! The deficiency of this vitamin in the cerebrospinal fluid often
occurs when the serum level is as high as 500 pg/ml. This is why, in Japan, the normal range for
this vitamin is 500-1300 pg/ml (Mitsuyama & Kogoh), not 200-900, as it usually is in the US and
possibly other countries. The result of this fact (that the lab normal range is actually set way too
low, by the pathologists and hematologists who run them) is that millions of patients with
inadequate B12 levels are passed as normal by the medical establishment, leaving them to be
diagnosed as Alzheimer’s (idiopathic) dementia and idiopathic depression, and treated only with
pharmaceuticals and psychotherapy, rather than with the natural substance that, if administered
early and copiously enough, will totally cure their condition (Dommisse, 1991; Goodman et al,
1996) - without any, or only minimal, side-effects, such as acne (which can often be eliminated
with natural vitamin E complex or zinc, depending on those blood-levels).
There is often also too strong a reliance on the Schilling’s Test, which is often negative
because it tests with free-B12, whereas dietary B12 is protein-bound, as pointed out by Carmel,
Sinow, & Karnaze; and by Doscherholmen et al..
The late geriatrician, Cees vanTiggelen, who practised in both Holland and Australia,
taught me that an adequate zinc level is required in the blood to catalyse the conversion of
hydroxycobalamin (as it occurs in the diet) to methylcobalamin, the only form that is able to
cross the blood-brain barrier (1984b). Also, that an excessive copper level will inhibit this
conversion as well. This observation is supported by the study of Nolan, in which he found that
excessive levels of copper, usually from copper plumbing, caused severe depression, memory
deficits, fatigue and insomnia (1983). Therefore, to assess B12 status without measuring the
serum zinc and copper levels in neuropsychiatric conditions is, at best, an incomplete work-up.
The serum B12 level can be optimal but the CSF level will be deficient (VanTiggelen et al,
1984a) - and this is the level that counts in CNS function. Alcoholism and other forms of liver
disease will also cause lack of conversion to CH3-B12 because this transformation occurs only in
healthy liver cells.
Treatment: There are 2 common misconceptions about treatment: (1) That most cases
require intramuscular B12; and (2) that an injection once every month or once every quarter is
sufficient to counteract the neuropsychiatric effects of this deficiency in all or most cases.
The Swedes Berlin H, Berlin R, and Brante already showed, in the journal Acta Medica
Scandinavica in 1968, and again in a 1985 letter to the British Medical Journal by R Berlin, that
high oral doses of cobalamin (w/o intrinsic factor) administered on a daily basis are as effective
as injections in correcting pernicious anemia. Despite the malabsorption due to lack of intrinsic
factor secreted by the cells lining the stomach, about 1% is still absorbed, and so doses of 1,000
mcg (or 2-5,000) enables the absorption of 10 (or 20-50) mcg, which is an ample amount to
maintain tissue levels adequately, after initial frequent intramuscular boosting of tissue stores.
The oral treatment method was eventually only reported to American physicians in Jan. 1991
(Lederle; Hathcock & Troendle). I personally decided, a long time ago, to maintain all my
patients’ serum levels above 1,000 pg/ml, which is an optimal or ideal serum level. This
substance is cheap and simple enough to take, esp. orally, that neglecting the covering of this
base in one’s practice should, in my opinion, be regarded as medical neglect.
It has long been recognized that the neuropsychiatric effects of this deficiency require
more-sustained and higher doses than the hematological manifestations of this deficiency do
(Smith; Whitehead & Chohan). And, in the presence of concomitant liver conditions and copper
toxicity (until the serum copper level can be reduced to its normal range), the best form of
treatment would be Methyl-B12 but, as far as I know, this form of the vitamin is only available in
Japan (Mitsuyama & Kogoh) and France (VanTiggelen, personal communication)! In
concomitant zinc deficiency, obviously, supplemental zinc, in doses sufficient to optimize its
serum level, can be given concomitantly with hydroxy- or cyano-cobalamin treatment.
There is one, fairly rare, cause of B12 deficiency that cannot be treated orally, no matter
how high the dose, and that is regional ileitis (Crohn’s Disease)(Dommisse, 1992), in which there
are no normal cells in the terminal ileum to absorb the B12 at that point in the digestive process.
These cases must receive the B12 by injection. Also, some people prefer an injection every 2, 3
or 4 weeks, rather than a 2-2,500 mcg tablet or sublingual lozenge daily or twice-daily. There are
also nasal gels available that do produce optimal serum levels, in my experience, and some
patients prefer this route to either the oral or parenteral one, but the Food & Drug Administration
in the US frowns on this method, saying that a substance administered through the nose cannot
be regarded as a food supplement! (Hathcock & Troendle)
References
Zucker DK, Livingston RL, Nakra R, Clayton P. B12 deficiency and psychiatric disorders: Case-report
and literature-review. BIOLOGICAL PSYCHI 16, 2(Feb):197-205, 1981.
Langdon FW. Nervous and mental manifestations of pre-pernicious anemia. J AM MED ASSOC 45:
1635, 1905.
Strachan RW, Henderson JG. Psychiatric syndromes due to avitaminosis-B12 with normal blood and
marrow. QUART J MED 34(1965), 135:303-17.
Lindenbaum J, Healton EB, Savage DG, et al.. Neuropsychiatric disorders caused by cobalamin
deficiency in the absence of anemia or macrocytosis. NEW ENG J MED 318, 26:1720-8, 1988.
MacCallum WAG: Recoverable psychiatric illness (esp. depression) occurring with low serum
vitamin-B12 levels. J IRISH MED ASSOC 1965, Dec.:187-92.
Perold JG. Vitamin B12 neuropathy in the absence of anaemia: A case report. S.AFR MED J 1981,
11 Apr.:570
Breedveld FC, Bieger R, vanWermeskerken RKA. The clinical significance of macrocytosis. ACTA
MED SCAND 209(1981):319-22.
Levitt AJ, Joffe RT: Vitamin-B12 in psychotic depression. BRIT J PSYCHI 1988; 153: 266-267.
VanTiggelen CJM, Peperkamp JPC, TerToolen JFW. Assessment of vitamin-B12 status in CSF. AM J
PSYCHI 1984a; 141, 1 (Jan.): 136-137.
Goggans FC. A case of mania secondary to vitamin B12 deficiency. AMERICAN JOURNAL OF
PSYCHIATRY 1984; 141, 2(Feb): 300-1.
Jacobs LG, Bloom HG, Behrman FZ. Mania and a gait disorder due to cobalamin deficiency. J AM
GERIATR SOC 1990; 38: 473-474.
Phillips Sl, Kahaner KP. An unusual presentation of vitamin B12 deficiency (depression, mania and
paranoia). AMERICAN JOURNAL OF PSYCHIATRY 1988; 145, 4(Apr): 529.
VerBanck PMP, LeBon O: Changing psychiatric symptoms (successive hypomania, depression and
paranoia) in a patient with B12 deficiency (before anemia and macrocytosis developed). J CLIN PSYCHI
1991; 52, 4: 182-183.
Reading CM. X-linked dominant manic-depressive illness: Linkage with Xg blood-group, red-green
color-blindness and vitamin-B12 deficiency. ORTHOMOLECULAR PSYCHIATRY 1979; 8, 2: 68-77.
Berlin H, Berlin R, Brante G. Oral treatment of pernicious anemia with high doses of vitamin-B12
without intrinsic factor. Acta Med Scand 184: 247, 1968.
Berlin R. Vitamin-B12 injections (ltr). Brit Med J 291, 6487(July 6):56, 1985.
Lederle FA. Oral cobalamin for pernicious anemia: Medicine's best-kept secret? (commentary). J AM
MED ASSOC 265, 1 (Jan. 2): 94-5, 1991.
Hathcock JN, Troendle GJ. Oral cobalamin for treatment of pernicious anemia? (editorial). J AM
MED ASSOC 265, 1(Jan. 2):96-7, 1991.
Newbold HL. Vitamin-B12: 'Placebo'or neglected therapeutic tool? Med Hypoth 28: 155-164, 1989.
Bell IR, Edman JS, Marby DW, et al.. Vitamin-B12 and folate status in acute geropsychiatric
inpatients: Affective and cognitive characteristics of a vitamin-'nondeficient'population. Biolog Psychi 27, 2
(Jan.15): 125-37, 1990.
Mitsuyama Y, Kogoh H. Serum and cerebrospinal fluid vitamin-B12 levels in demented patients with
MH3-B12 treatment - Preliminary study. JAPAN J NEUROL & PSYCHI 1988; 42, 1: 65-71.
Ikeda T, Furukawa Y, Mashimoto S, Takahashi K, Yamada M. Vitamin-B12 levels in serum and
cerebrospinal fluid of people with Alzheimer's disease. ACTA PSYCHIATRICA SCAND 1990; 82, 4 (Oct.):
327-329.
Nijst TQ, Wevers RA, Schoonderwaldt HC, Hommes OR, DeHaan AF. Vitamin-B12 and folate concentrations in serum and cerebrospinal fluid of neurological patients, with special reference to multiple sclerosis
and dementia. J NEUROL NEUROSURG & PSYCHI 1990; 53, 11(Nov.):951-954.
Regland B. VITAMIN-B12 DEFICIENCY IN DEMENTIA DISORDERS (monograph/ doctoral thesis,
comprising 6 papers, with co-authors). Dept of Psychi. and Neurochem., University of Goteborg, Sweden,
1991(Jan.).
Dommisse JV. Subtle vitamin-B12 deficiency and psychiatry: An often-unnoticed but devastating
relationship? MEDICAL HYPOTHESES 1991; 34: 131-140.
Dommisse JV. A nutritional and metabolic approach to memory-loss: 18 years'experience. Chapter 1
in Section 3 of THE SCIENCE OF ANTI-AGING MEDICINE (Klatz R, Goldman R, eds). Chicago: The American
Academy of Anti-Aging Medicine, 1996:119-31.
Goodman M, Chen XH, Darwish D. Are US lower normal B12 limits too low? J AM GERIAT SOC
1996 Oct;44(10):1274-5.
Zisselman MH, Kim E, Sharretts RE, et al. Case report: The psychiatric manifestations of B12
deficiency. PRIMARY PSYCHIATRY 1996; 3, 1: 50-55.
Dommisse JV. The psychiatric manifestations of B12 deficiency. PRIMARY PSYCHI 1996, 3,
4(Apr):18-21.
Dommisse JV: The expert speaks: The psychiatric manifestations of vitamin B12 deficiency.
CLINICAL PEARLS NEWS (I.T. Services, 3301 Alta Alden #2, Sacramento, CA 95825) 1998, March.
Spector R, Cancilla P, Damasio AR. Is idiopathic dementia a regional vitamin-deficiency state? MED
HYPOTH 1979;5:763-7.
Evans DL, Edelsohn GA, Golden RN. Organic psychosis without anemia or spinal cord symptoms in
patients with vitamin-B12 deficiency. AM J PSYCHI 1983;140,2(Feb):218-21.
VanTiggelen CJM. Alzheimer's Disease and alcoholic dementia: Association with zinc deficiency and
cerebral vitamin B12 deficiency. ORTHOMOLEC PSYCHI 1984b;13,2:97-104.
Nolan KB: Elevated copper blood-levels (often due to contaminated drinking-water) can be toxic,
causing profound mental and physical fatigue, poor memory, severe depression, and insomnia.
NUTRITIONAL REVIEWS 1983; 41: 318-20.
Gross JS, Weintraub NT, Neufeld RR, Libow LS. (Latent) Pernicious anemia in the demented patient
without anemia or macrocytosis: A case for early recognition. J AMER GERIAT SOC 1986;34,8:612-614.
Karnaze DS, Carmel R. Low serum-cobalamin levels in (29% of cases of) primary degenerative
dementia: Do some patients harbor atypical cobalamin-deficiency states? ARCH INTERN MED
1987;147,3:429-431.
Freedman ML. B12-deficit may be a common cause of dementia. Joint annual meeting of the American
Geriatrics Society and the American Federation for Ageing-Research. Reported in CLINICAL PSYCHIATRY
NEWS 1988; 16,9:10.
Warren T. BEATING ALZHEIMER'S. Garden City Park, NY: Avery Publishing Group, 1991.
Solomon JG. Remediable causes of dementia. VIRGINIA MED 1979;106:459-62.
Dommisse JV. Dementia remedies confirmed in practice. VIRGINIA MED 1979;106,8(Aug):567.
Cole MG, Prchal JF. Low serum vitamin-B12 in Alzheimer-type dementia. AGE AGEING
1984;13:101-5.
Carmel R, Sinow RM, Karnaze DS. Atypical cobalamin deficiency (due to proteinbound-cobalamin
malabsorption). J LAB CLIN MED 109(1987), 4(Apr):454- 63, 1987.
Doscherholmen A, Hagen PS, Liu M, Olin L. A dual mechanism of vitamin B12 plasma absorption. J
CLIN INVESTIG 1957; 36: 1551-1557.
Smith ADM. Megaloblastic madness. BRIT MED J 1960, 2: 1840.
Whitehead JA, Chohan MM. Paraphrenia and pernicious anemia. GERIATRICS 1972, May:148-158.
Dommisse JV: Bipolar disorder and Crohn's Disease/ vitamin-B12 deficiency (ltr). JOURNAL OF
CLINICAL PSYCHIATRY 53(1992), 1(Jan):29.
Dean W, Morgenthaler J. SMART DRUGS AND NUTRIENTS: How to Improve Your Memory and
Increase Your Intelligence, Using the Latest Discoveries in Neuroscience. Santa Cruz, CA: B&J Publications,
1991.
UMRP Editors. AMAZING MEDICINES THE DRUG COMPANIES DON'T WANT YOU TO
DISCOVER. Tempe, AZ: University Medical Reasearch Publishers, 1993.
Folic Acid (formerly Vitamin-B11)
A deficiency of this vitamin, also associated more often with a macrocytic anemia
(Dommisse, 1980) than with any psychiatric condition, has been shown to be a fairly common
cause of depression (Abou-Saleh and Coppen, 1986; Guadirian et al, 1980; and Reynolds et al,
1970) - though you would not think so if you were to judge by how seldom the level is even
measured in the treatment of depression, let alone boosted. Folic acid is required in certain vital
enzyme-reactions that occur in the brain, in the formation of the neurotransmitters involved in
mood, namely serotonin, dopamine and noradrenaline. Reynolds et al (1984) and Botez and
Reynolds (1979) have shown that these reactions are accomplished by transmethylation and
hydroxylation effects. Thornton (1977) demonstrated that prolonged postpartum depression will
sometimes only respond when folic acid is given to the patient. I have cured several cases of
depression by using only folic acid, when it is deficient. The antidepressant response to the oral
treatment of 1-3 mg daily, after meals, is usually within a few days.
Although folic acid and vitamin-B12 are well-known as a collaborative team in the
prevention of megaloblastic anemia (Dommisse, 1980), folic acid'
s role in the prevention of
neuropathy, spinal cord damage and cerebral effects such as in the development of dementia, is
less well known. Until fairly recently it was felt that all the neuropsychiatric effects of whatever
caused megaloblastic anemia were due to the B12-deficiency component of that syndrome. That
is now known not to be the case and that folic acid has certain unique functions in the central
nervous system. Senile dementia of the Alheimer type (SDAT) is also sometimes caused by folic
acid deficiency (Kay et al; Enk et al; Botez et al; Melamed et al; Sapira et al; Sneath et al;
and Strachan and Henderson, 1967) and I have seen 2 such cases in my practice. The response
to the treatment in this case is much slower, because of the chronic nature of the changes which
have caused the dementia. I do wonder whether these are not also actually cases of B12
deficiency dementia but that the serum B12 level was recognized as being deficient when it may
have been.
Minimal brain dysfunction/ attention-deficit disorder has been seen in an 8-year-old girl
who had had transient severe folic acid deficiency in infancy (Shapira et al, 1983). And mixed
bags of psychiatric disorders were often found to have lower average serum folate levels than
control groups (Thornton and Thornton; Editorial, 1976; Howard, 1975; and Kariks and
Perry, 1970).
Folic acid excess has also been seen to cause or exacerbate psychiatric disorders (Prakash
and Petrie, 1982), but, since the authors did not measure B12-levels on their patients, one cannot
be sure that they didn'
t simply have the psychiatric effects of B12-deficiency, which are known to
be exacerbated by folic acid.
The red-cell folate level is a much more accurate determinant of folate status as recent
folate-rich diet, supplements and, especially, IV vitamins, given in emergency rooms of hospitals,
will give a falsely-high impression of overall sustained folate status. However, since, unlike
B12, the deficiency is easily corrected with amounts of folate commonly occurring in
multivitamins - which I strongly and repeatedly recommend to all my patients to take - I tend to
forgo ordering this level as well; it costs $30-50 in the US.
References
Dommisse JV: Folic acid and pregnancy-anemia. S.AFR MED J 59, 21(May 16):738-9, 1981.
Abou-Saleh MT and Coppen A. The biology of folate in depression: Implications for nutritional
hypotheses of the psychoses. JOURNAL OF PSYCHIATRIC RESEARCH 20(1986), 2:91-101.
Guadirian AM, Ananth J, Engelsmann F. Folic acid deficiency and depression. PSYCHOSOMATICS
21(1980), 11:926-9.
Reynolds EH, Preece JM, Bailey J and Coppen A. Folate deficiency in depressive illness. BRITISH
JOURNAL OF PSYCHIATRY 117 (1970): 287-92.
Reynolds EH, Carney MWP and Toone BK. Methylation and mood. THE LANCET 1984, ii, July 28
(8396): 196-8.
Botez MI and Reynolds EH, eds. FOLIC ACID IN NEUROLOGY, PSYCHIATRY AND INTERNAL
MEDICINE. NewYork: Raven Press, 1979.
Thornton WE. Folate deficiency in puerperal psychosis. AMERICAN JOURNAL OF OBSTETRICS
AND GYNECOLOGY 129 (1977), 2 (Sep 15): 222-3.
Enk C, Hougaard K, Hippe E:
Reversible dementia and neuropathy 16 years after partial
gastrectomy. SCAND J HEMATOL 25 (1980): 63-6.
Botez MI, Fontaine F, Botez B, Bachevalier J: Folate-responsive neurological and mental disorders:
Report of 16 cases. EUR NEUROL 16 (1977): 230-46.
Melamed E, Reches A, Herschko C: Reversible CNS-dysfunction in folate deficiency. J
NEUROLOGICAL SCI 25 (1975):93-8.
Sapira JD, Tullis S, Mullaly R: Reversible dementia due to folate deficiency. SOUTHERN MED J 68
(1975), 6:776-7.
Strachan RW, Henderson JG: Dementia and folate deficiency. QUARTERLY J MED 34 (1967), 142
(Apr.):189-204.
Shapira Y, Maayan C, Statter M, Ben-Zvi A: Minimal brain dysfunction: A possible late sequela of
transient infantile folic acid deficiency. J PEDIATRICS 103 (1983), 4 (Oct.):671-2.
Editorial: Folic acid and the nervous system. THE LANCET 1976, ii, Oct.6:836.
Howard JS: Folate deficiency in psychiatric practice. PSYCHOSOMATICS 16(1975), Jul/Aug/Sep:112-5.
Prakash R, Petrie WM: Psychiatric changes associated with an excess of folic acid. AM J PSYCHI
139(1982), 9(Sept.):1192-3.
Pyridoxal phosphate/ Pyridoxine HCl (Vitamin-B6)
Pyridoxine, pyridoxamine and pyridoxal are the 3 related substances that make up what
we collectively refer to as vitamin B6. Actually, pyridoxal phosphate is the active version of this
vitamin. Vitamin B6 deficiency is the third in the triumvirate of B-vitamin deficiencies which
are considered the main causes of depression, among all nutrients, with the possible exception of
omega-3 oils (Rudin, 1987). This depressive effect of a B6 deficiency was first discovered in
relation to its depletion by the oral contraceptive pill, in numerous papers in the late 60'
s and
early 70'
s (Daly et al; West; Goldzieher et al; Adams et al; Winston; and Leeton). Many of
these papers showed that it was the interruption in the formation of the neurotransmitter
serotonin from L-tryptophan, which requires B6 for this reaction, which was the cause of the
depression. The estrogen component of the contraceptive pill was found to competitively-inhibit
B6.
However, regardless of what causes the low vitamin B6 serum-level, depression will
often be the result. Thus, for example, Stewart et al, including Prof. Herman Baker (1984), who
is with us here at this conference, found that 20% of depressed out-patients had abnormally low
B6 levels, while only 5% of a control-group (some of whom may also have been depressed but
not diagnosed as such) had low levels. Since PMS is considered to be at least partly a manifestation of underlying depression, perhaps it is therefore not surprising that women with low B6
levels have often been found to suffer from PMS, which is relieved by vitamin B6 tablets (Stokes
and Mendels, 1972). Hyperventilation syndrome, which is related to panic and depressive
disorders, has also been found to respond to combined treatment with B6 and L-tryptophan (Hoes
et al, 1981).
Vitamin B6 deficiency has also been associated with tardive dyskinesia (Tkacz, 1984),
hyperactive children (Coleman et al, 1979), infantile autism (Rimland et al, 1978; and
Martineau et al, 1981), childhood seizures (Report of Council, 1951), morning-sickness in pregnancy (Wheatley, 1977) and carpal tunnel syndrome (Harrison et al, 1983). I, and other
nutritionally-oriented psychiatrists, see little or no tardive dyskinesia in our patients, and I believe
the reason is that we keep their B6 and several other nutrient levels up (see next section, below).
Diagnosis: Despite all this documentation of the effects of vit.B6/ pyridoxal deficiency,
it is hardly ever considered as a cause or contributing factor in depression and these other
conditions, even in patients who are at risk for the deficiency because of poor diet, smoking and
drinking, being on the oral contraceptive pills, etc.. In Spain, I believe, oral contraceptive pills
are not available w/o 25mg of B6 in them; this strikes me as a very sensible idea that should be
applied everywhere. There is a serum level available, although it is rather expensive, running at
around $70 at all labs in the US.
Treatment: Since this deficiency is much easier to correct than a B12 deficiency, with
doses of 25-100 mg once or twice daily (amounts usually present in therapeutic multivitamin or
B-Complex tablets or capsules), I rarely order a serum level but make sure that all my patients
take a therapeutic multivitamin-with-minerals pill or pills every day, to cover the need for many
vitamins and minerals whose levels I cannot - or thus need not - obtain.
References
Rudin DO. THE OMEGA-3 PHENOMENON. NewYork: Rawson Associates, 1987.
Daly RJ, Kane FJ and Ewing JA. Psychosis associated with the use of a sequential oral contraceptive.
THE LANCET 1967, ii: 444-5.
West J. Mood and the pill. BRITISH MEDICAL JOURNAL 1968, 4:187-8.
Goldzieher JW, Moses LE, Averkin E et al. Nervousness and depression attributed to oral contraceptives - a double-blind placebo-controlled study. AMERICAN JOURNAL OF OBSTETRICS & GYNECOLOGY 111 (1971): 1013-1020.
Adams PW, Rose DP, Folkard J et al. Effects of pyridoxine hydrochloride (vitamin B6) upon depression associated with oral contraception. THE LANCET 1973, i: 897-904
Winston F. Oral contraceptives, pyridoxine and depression. AMERICAN JOURNAL OF PSYCHIATRY 130 (1973), 11:1217-21.
Leeton J. Depression induced by oral contraception and the role of vitamin B6 in its management.
AUSTRALIA & NEWZEALAND JOURNAL OF PSYCHIATRY 8 (1974), June: 85-88.
Stewart J, Harrison W, Quitkin F, Baker H: Low B6 levels in (20% of) depressed out-patients.
BIOLOGICAL PSYCHI 19(1984), 4: 613-616.
Stokes J, Mendels J. Pyridoxine and premenstrual tension. THE LANCET 1972, i: 1177-1178.
Hoes MJAJM, Colla P and Folgering H. Hyperventilation syndrome, treatment with L-tryptophan and
pyridoxine; predictive values of xanthurenic acid excretion. JOURNAL OF ORTHOMOLECULAR
PSYCHIATRY 10 (1981), 1 (Jan): 7-15.
Coleman M, Steinberg G, Tippet J et al. The effect of pyridoxine-administration in a subgroup of
hyperkinetic children: A double-blind cross-over comparison with methylphenidate (Ritalin). BIOLOGICAL
PSYCHIATRY 14 (1979), 5: 741-751.
Rimland B, Callaway E and Dreyfus P. The effect of high doses of vitamin B6 on autistic children: A
double-blind cross-over study. AMERICAN JOURNAL OF PSYCHIATRY 135 (1978), 4 (Apr): 472-475.
Martineau J, Garreau B, Barthelemy C et al. Effect of vitamin-B6 on average evoked potentials in
infantile autism. BIOLOGICAL PSYCHIATRY 16 (1981), 7: 627-641.
Report of the Council. Pyridoxine hydrochloride (vitamin B6). JOURNAL OF THE AMERICAN
MEDICAL ASSOCIATION 147 (1951): 322-325.
Wheatley D. Treatment of pregnancy-sickness. BRITISH JOURNAL OF OBSTETRICS & GYNAECOLOGY 84 (1977): 444-447.
Harrison W, Stewart J, Lovelace R and Quitkin F. Case report of carpal tunnel syndrome associated
with tranylcypromine (Parnate)/ inhibition of vitamin-B6. AMERICAN JOURNAL OF PSYCHIATRY 140
(1983), 9: 1229-1230.
Bernard P. Therapy of side-effects of oral contraceptive agents with vitamin B6. ACTA
VITAMINOLOGY & ENZYMOLOGY 1982; 4, 1-2: 45-54.
Tkacz C, Hawkins D. A preventive measure for tardive dyskinesia. J INTERNAT ACAD PREVENT
MED 8 (1984), 5: 5.
Dommisse JV: Nutritional treatment of tardive dyskinesia. AMERICAN JOURNAL OF PSYCHIATRY 148(1991), 2(Feb):279.
Protocol for Preventing - or Successfully
Treating - Tardive Dyskinesia
The main nutrients that seem to be involved are: vitamin E (by its antioxidant action)
(Lohr et al); vitamin B6; lecithin; manganese (Kunin); niacin; and (omitted in my letter in the
Am J Psychi in Feb 1991) vitamins A (or its precursor, beta-carotene) and C, 2 further antioxidants. Since all these nutrients have the potential of toxicity, it is important to not just "throw
them at the patient" with disregard for that potential. This is particularly true for manganese,
which, interestingly-enough, causes parkinsonism when at toxic levels in the blood (Seth and
Chandra, 1988), demonstrating the nutritional phenomenon that nutrient excess will sometimes
produce the same symptoms or effects as the deficiency will.
It is best to start out by measuring the levels of some of these nutrients in the patient'
s
blood, especially vitamin E, B6, and Mn, which are potentially the most toxic (Schaumburg et al,
1983; Berger & Schaumburg, 1984; and Seth & Chandra, 1988). In the case of Mn and alphatocopherol, it is best to just treat to the point where the levels are in the high end of the normal/
therapeutic ranges for these nutrients, because levels above that are liable to cause symptoms.
Although a relatively mild toxic syndrome has been found in people who take massive doses of
vitamin B6 (Seth & Chandra; Schaumburg et al), I have measured levels much higher than the
normal range in patients who were actively taking up to 100mg B6 twice daily and who did not
have any such toxic symptoms. The normal range at the reference-laboratory I use for this test
(Nichols Institute, in California) is 12.3-37.4 ng/ml. In other labs the normal range extends up to
52. I have found that levels under 100 ng/ml are safe. A maintenance dose of 25mg per day is
usually enough to secure levels between 20 and 100ng/ml. This nutrient should be taken after the
evening-meal as it is potentially helpful with sleep-induction and -maintenance, through its
catalytic role in the formation of serotonin from l-tryptophan.
Vitamin E: 400-800 I.U. per day. Less is insufficient to treat; more often raises the level
above the normal range. This vitamin acts against TD by its antioxidant effects, as free radicals
are considered probably instrumental in the pathogenesis of TD. Too often nowadays, with vit. E
being the big nutrient for cholesterol and cardiovascular reasons, and for fibrocystic disease of
the breast, this vitamin is being prescribed in doses that are toxic, such as 1,000-1,600 IU/day. It
is very important to use not just alpha-tocopherol but the Mixed-Tocopherol Natural Complex,
such as the ones by Country Life, the AC Grace Co. or Allergy Research Grp. To prevent heart
disease, gamma-tocopherol is now considered to be possibly even more important than alphatocopherol (Ohrvall et al; Ziouzenkova et al). The exclusive focus on - and use of - alphatocopherol in many studies may explain the conflicting reports about the efficacy of ‘vit.E’ in the
cardiovascular literature. It is likely that gamma-tocopherol, or the entire natural vitamin E
complex, is just as important in preventing and treating tardive dyskinesia as it is in
cardiovascular disease.
Lecithin: 1200mg caps: 2-3 caps, 2-4 times per day. The only real (fairly rare) limiting
factor is diarrhea. This B-vitamin'
s action is cholinergic, as it breaks down into choline, which is
taken up into the acetylcholine system in the brain. This is thought to counter the dopaminergic
rebound that is considered to be the mechanism of the production of TD (Growdon et al).
Manganese (Kunin): If the patient'
s blood-level is below the middle of its normal range,
have the patient take one tablet of about 10-25 mg elemental manganese (100-250 mg chelate)
daily, after a meal (in case of slight gastric irritation; if gastric irritation still occurs, have patient
crush the tablet and mix it into their food). If the level is just below normal, they should take 4050 mg elemental Mn daily, and, if far below normal, twice a day. Re-measure level in 3 months
and adjust dosage.
Niacin (Kunin): It is not very useful measuring the blood-level here, partly because it is
hardly ever deficient, except in severe alcoholics with poor nutritional intake, and partly because
the limiting factor doesn'
t appear to be the blood-level but a flushing reaction to the vitamin in
some people'
s skin, seemingly unrelated to level. Start with a lowish dose of the plain tablet,
about 25 mg, and, if tolerated, build up to a sustained-release tablet/ capsule of 500 mg twicedaily. A useful tip is that a baby-aspirin, taken an hour before this vitamin, can prevent the
flushing reaction, but it does not prevent the potential liver-damage, which needs to be
monitored-for.
Vitamin C (Tkacz & Hawkins, 1981): 3000 mg per day cannot do any harm and is much
more efficacious than the RDA of 60-100 mg per day. Its action seems, like that of vitamin E, to
be an antioxidant one. There doesn'
t seem to be much point in the expense of obtaining a serum
level, except that, if the level is high-normal on the patient'
s diet and lifestyle, perhaps that is one
nutrient they won'
t need to take.
Beta-Carotene: The dosage is 25,000-50,000 I.U. daily. Only an amount sufficient to
produce optimal levels of vitamin A will convert to that vitamin. Therefore this is the only sensible way to take vitamin A supplements, since vitamin A, being fat-soluble, is one of the potentially toxic nutrients when taken in excess.
Some patience - several months - is required in awaiting the effects of these nutrients as
nutrition works more slowly than drugs and we are dealing here with a condition that has taken a
long time to develop and is often chronic when not treated in this comprehensive way. It is
interesting to note that tardive dyskinesia is virtually not seen in psychiatric practices that utilize
large doses of vitamins and minerals in their treatment of psychosis. This may be the single
greatest contribution of the so-called ‘orthomolecular’ psychiatrists to the treatment of
schizophrenia and other psychotic states (Dommisse, 1991).
References
Lohr JB, Cadet JL, Lohr MA et al. alpha-Tocopherol in tardive dyskinesia. THE LANCET 1987, i,
April 18: 913-914.
Kunin RA. Manganese and niacin in the treatment of drug-induced dyskinesias. J ORTHOMOLEC
PSYCHI 5(1976), 1(Jan):1-24.
Seth PK, Chandra SV. Neurotoxic effects of manganese. Chapter 2 in METAL NEUROTOXICITY
(Bondy SC, Prasad KN, eds), CRC Press, BocaRaton, Florida, 1988.
Schaumburg HH, Kaplan J, Windebank A, et al. Sensory neuropathy from pyridoxine abuse: a new
megavitamin syndrome. N ENGL J MED 1983, Aug 25; 309(8): 445-448.
Berger A, Schaumburg HH. More on neuropathy from pyridoxine abuse (ltr). N ENGL J MED 1984,
Oct 11; 311(15): 986-987.
Tkacz C, Hawkins D. A preventive measure for tardive dyskinesia. J ORTHOMOLECULAR PSYCHI
1981; 10(2): 119-123.
Growdon JH, Cohen EL, Wurtman RJ. Treatment of brain disease with dietary precursors of
neurotransmitters. ANNALS OF INTERNAL MEDICINE 1977; 86, 3(Mar):337-9.
Ohrvall M, Sundlof G, Vessby B. Gamma-, but not alpha-, tocopherol levels in serum are reduced in
coronary artery disease. J INTERN MED 1996 Feb;239(2):111-7.
Ziouzenkova O, Winklhofer-Roob BM, Puhl H, et al.. Lack of correlation between alpha-tocopherol
content of plasma and LDL, but high correlations for gamma-tocopherol and carotenoids. J LIPID RES 1996
Sep;37(9):1936-46.
Dommisse JV. Nutritional treatment of tardive dyskinesia. Am J Psychi 1991; 148,2(Feb):279.
A Radical New Approach to Hypothyroidism
After 11 years of treating hundreds of hypothyroid patients with a pioneering combination
of both the usual thyroxine (T4) thyroid hormone treatment (Levoxyl, Synthroid) and either
dried hog thyroid extract (Armour Thyroid), which contains both T4 and triiodothyronine (T3)
(just as in humans), or Cytomel, which is pure T3 (Dommisse, 1991 & 1993), I am gratified to
report that the prestigious New England Journal of Medicine has finally, on 11 Feb. 1999,
published a paper showing that many hypothyroid patients function significantly better when 50
mcg of their previous T4-only treatment is substituted with 12.5 mcg of T3 (Bunevicius et al,
1999).
The study was conducted on 33 patients with hypothyroidism. Each patient was studied
for two five-week periods. During one period, the patient received his or her usual dose of
thyroxine. During the other, the patient received a regimen in which 50 mcg of the usual dose of
thyroxine was replaced by 12.5 mcg of triiodothyronine. The order in which each patient received
the two treatments was randomized. Biochemical, physiologic, and psychological tests were
performed at the end of each treatment period.
Results. The patients had lower serum free and total thyroxine concentrations and higher
serum total triiodothyronine concentrations after treatment with thyroxine plus triiodothyronine
than after thyroxine alone, whereas the serum thyrotropin concentrations were similar after both
treatments. Among 17 scores on tests of cognitive performance and assessments of mood, 6 were
better or closer to normal after treatment with thyroxine-plus-triiodothyronine. Similarly, among
15 visual-analogue scales used to indicate mood and physical status, the results for 10 were
significantly better after treatment with thyroxine-plus-triiodothyronine. The pulse rate and serum
sex hormone-binding globulin concentrations were slightly higher after treatment with thyroxineplus-triiodothyronine, but blood pressure, serum lipid concentrations, and the results of
neurophysiologic tests were similar after the two treatments.
Conclusions. In patients with hypothyroidism, partial substitution of triiodothyronine for
thyroxine may improve mood and neuropsychological function; this finding suggests a specific
effect of the triiodothyronine normally secreted by the thyroid gland.
A steady progression of publications over the past 15 years or so have attested to the
greater efficacy of T4+T3 vs. T4-only treatment in various types, grades, and manifestations of
hypothyroidism (Joffe et al; Joffe & Singer; Cooke et al; Dullaart et al; Escobar-Morreale et
al), or have indicated that perhaps it is not acceptable for patients to run low free-T3 serum levels
(unless they have certain cardiac arrhythmias) (Palazzo & Suter; Chopra; DeGroot). Still
further evidence of the shift toward including T3 in both the measuring and treating of the
various forms of hypothyroidism is provided by yet another paper published recently: The multicenter Italian '
Evaluation of the adequacy of levothyroxine replacement therapy in patients with
central hypothyroidism'has just reported that "both FT4 and FT3 serum levels ... are necessary
for a more accurate disclosure of over- or under-treated patients." (Ferretti et al, 1999).
Only limited points can be made here: (1) The protocol used, while possibly ideal for
research purposes, was not necessarily optimal for each patient in terms of optimizing both the
FT4 and FT3 serum levels in each patient, leaving room for even greater benefits with an
individualized approach; (2) It is not surprising that it took a team from outside the US - but
containing an American psychiatrist (Prange) who has published on the great benefits of T3 in
refractorily-depressed patients - to introduce this treatment-proposal to mainstream medicine in
the US; (3) Despite the limitations of dosage-flexibility required for the research protocol, there
were absolutely no advantages for the T4-only controls [while there was definite improvement in
(a) 6 of 17 parameters of mood and cognition; (b) 10 of 15 parameters of visual-analogue scales;
plus (c) greater sex-hormone-binding capacity (a significant marker for thyroid function), in the
combination-treatment parts of the study.]
(4) This paper shows, for the first time, the accuracy of the assumption of "but a few
practitioners, who are often thought by their colleagues to be practicing on the fringes of
medicine" (Dr Anthony Toft's editorial on pp. 469-70 of the same issue of NEJM), that the T3
secreted by the thyroid gland - and T3 that can be prescribed in treating hypothyroidism - is vital
for optimal thyroid function. (5) It is possibly purely speculative that "a substantial
minority"(Toft) of T4-only-treated hypothyroid patients are dissatisfied with their treatment,
especially in the absence of being offered T3 as well in their treatment (and not just a higher dose
of T4), and especially as they may simply not know any better! (6) While T3 levels in cerebral
cortical tissue were supposedly not reduced in the T4-only parts of the study, numerous
psychiatric studies, only a handful of which can be referenced here, have shown mood and
cognitive advantages for T3+T4 over T4-only in treating hypothyroid depressed patients (Joffe et
al; Joffe & Singer; Cooke et al; Arem, 1999), raising the question: what is a normal cerebral
cortical tissue T3 level?
And lastly (7), the editorial'
s objections to the shorter half-life and greater serum-level
fluctuations of T3 and thyroid extract are easily overcome by twice-daily, after-breakfast and
after-supper, prescribing of same; and the greater elevation of the free-T3 level than the free-T4
level of some patients on thyroid extract can easily be compensated-for by using a combination
of both thyroid extract twice-dly and dly T4 - or titrated doses of twice-dly T3 and daily T4 - in
dosages titrated by regular measurement of both FT4 and FT3 serum levels every time that
treatment is monitored with blood-levels.
It should be pointed out that this recent paper from Lithuania only addresses one of the 4
or 5 ways in which my approach is different from that of the mainstream in US medicine. It does
not address the issue of whether '
the bar is too high'for hypothyroidism-in-general to be
diagnosed often enough; e.g., whether grade-3, the mildest grade of primary hypothyroidism,
and many cases of secondary, tertiary and non-thyroidal-illness hypothyroidism, that are not
currently treated, should be treated. My answer to all these questions is, by and large, yes; the
current standard approach'
s answer is, by and large, no. Since I have never seen a lack of
positive response when I have treated these '
marginal'cases, I have to assume that my approach is
correct and the standard one is leaving millions of patients under-diagnosed and under-treated.
No matter how certain one may be that one'
s approach is the correct one, it is still very
hard to '
paddle against the stream'
, especially when '
the stream'consists of the considered opinion
of all the top endocrinologists in the US and one is not even an endocrinologist, let alone
considered a top one! But, whenever I have come into an argument about this issue, I have
insisted that rank is not pulled and that the argument revolve strictly around the known
physiology, pathology and medicine of serum thyroid hormone levels and on its own merits. Noone has been able to show that I was wrong, but few have conceded defeat either. Now, finally, I
have received '
official'vindication for an important aspect of my approach from an article that is
still a halting first step in the direction that I have been going for 11 years. What has made the
battle a whole lot easier has been the fact that the patients have trusted that, the better they felt
and functioned on the combination treatment, the more they knew it was the right one and they
have stuck with it, even when advised to abandon it by endocrinologists in prestigious
institutions. The latest development in the loosening of the strangle-hold that T4-only
treatment has in hypothyroid patients has come in the form of a book written by a professor of
endocrinology at Baylor Medical College in Houston, Texas, and published in June of this year
by Ballantine Books, a division of Random House (1999). Dr Ridha Arem makes the astounding
admission that he is convinced that some patients with ‘normal thyroid blood values’ are actually
hypothyroid and that he puts them on a therapeutic trial of thyroid hormone treatment. It appears
that this has always produced relief of hypothyroid symptoms in the patient and he has not
discontinued any of these patients’ treatment.
He makes the further observation that some patients on T4-only treatment do not do well
enough and are not returned to their pre-hypothyroid normal state, either physically or mentally/
emotionally - and he puts them on Cytomel, 5-10 mcg 2-3 times daily. All of them have
improved and been restored to their normal level of functioning.
After reading this book, I called Dr Arem and asked him whether, rather than have to
come to the conclusion that patients can be hypothyroid with ‘normal blood-levels’, wouldn’t it
be better to re-think which blood-tests should be done and how they should be interpreted? I
suggested that, while the ultra-sensitive TSH is a very accurate test for measuring the TSH,
perhaps the TSH is not the best yardstick of thyroid function, since there are several other
influences that determine its serum level. Wouldn’t it be better to use the free-levels of T4 and
T3, the only accurate measures of the function of these two hormones, as the more-appropriate
gauges of the degree of thyroid function? I told him that this is what I have been doing already
for the past 11 years. He was very intrigued and will be getting back in touch with me about
some possible future publishing collaboration.
I have held, since 1988, that in most patients whose free-T3 serum levels are suppressed,
for whatever reason, this functional deficit needs to be corrected before the patients can quickly
return to normal health. Usually, the only way to achieve optimization of both the free-T4 and
-T3 levels is by prescribing a combination of both T4 (e.g., Levoxyl) and Armour Thyroid
(T4/T3) or Cytomel (T3). Yet I have been unique in prescribing a combination of any two
thyroid hormone preparations! What does that tell one about the closeness-to-optimal of the
millions of hypothyroid patients'free-T4 and free-T3 serum levels in the US? About the fact that
no-one prescribes more than one thyroid preparation?; and that “Armour Thyroid is an outdated
treatment and that it and Cytomel, both containing T3, are '
dangerous thyroid hormones'
? Any
thyroid hormone containing T3 is dangerous if the free-T3 serum level is not routinely obtained
in monitoring treatment (and this level is seldom normally obtained) but if the T3-containing
preparation is prescribed twice-daily (which minimizes its fluctuating serum levels), and the freeT3 serum level is always obtained, this dual method of treating hypothyroidism is not only safe
but also optimizes and totally restores thyroid function to normal. Anything less than that is lessthan-optimal!
I completed a long paper on my approach to hypothyroidism in May and it is now
awaiting publication.4
References
Dommisse JV. T3 is at least as important as T4 in all cases of hypothyroidism. J CLIN PSYCHI
1993;54,7(July):277-8.
Dommisse JV. Pseudotumor cerebri in two patients with lithium-induced hypothyroidism. J CLIN
PSYCHI 1991;52,5(May):239.
Bunevicius R, Kazanavicius G, Zalinkevicius R, Prange AJ. Effects of thyroxine as compared with
thyroxine-plus-triiodothyronine in patients with hypothyroidism. N ENGL J MED 1999;340:424-9.
Dommisse JV. Hypothyroidism: Sensitive diagnosis and optimal treatment of all types and grades.
IN PRESS, 1999.
Joffe R, Blank DW, Post RM, Uhde W. Decreased triiodothyronines (T3) in depression: A preliminary
report. BIOLOGICAL PSYCHI 1985;20:922-5.
Joffe RT, Singer W. A comparison of triiodothyronine (T3) and thyroxine (T4) in the potentiation of
tricyclic antidepressants. PSYCHIATRIC RES 1990;32:241-51.
7. Palazzo MG, Suter PM. Thyroid hormone receptor expression in 'sick euthyroid'syndrome.
LANCET 1990;335,Mar.17:662-3.
8. Cooke RG, Joffe RT, Levitt AJ. T3 augmentation of antidepressant treatment in T4-replaced
thyroid patients. J CLIN PSYCHI 1992;53,1(Jan):16-18.
9. Dullaart RP, vanDoormaal JJ, Hoogenberg K, Sluiter WJ. Triiodothyronine rapidly lowers plasma
lipoprotein(a) in hypothyroid subjects. NETH J MED 1995 Apr;46(4):179-84.
10. Escobar-Morreale HF, del Rey FE, Obregon MJ, de Escobar GM. Only the combined treatment with
thyroxine and triiodothyronine ensures euthyroidism in all tissues of the thyroidectomized rat.
ENDOCRINOL 1996 Jun;137(6):2490-502.
11. Chopra IJ. Clinical Review 86: Euthyroid sick syndrome: Is it a misnomer? J CLIN ENDOCRINOL
METAB 1997, Feb;82(2):329-34.
12. DeGroot LJ. Dangerous dogmas in medicine: The nonthyroidal illness syndrome. J CLIN
ENDOCRINOL METAB 1999 Jan; 84(1):151-64.
13. Ferretti E, Persani L, Jaffrain-Rea ML, et al.. Evaluation of the adequacy of levothyroxine
replacement therapy in patients with central hypothyroidism. J CLIN ENDOCRINOL METAB 1999
March;84,3:924-9.
14. Arem R. THE THYROID SOLUTION: A Mind-Body Program for Beating Depression and
Regaining your Emotional and Physical Health. NewYork: Ballantine Books, June 1999.
Natural Sex Hormone Replacement Therapy
I have been using compounded prescriptions of natural estrogens, progesterone and
testosterone in peri- and post-menopausal women, and natural testosterone in middle-aged and
elderly men, with low levels of these hormones (for their gender) for the past 2 years. I started
out by prescribing pregnenolone, the ‘mother’ hormone, in women, and dehydroepiandrosterone
in men. The initial response was favorable but in time, within a year or so, most patients did not
produce enough of the target end-hormones, at least not usually in balanced amounts, even with
doses of 800-1,000mg daily of these precursor-hormones. So I resorted to the natural endhormones, always going according to optimal blood-levels. My assessment of the literature on
this subject (Hormone Replacement Therapy, HRT) is that the natural substances are far superior
in their effects and in their side-effect profiles. Theoretically at least, it seems to me that altering
the hormone molecular structure, so that the drug companies can obtain proprietary rights over
what would otherwise be a natural substance (which is in the public domain and not available for
corporate take-over) is asking for trouble with side-effects, including the risk of cancer.
Growth Hormone Boosting
Once the growth-plates in our long bones have fused, growth hormone no longer causes
any increase in our height, but its other functions continue: Maintaining youthfulness, musclestrength, skin-thickness, memory, mood, sex-drive, and numerous other desirable attributes.5
In December 1996, Drs Clark and Kendall, in the Department of Medicines Management
at Keele University in the UK, reviewed the upshot of numerous studies on the effects of this
hormone injection in adults who were deficient in growth hormone. They said this condition is
now recognized as a clinical syndrome with characteristic signs and symptoms. This treatment
produced improvements in insulin-like growth factor levels, decreases in total fat mass, and
increases in lean body mass, with no overall effect on total body weight. Other effects included
variable serum cholesterol levels, bone mineral density and quality of life. A team of researchers
at the Sahlgrenska University Hospital in Goteborg, Sweden, focused on the effect of this GH
injection on raising the metabolic rate, and on decreasing body fat by decreasing the serum level
of leptin (Karlsson et al, 1997).
Until the past year or two, growth hormone as a supplement has only been available as an
expensive ($14) daily injection, for life. Its cost and inconvenience put it out of reach of most
mortals and it was only commonly used by movie stars who wanted to maintain their youthful
appearance for as long as possible. Then, in 1981, scientists discovered that another method of
boosting one'
s GH function is by taking a combination of certain amino-acids by mouth, mostly
at bed-time, which causes the release of one'
s own GH from the pituitary gland (Thorner, 1997).
MO Thorner and colleagues, in the dept of medicine at the U of Virginia, reported that aging,
nutrition, the feedback effect of IGF-1, and body composition all play a role in the decline of GH
secretion (1997). In GH-deficient adults there is an increase in the amount of intra-abdominal fat
and this process increases with age. This causes serious metabolic consequences, including
insulin resistance and increased cardiovascular risk. The GH axis can be stimulated by certain
chains of amino-acids known as growth-hormone-releasing peptides (GHRPs). The GHRP/GH
receptor has been cloned and orally-active GHRP mimetics have been developed. One such
compound, MK-677, stimulates the amplitude of pulsatile GH secretion and its effects persist for
24 hours. With repeated night-time dosing, a youthful pattern of GH secretion can be achieved
within one month. These GH secretagogues may have a therapeutic role in short-stature children
as well as GH-deficient adults, including older adults, whose body composition stands to be
improved by this treatment.
Arvat, Camanni and Ghigo, in the department of internal medicine at the
University of Turin in Italy, reported in November 1997 that such GHRPs are synthetic
molecules with strong, dose-related and reproducible growth-hormone(GH)-releasing activity in
humans. They act at both the pituitary and hypothalamic level, where specific receptors have
been located. Their action is increased in obese patients and others who are GH-deficient, and
markedly decreased in hypothyroidism and adrenal cortical over-activity (and cortisone-type
treatment). And Greta vandenBerghe and colleagues, in the department of critical care medicine
at the U of Leuven in Belgium, reported in February 1998 that the low activity state of the
thyroid and GH axes in prolonged critical illness appears to have a combined neuro-endocrine
cause, since these axes are both readily activated by the co-infusion of thyrotropin-releasing
hormone (TRH) and GH secretagogues. Two months later, the Turin team summarized the ‘state
of the art’ of GH secretagogue treatment as “enhancing the activity of the GH/IGF-1 axis”, thus
“children, elderly subjects, critically ill and GH-deficient obese and other adult patients” can
benefit from this treatment.
I tried this in dozens of patients for several months but found inconsistent results in the
boosting of IGF-1 serum levels. So I reverted to my old, tried-and-true approach: Measuring the
blood-levels of the amino-acids, as well as of IGF-1, first, and then tailoring the dosages of the
various necessary amino-acids according to the patient'
s own baseline plasma levels of these
amino-acids, and omitting any dosage of those that were already optimal. This was much more
successful.
Then, recently, scientists succeeded in putting the string of amino-acids and peptides that
comprise this actual hormone itself (not just a hormone booster) into a polymer matrix that
renders it absorbable through the mucous membrane of the mouth. It is still too soon for there to
be much published research on these oral GH preparations but, since they are classified as dietary
supplements, they can be sold over-the-counter. Several such oral spray preparations are now
available, at a fraction of the cost of the shots and at only a slight disadvantage as far as efficacy
in raising IGF-1 is concerned. The serum level of insulin-like growth factor number 1 (IGF-1) is
the only practical way in which growth hormone, which is secreted by the pituitary gland in 6
brief bursts each night, can be measured. I started out recommending a homeopathic version of
this substance because it was the cheapest available one, but have recently found one that is
significantly stronger in dosage and only fractionally more costly, Eden GH-1. Because of the
nightly physiological function of GH, I believe one can save money by only spraying it into the
mouth at bed-time and not during the day. So far, the effect, both in raising the IGF-1 level and
in symptom-relief and sense of well-being, have been very encouraging.
Even more successful, for those who can afford both approaches, is to take both
the oral growth hormone spray and the customized dosages of the GH-releasing amino-acids. I
have seen increases in the IGF-1 serum level of as much as 130 points in several patients within a
3-month period!
The advantage of obtaining an amino-acid panel (including arginine, ornithine, glutamine,
glycine, lysine levels), and a carnitine level, separately, is greater than just for the boosting of
GH: There are several amino-acids that are not involved in GH-boosting but are nevertheless
vital in other health functions (see references, from Braverman to Banderet) e.g., Tryptophan,
phenylalanine and tyrosine are the amino-acids from which the brain neurotransmitters serotonin,
dopamine and norepinephrine/ noradrenaline are formed, in the presence of vitamin B6 and other
vitamins, and minerals, as catalysts. Deficiencies of any of these elements can cause depression
and other mood disorders, and it makes much more sense to correct them than to automatically
jump to the prescription of some or other drug to treat the condition by artificially elevating the
neurotransmitters, don'
t you think?
Many other amino-acids are involved in other essential functions, such as musclestrength, memory, immune system strength, etc., and, if that function is lacking, that AA can be
prescribed in the appropriate dosage and the level monitored to reach the optimal range. And,
e.g., Phosphatidyl serine has also been found, by Paris Kidd, to be important in memory
functions; and gamma-amino-butyric acid (GABA) can have a powerful anti-anxiety effect, even
an anti-manic effect, if prescribed for an anxious or bipolar patient with a low plasma level of
this AA. I have proven this in scores of patients over the past 2 years.
References
Clark W, Kendall MJ. Growth hormone treatment for growth hormone deficient adults. J CLIN
PHARM THER 1996 Dec;21(6):367-72.
Karlsson C, Stenlof K, Johannsson G, et al.. Effects of growth hormone treatment on the leptin system
and on energy expenditure (and body fat mass) in abdominally-obese men. EUR J ENDOCRINOL
1998;138(4):408-14.
Thorner MO et al. Aging, nutrition, the feedback effect of IGF-1, and body composition, all play a
role in the decline of GH secretion. RECENT PROG HORM RES 1997;52:215-44; discussion 244-6.
Arvat E, Camanni F, Ghigo E. Age-related growth-hormone-releasing activity of growth hormone
secretagogues in humans. ACTA PAEDIATR SUPPL 1997 Nov:423():92-6.
vandenBerghe G, deZegher F, Baxter RC, et al.. Neuroendocrinology of prolonged critical illness:
Effects of exogenous thyrotropin-releasing hormone and its combination with growth hormone secretagogues.
J CLIN ENDOCRINOL METAB 1998 Feb:83(2):309-19.
Ghigo E, Arvat E, Camanni F. Orally-active growth hormone secretagogues: State of the art and
clinical perspectives. ANN MED 1998 Apr:30(2):159-68.
Braverman ER, Pfeiffer CC. THE HEALING NUTRIENTS WITHIN: Facts, Findings and New
Research on Amino Acids. New Canaan, CT: Keats Publishing, Inc., 1987.
Wurtman RJ, Wurtman JJ. NUTRITION AND THE BRAIN, Vol. 3. NewYork: Raven Press, 1979.
Gelenberg AJ. Nutrition in psychiatry: We are what we eat? (editorial). J CLIN PSYCHI 1980;
41,10:328-9.
Growdon JH, Cohen EL, Wurtman RJ. Treatment of brain disease with dietary precursors of
neurotransmitters. ANN INT MED 1977;86,3(Mar):337-9.
Young SN, Chouinard G, Annable L. Tryptophan in the treatment of depression. ADV EXP MED
BIOL 1981;133:727-37.
Rao B, Broadhurst AD. Tryptophan and depression. BRIT MED J 1976;Feb:460.
Chouinard G, Young SN, Annable L. Effectiveness of tryptophan in acute mania comparable to that of
lithium. Poster presentation, annual convention of the SOC for BIOLOGICAL PSYCHI, 1983. Abstracted in
CLINICAL PSYCHIATRY NEWS 1983, Aug..
Sabelli HC et al. Clinical studies on the phenylalanine hypothesis of affective disorder: Phenylalanine
dietary supplements. J CLIN PSYCHI 1986;47,2:66-70.
Gelenberg AJ, Wojcik JD, Growdon JH, Sved AF, Wurtman RJ. Tyrosine for the treatment of
depression. AMER J PSYCHI 1980;137,5(May):622-3.
Goldberg IK. L-tyrosine in depression. LANCET 1980;Aug16:364.
Banderet LE, Lieberman HR. Treatment with tyrosine, a neurotransmitter-precursor, reduces
environmental stress in humans. BRAIN RES BULL 1989;22:759-62.
Conclusion
Let me make the following points: (1) The correction of numerous deficiencies in any
one patient has a far greater effect than the correction of any one of those deficiencies would
have had. It is the synergistic effect of the optimization of several elements that has had the
profound, probably permanent, effect on most of my patients. Since, as a Senate document
reported in the 70'
s, the food from American farms contained only 15% of the minerals it
contained just 50 years previously, many of us are at risk for mineral deficiencies, which also
lead to vitamin, amino-acid and hormonal deficiencies, compromised immune systems, candida
yeast overgrowth, food-allergies, etc..
(2) What we are witnessing in the past few years is nothing less than a massive
paradigm-shift (Barker JA, 1992) in medicine, an entirely new way of looking at medical and
psychiatric problems. So I am claiming that, whatever distance nutritional-medical people have
traveled along their path so far, this is the approach of the future. History will have to be the
judge of this claim. For now, let me remind you that Thomas Edison already remarked, a century
ago, that the physician of the future would not employ medicines, surgery or other artificial
procedures or mediums to cure illness but would guide the patient in the best way to structure
his/ her natural diet and lifestyle in such a way as to achieve maximum health. And, at about the
same time-period, Sigmund Freud predicted that psychoanalysis would fall away as a method of
treatment once physicians were able to find the organic/ biological/ neurochemical underpinnings
of much of the area of mental and emotional illness, and correct them biochemically.
1992.
Reference
Barker JA. Paradigms: The Business of Discovering the Future. NewYork: HARPERBUSINESS,
Contents may be copied, with appropriate
acknowledgement.
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