Download The Complicated Patient – A Roadmap to Assessment

The Complicated Patient –
A Roadmap to Assessment and Therapy
Dr. Paul Anderson
Summary
Being an integrative practitioner might make you the best trained and
able to deal with the complicated patient but it sure can make your
day long and complicated. In this final session Dr. Anderson will
outline a process for assessing, quantifying and laying out a treatment
plan for this challenging group of patients. The presentation will
focus on top down assessment and categorizing therapies by the stage
of the illness the patient is in (or “peeling the onion”). An
appropriate thought process in which any appropriate modality can be
inserted as well as a mechanism for reassessment will be outlined.
Topic Summary
Modern chronic illness is more complex and difficult
to assess and treat than ever before. Aggravating
factors such as infectious and immune effect,
genomic variations, toxicants and others make the
chronically ill patient complex.
This session is designed to list the research behind
these crossover points and to describe clinically
relevant ways of untangling the clinical picture.
Outline
In this session Dr. Anderson will answer the questions:
1. My patients come in with so much going on; how do I
know where to start?
2. They expect a quick fix of all complaints; how can I
reset their expectation that this will take time?
3. What is the best way to make sure that we work
together in alignment and how do I make them see they
are making progress on a long road to healing?
4. Obviously this topic cannot be fully explored in one
session or one day – but in addition to the above
resources will be given for the practitioner to explore
the topic more completely.
Effectors in Chronic Illness
Effectors:
1
7
1. Cell Function
2. Toxin
2
6
3. Biofilm
2
Sick
4. Immunology
5. Endocrine
6. Psychosocial
7. Digestive - GI
3
5
4
Note:
Chronic Disease of any
kind is (in the absence
of genetic or acquired
immune deficiency) is
never a single issue. In
some proportion the
effectors listed feed
into the terrain that
allows the chronic
illness to exist.
How to think through the
complex chronically ill
persons case.
Ideas - Concepts:
Therapeutic
integration
and intensity:
First Acute Illness
LOW
First / Early “clean” Chronic Illness
MEDIUM
Chronic Complicated Illness State
HIGH
Breadth and Depth of co-infection / co-morbidity etc
Effectors in Chronic Illness
Effectors:
1
7
1. Cell Function
2. Toxin
2
6
SICK
2
3. Biofilm
4. Immunology
5. Endocrine
6. Psychosocial
7. Digestive - GI
3
5
4
Note:
Chronic Disease of any
kind (in the absence of
genetic or acquired
immune deficiency) is
never a single issue. In
some proportion the
effectors listed feed
into the terrain that
allows the chronic
illness to exist.
Effectors in Chronic Illness
Effectors:
1. Cell Function
2. Toxin
1
7
2
SICK
2
3. Biofilm
4. Immunology
5. Endocrine
6. Psychosocial
7. Digestive - GI
3
6
5
4
Note:
No person
experiences these
“layers” equally – and
– they will change in
proportion over time.
So you must meet the
case where it is and
then monitor and
adjust as the case
evolves.
Effectors in Chronic Illness
Effectors:
7
1
1. Cell Function
2
2. Toxin
3. Biofilm
4. Immunology
6
SICK
2
5. Endocrine
6. Psychosocial
7. Digestive - GI
3
4
5
Note:
In my experience as the
case begins to clear up
the residual effectors
that take the longest
can be these, although
each person has their
own “order” they heal
in.
Effectors in Chronic Illness
Effectors:
1
1. Cell Function
2
2. Toxin
3. Biofilm
3
SICK
2
4
4. Immunology
5
5. Endocrine
6. Psychosocial
7. Digestive - GI
7
6
Note:
All contributory factors
must be consistently
monitored even when
they seem “normal”
until the patient is
healed – then a critical
assessment of the
initial inciting
“weaknesses” must be
done to focus
prevention.
Effectors in Chronic Illness
Effectors:
1
1. Cell Function
2
2. Toxin
3. Biofilm
3
SICK
2
4
4. Immunology
5
5. Endocrine
6. Psychosocial
7. Digestive - GI
7
6
Note:
In the preventive stage
any area may be the
weak point.
All areas should be
tonified and watched
long term even in
remission.
So:
Although we should not overcomplicate cases:
We do need to take a step back in cases that are not clearing (or
are getting worse) and recognize the effects our ever more toxic
world, stronger infections, weaker immunity, biofilms etc have on
the depth and breadth of our patients illnesses.
Some Cases
Slide Content (c) 2016 PS Anderson
14
Neuropsychiatric Case
Slide Content (c) 2016 PS Anderson
15
Case - PT
• 52 YO Female
– Multiple psychiatric diagnoses that were
resistant to multiple psychiatric medications
over a 1 year trial.
– Psychiatrists were frustrated and began adding
medications without D/C of prior medications.
– Patient presented with components of Bipolar I,
Anxiety, and multiple other complaints.
Case - PT
• Patient agreed to getting a PICC line set,
and an intensive course of IV treatment.
• IV included two to three times weekly
administration (in succession below) of:
1. IV – Phospholipids
2. IV Nutrients (Vit-Min- Amino Acids formula)
3. IV Glutathione Push at the end of Tx (1 – 4
grams)
Case PT
• Patient responded well acutely to the protocol.
• She did better as we ramped the magnesium up
in the Vit-Min AA protocol to a total of 4 grams
magnesium sulfate per Tx.
• Patient was instituted on oral nutrients between
IV Tx: (PTC, Mg, 5HTP, B-Complex, Multi-Vit).
– After 3 weeks we began a slow medication taper.
Case - PT
• We tapered the SSRI class of drugs first.
– Patient responded well.
• Patient eventually completed 40 Tx
– 2-3X a week for 30 Tx
– Then weekly for 4 Tx
– Then bi-monthly for the balance of Tx.
– Patient continues to this day (> 6 years later) on only
oral nutrients and one low dose medication.
Case: LK
PANS – and other issues…
Slide Content (c) 2016 PS Anderson
20
PANS
PANS (Pediatric Acute-onset Neuropsychiatric Syndrome) is when an
infectious trigger, environmental factors, and other possible triggers
create a misdirected immune response results in inflammation on a
child’s brain. In turn, the child quickly begins to exhibit life changing
symptoms such as OCD, severe restrictive eating, anxiety, tics,
personality changes, decline in math and handwriting abilities,
sensory sensitivities, and more.
PANS was introduced in 2012 by Dr. Susan Swedo in the paper From
Research Subgroup to Clinical Syndrome: Modifying the PANDAS
Criteria to Describe PANS (Pediatric Acute-onset Neuropsychiatric
Syndrome).
Case - LK
• Patient: 18 year old male.
• Date of first visit: August 2014
• Onset of illness: Early 2007 (following an acute
illness)
– Patient and mother report that he was “very
normal” prior to the onset in 2007.
• Primary presenting symptoms:
–
–
–
–
–
Fatigue
Poor infection resistance
Allodynia
Circadian disturbance
Increasing agoraphobia
Prior Diagnosis and Treatment
• From incident in 2007 through 2011:
– Initially unknown trigger or illness – just sicker and
sicker all the time
– August 2011 a presumptive diagnosis:
• “Unknown immune deficiency”
• Therapy with IV-Ig – some help
Prior Diagnosis and Treatment
• 2011 New diagnosis:
– After the above patient was diagnosed with
elevated ASO and Positive titers
– PANDAS / PANS
• Treated with oral antibiotics, higher IV Ig doses
• Patient flared so bad in late 2011 they were put on a slow
Prednisone taper starting at 40mg.
Prior Diagnosis and Treatment
• 2011 New diagnosis:
– With the therapy for the PANDAS / PANS (and as
ASO/Cultures improved)
• Less fatigue
• MORE anxiety
• Much MORE pain (“worst ever”)
• Pain and Anxiety increase has the family on
suicide watch.
• Updates: then through our first visit:
– Was currently on 1 mg Prednisone (taper from prior
doctor – associated this dose with more symptoms).
– Did try a biofilm nasal spray which seemed to help
his symptoms
Initial Assessment in August 2014
• Ongoing chronic illness since unknown trigger in 2007
• Prior Dx & Rx appeared to help some areas and not others
– IV-Ig and some nutrient IV therapy helped most
– Antibiotic therapies also seemed to modify the disease state
• Need for:
– Acute adjustment in the steroid Rx
– New lab assessment required
– Genomic assessment also required
Initial Orders:
• Order serum labs
• Send me the genomic assessment
• Increase the supportive IV Nutrient therapies
– Increase nutrients slowly as indicated on SNP
assessment
– Attempt two IV per week separated by 1-2 days
• Consider support to the IV therapies:
– Based on the labs and SNP assessment possibly
increased ID support, Biofilm therapies, HBOT etc.
• Continue the basic nutrients and SQ-Ig injections
Initial Report to Referring
Providers
• Background adrenal / steroid support:
- Leave the 1 mg Prednisone for now, but to stabilize his system
during this phase of the treatment we would add Hydrocortisone 10 mg in the
AM (with the prednisone) and 10 mg at lunch.
- This is well below the adrenal suppressive dose and will allow his system
to more comfortably tolerate therapy.
• IV:
- Continue IV nutrients as before with steady escalation in doses as
tolerated, and I will review all IV plans and orders prior to administration
with each change.
Initial Report to Referring
Providers
• IgG therapy:
- Continue this as before
• GcMAF: (Was a request of the parents that I
comment on this)
- As I looked over everything and listened to the history I believe this would be a
positive addition for his immune function in the near future. I would recommend a
Nagalase level be done as baseline soon (as this is a long lead time lab) and then that we
consider GcMAF theray in the next month or two. I can supply dosing strategies should
that be required.
• Genomic Assessment:
- Please see the addenda after this letter.
- I am placing interpretation of the genomic areas of stress I see and their corresponding nutritional
supports in that report.
- I would think that adding them to the IV slowly over time and orally as tolerated would be the best
plan.
Additional Labs Ordered:
• Confirmation of improved IgG levels (with infusions)
• Confirmation of persistent IgA insufficiency
• Confirmation of ongoing positive ASO and Anti-DNase B
Strep Ab’s
• Elevated Reverse T3
• Reactivated EBV (elevated EaIgG) and CMV at likely
active titers (IgG at 10X elevation).
• Negative ANA, HCYS at 11.2, CBC-CMP WNL, IgM and E
normal
Primary Genomic Assessment:
• Phase-1 detox is relatively clear
– There is one homozygous SNP at CYP2E1*1B
G9896C rs2070676
•
Metabolizes several precarcinogens, drugs, and solvents to reactive metabolites. Inactivates a
number of drugs and xenobiotics and also bioactivates many xenobiotic substrates to their
hepatotoxic or carcinogenic forms. This protein localizes to the endoplasmic reticulum and is
induced by ethanol, the diabetic state, and starvation. The enzyme metabolizes both endogenous
substrates, such as ethanol, acetone, and acetal, as well as exogenous substrates including benzene,
carbon tetrachloride, ethylene glycol, and nitrosamines which are premutagens found in cigarette
smoke. Due to its many substrates, this enzyme may be involved in such varied processes as
gluconeogenesis, hepatic cirrhosis, diabetes, and cancer.
Primary Genomic Assessment:
• Phase-2 has some acetylation issues (NAT)
as well as slow SOD activity.
– This indicates a higher use of B-5 (for
acetylation)
– Also higher need for Trace minerals
(especially Mn, Cu, Fe)
Primary Genomic Assessment:
• Plasma Cell activity: Generally reasonable but the one SNP
in the IgG area found did have a homozygous defect.
– This is likely part of the reason IgG therapy helps and should
continue.
– Homozygous - FCGR2A rs1801274 association with Kawasaki
disease Duan J, Lou J, Zhang Q, Ke J, Qi Y, Shen N, et al. (2014)
A Genetic Variant rs1801274 in FCGR2A as a Potential Risk
Marker for Kawasaki Disease: A Case-Control Study and MetaAnalysis. PLoS ONE 9(8): e103329.
doi:10.1371/journal.pone.0103329
Primary Genomic Assessment:
• Other Immune:
– Homozygous - IFIH1 (HLA) rs1990760 - IFIH1 Is Associated with
Increased Sensitivity to IFN-α and Serologic Autoimmunity in
Lupus Patients - J Immunol. 2011 Aug 1; 187(3): 1298–1303.
– Homozygous - IL5 rs2069812 - Turk J Hematol 2014;31:17-24:
The lack of other variants in the IL-5 gene of patients and
controls suggests that rs2069812 may be a regulatory SNP
and may have a role in B-lymphocyte development,
constituting a genetic risk factor in antibody development.
Primary Genomic Assessment:
• Other Immune:
– Homozygous - HLA rs2155219 - Associated with significant
atopy - Hum Mol Genet. 2013 Dec 1; 22(23): 4841–4856.
– Homozygous – SHMT2 rs34095989 - SHMT: Serine Hydroxy
Methyltransferase (Helps to shift the emphasis of the
methylation cycle toward the building blocks needed
for new DNA synthesis and away from the processing of
homocysteine to methionine.)
Primary Genomic Assessment:
• Methylation “family”: This group is generally
experiencing a broad base of SNP activity in
heterozygous formations.
– This indicates that as opposed to a large effort to
support one area (such as MTHFR) the better
tolerated, and more helpful, path is broad based
active B-Vitamin plus Trace Mineral co-factor
support.
Primary Genomic Assessment:
• Retinoid conversion: He has 3 of 3 tested
heterozygous BCMO SNP’s.
– In the long run he will need retinal palmitate (fat soluble
Vitamin A) at doses of 25,000 to 50,000 IU per week
tapered to 5,000-10,000 IU for maintenance. This is
because his Carotenoid to Retinoid conversion in globally
hampered. This has potential effect on eye, gonad and
epithelial tissue function.
Primary Genomic Assessment:
• Mitochondrial: If one looks at this area it is
deceivingly “normal” but the homozygous NDUFS
SNP’s as well as some others mean that
conversion of B-3 to active NAD forms as well as
efficiency of Co-Q-10 are hampered.
– In the long run the Niacinamide in the IV B-Vitamins
will help, and an NAD supplement with Co-Q-10
would be useful.
Mitochondrial Support
The role of mitochondrial dysfunction in disease:
Damage to cell organelles (mitochondria, nucleus,
ER, membrane) disrupts active transport, enzyme
production and function & cell reproduction.
These changes disrupt cell osmotic balance,
transporters and other factors causing degenerative
changes in the cell, tissue and eventually the person.
Mitochondria: ELECTRON TRANSPORT / OX-PHOS – 1
•
TCA cycle and Glycolysis only
form a few ATP molecules each.
•
Most of the ATP from glucose
metabolism comes from the
electron transport system.
•
The main function of all the
earlier steps is to make the
Hydrogen of the Glucose
molecule available in forms that
can be utilized for oxidation.
Mitochondria: ELECTRON TRANSPORT / OX-PHOS – 2
• Oxidation of Hydrogen is accomplished by Splitting the
Hydrogen Atom into:
– Hydrogen Ion
– Electron
• Electron used to change dissolved O2 from fluids to
Hydroxyl ions.
• Hydroxyl ions combine to form H2O
• During these reactions, ATP produced.
• Occurs in the Mitochondria
• Occurs via Enzymatically Catalyzed Reactions
Mitochondria: ELECTRON TRANSPORT / OX-PHOS – 3
SNP’s and Poisoning can disorder mitochondrial
function:
• Inhibition is Blocking the respiratory chain at places
other than the ADP+P position.
– Many poisons can do this:
•
•
•
•
Barbiturates
Rotenone (insecticide)
Sulfuric Acid, CO, Cyanide
Antibiotics: Oligomycin, Piericidin-A
• Uncoupling (derailing) Ox-Phos:
– Ox-Phos is the addition of ‘P’ to ADP = ATP
– Uncoupling is the dissociation of oxidation from
phosphorylation
(Incr. permeability of mitochondria to protons / reduces electromechanical potential – short circuits
ATP-synthase [ATPase])
• 2-4-dinitrophenol, dinitrocresol, pentachlorophenol
Mitochondria: ELECTRON TRANSPORT / OX-PHOS SNP’s –
4
• The chemiosmotic mechanism
of Oxidative Phosphorylation
resulting in the formation of
large amounts of ATP.
• At the mitochondrial
membrane.
COX series
NDUFS series
UQCRC series
ATP5 etc series
Cofactors to consider:
•
•
•
•
•
•
•
Nicotinamide / NADH
Co-Q-10
Riboflavin-5-phosphate
Iron
Proline
Ca, Mg, K, Zn,Cu,Cr [positive]
Cd [negative = mito poison]
•Structure 19, 833–843, June 8, 2011
•African Journal of Food Science Vol. 4(5) pp. 200-222, May 2010
•J. Anim. Sci. Vol. 91, E-Suppl. 2/J. Dairy Sci. Vol. 96, E-Suppl. 1
Mitochondrial Damage
• Big topic – Involved in the pathology of most
chronically ill people
• Slow to repair, but as it does the major symptoms
lessen or are eliminated
• Concepts are:
– Clean up (curcumin)
– Restore energy (LAMC [Poly-MVA], B-Vitamins, Iron
[ferritin over 30-40 minimum], Thyroid - Adrenal,
HBOT etc.)
– Repair (Phospholipids, ALA, Carnitine, Taurine)
– Attend to cell ReDox: Omegas / Tocopherols /
Ascorbate / Glutathione
Mitochondrial Damage
• Can people tolerate those mitochondrial
therapies all at once?
• If not what does that look like?
• What order should those therapies follow?
Progression of Therapies
• Began supportive / mito-tx IV therapies
• Began trial of HBOT after the IV therapies
• Began adrenal rebalancing therapy and steroid adjustment
• Planned for IV Anti-infective treatments
– Implemented in the first 60 days of therapy
• Planned for biofilm treatments
– Implemented in the first 60 days of therapy
• Continued the SQ – Ig therapy
Rx Progression 02-2015 through 082015
• IV Therapies:
– Mito and Cell Support Formulas
– Anti-infective and Immune Support Formulas
– Biofilm augments
• HBOT:
– Trial at 45 min 1.3 + ATA
– Increased time and O2 over time
– Family purchased a chamber in 04-2015 – doing home
HBOT 4-6 days a week
• Additional palliative therapies:
– Adjusted oral supps and meds as needed
– Added GI support
– Added and adjusted medical cannabinoid therapies
Case Progression 02-2015 through
08-2015
• IV Therapies:
– Adjusted the additives as tolerated and progressed doses
through time
– Increased the intensity of and frequency of the immune
therapies
• HBOT:
– After initial trial doses the patient noticed a great deal of
help in many areas of compliant (pain, sleep, energy…)
– Worked up to 90 min Tx with cycling air breaks
• Additional palliative therapies:
– Worked with balancing CBD Rx and use of additional THC
product later in the day
– Gave patient instructions on home preparation of mixed
constituent product
A lot of “up and down” through early therapy:
02-2015 follow up notes:
• URINARY: Bladder "shyness" worse. CBD helps and heat helps.
• SLEEP: Was waking at 6am least week. Now 10:30-11am and
going to bed around 11pm-midnight. Hard to fall back to
sleep in am once he wakes. and sleeping 10-12 hours.
• EENT: Ear sore and tested and it was yeast. Consistent
running nose and mucus in thought- does not feel like he has
a cold. Yellowish.
• ENDO: Wakes feeling very cold and needs to take a bath.
• GI: Oxy powder (Mg Oxide) for GI motility.
• GI: Random nausea- a couple times past few month he felt
like he was going to throw up for now reason may have been
zinc on an empty stomach. Pressure build in stomach and he
feel like he needs to burp it Burps up mucus. and he needs
to swallow it down again.
02-2015 Plan:
•
•
•
•
•
•
Adjusted Mito-Tx, IV formulas
Added Thyroid and Adrenal support
Increased GI support
Added Xylitol nasal spray and saline
Added consideration to use BEG spray
Encouraged patient and family to stick with
the plan. Family is frustrated but also sees
some movement forward which is of some
encouragement.
06-2015 Follow up:
"Progress is slow but steady. Likely about
30% improvement from baseline"
Biggest gains are in:
- Energy
- Social interaction
- Functionality
- Decreased neurological agitation
- Less anxiety
06-2015 through 07-2016
• Some gains and some aggravations. Trend is better.
• In 01-2016 changed ABX and added the oral Biofilm
protocol with ‘Biosolve’ (see Biofilm notes).
– After one month at full dose LK aggravated with a
PANS flare. I met with he and his mother and we
agreed this was breaking through a huge barrier to
progression but also that we needed more gentle
progress with the new biofilm therapy and new ABX.
06-2015 through 09-2016
• Over the 1.5 years the family and LK believe he is
definitely moving toward better health and less
PANS Sn/Sx.
• There is still much to do and he does flare, but
he has a life, and quality of life he has not had in
years.
Summary
Slide Content (c) 2016 PS Anderson
56
Effectors in Chronic Illness
Effectors:
1
7
1. Cell Function
2. Toxin
2
6
3. Biofilm
4. Immunology
5. Endocrine
6. Psychosocial
7. Digestive - GI
Slide Content (c) 2016 PS Anderson
5
2
Sic
k
4
3
Note:
Chronic Disease of any
kind is (in the absence
of genetic or acquired
immune deficiency) is
never a single issue. In
some proportion the
effectors listed feed
into the terrain that
allows the chronic
illness to exist.
57
Ideas - Concepts:
Therapeutic
integration
and intensity:
First Acute Illness
LOW
First / Early “clean” Chronic Illness
MEDIUM
Chronic Complicated Illness State
HIGH
Breadth and Depth of co-infection / co-morbidity etc
Slide Content (c) 2016 PS Anderson
58
1. Meet and assess each patient where they
are regardless of which disease label they have.
As a cornerstone of being able to apply balanced
and effective integrative care to patients the
ability to assess their state of health and vitality
while targeting treatment to their individual needs
is paramount. The beauty of integrative medicine
is that its many modalities have the most depth
when incorporating into a complicated chronic
illness care plan. In this the integrative plan can
meet the person where they are and provide multimodality support.
2. Employ the most well rounded treatment,
from any provider needed, and continue this
through each phase of their care.
After the above assessment, the application of
integrative medicine and any other needed
modalities can commence. Many times the
practitioner has to stratify the modalities applied
in a least to most important manner and decide
what the patient needs and can realistically
employ at their stage of health. In doing so the
best support for the moment can be brought to
bear on their case, and the likely “next steps”
will be waiting in the wings for them as they
progress or aggravate.
3. Regardless of where you have to start
therapeutically always continually assess and
treat the determinants of health.
In the chronically ill person a conundrum often exists as
to how many of the “basics” need to be or are
implemented during an acute or severely chronic state.
Examples might be “just how concerned with ______
should I be while I am so ill?” The blank can be diet,
clean foods, exercise, mental emotional and spiritual
practice etc. The answer is both fluid (based on the case
and vitality of the patient) as well as dogmatic (the basic
determinants of health are always important).
3. Regardless of where you have to start
therapeutically always continually assess and
treat the determinants of health.
Rectifying this dissonance is key to appropriate clinical
management. In reality the process is typically a
discussion like this: “I realize you are in an acute state
and feel horrible. I am going to discuss what we call your
determinants of health so they are on your mind. What
we will do is work toward these things being a larger and
larger part of your care over time. And the reason for
their importance is that eventually in order to keep you
well these factors have to be consistently addressed –
even if we are not doing a lot with them immediately.”
4. Embrace the seeming failures of
treatment and “odd reactions”.
I often tell patients that their body will process
healing unlike anyone else, and their body has a
language it speaks. The language is not verbal
however, but rather presentation of signs and
symptoms trying to tell us something. At this time I
also tell them we learn more from what seemed to
go wrong than what went right.
4. Embrace the seeming failures of
treatment and “odd reactions”.
Our goal is to not allow whatever went wrong to continue
but rather let the body (and our knowledge of medicine)
gain a new answer as to what to change or do next. I can
personally say that the majority of things I know to do
with very ill patients came not from medical school or
educational offerings but rather listening to this language
spoken by sick patient’s bodies and then finding the
reason for and answer to that communication.
5. The progress of care is non-linear and so the
therapies employed will necessarily be non-linear
in their application.
Just as we are going to meet the person where they are
with their integrative care, we are also going to change
the level and intensity of interventions as the person and
their body process their specific healing path. This means
communicating the need for follow up and reassessment
with the patient, and being ready and able to adjust
therapies.
5. The progress of care is non-linear and so the
therapies employed will necessarily be non-linear
in their application.
Often as the higher force interventions complete their
work there is a rapid need for more healing support. In
this manner the patient is not told something like
“everyone with your illness needs X weeks of Rx-1 then
needs Y weeks of Rx-2…” If integrative medicine is given
in too linear or formulaic a manner, it may over treat
some areas while missing healing opportunities in the
chronically ill patient.
So
• Give yourself and your patients time
• Keep your mind open
• Learn from success and learn more from
failures
• Get help if you need it
Based on the principle of ‘Tolle Totum’ I am
developing a multi-media program for
advanced treatment skills. This will include
live seminars, mentoring and web based
programs for advanced chronic illness and
cancer treating physicians. It elevates the
ideas of truly integrative healthcare and
modality integration which can effectively and
successfully be used to all forms of chronic
disease Oncologic, Immunologic, Infectious or
whatever presents.
Slide Content (c) 2016 PS Anderson
68
Thank you!
Watch this site for webinars, documents, our new Fellowship Program and
upcoming learning opportunities:
WWW.ConsultDrA.com
“Treat the Whole Person”
Integrative Oncology & Chronic Illness Series:
Advanced Applications in Medical
Practice
May 19-21 (Scottsdale, AZ)
Slide Content (c) 2016 PS Anderson
69
Thanks
and
Be Well!
Slide Content (c) 2016 PS Anderson
70