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Commentary on Nutritional Treatment
of Mental Disorders
from Willam Walsh, Ph.D., Senior Scientist, Pfeiffer Treatment Center
www.hriptc.org
(The following information is taken from Dr. William Walsh's discussion on Safe Harbor's "Integrative Psychiatry" email list for professionals. To preserve Dr. Walsh's wealth of information, we have posted his comments here, with the notation of added commentary [with the date] as discussion goes on.)
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Index
SAMe
SAMe is very promising for undermethylated persons and a bad idea for those who suffer from a genetic tendency for overmethylation. I don't particularly like the "allopathic" method you referred to which is simply trial & error. SAMe can do great harm if given to the wrong person. I hate going to funerals. (17 Dec, 2002)
The mechanisms of action of SAMe and TMG are quite different. Most of our methyl groups come from dietary methionine. The methionine is converted to SAMe in a reaction with magnesium, ATP,
methionine-adenosyl-transferase, and water. SAMe is a relatively unstable carrier of methyl groups and is the primary source of methyl for most reactions in the body. Once the methyl group has been donated, the residual molecule is s-adenosyl-homocysteine which converts to homocysteine. TMG (betaine) is a biochemical which can donate a methyl group to homocysteine, thus converting it back to methionine. The TMG route is secondary to the 5-methyl-tetrahydrofolate/B-12 reaction which the primary route for restoring methionine. Methionine and SAMe supplements directly introduce new methyl groups into the body. TMG can provide a methyl group only to the extent that there is insufficient folate/B-12 to do the job. In some persons, the methylation effect of TMG is very minimal. In addition, persons who are undermethylated have a SAM cycle which is "spinning very slowly", much like a superhighway with little traffic. The answer for them is NOT to more efficiently convert the small amount of homocysteine to methionine (using TMG), but rather to directly introduce more methionine or SAMe into the body. A small percentage of persons with
sufficient dietary methionine cannot efficiently produce SAMe --- These persons need supplemental SAMe, and not methionine or TMG and are the exception to the rule. In most other cases, methionine supplements alone are sufficient. TMG is a great way to treat individuals with dangerously high homocysteine levels. TMG can be very useful in augmenting methionine therapy along with B-6/P-5-P , serine, etc. The challenge is to supply enough methyl groups to help the patient, without creating dangerously high levels of homocysteine. Use of TMG is an "insurance policy" against this happening. (Jan 22, 2003)
A quick way to test for need for methylation therapy is to carry out a cautious trial of SAMe. Within a week or two you should have your answer. If she clearly is improving on the SAMs (which is frightfully expensive)..... you can get usually the same benefits (albeit more slowly) using methionine plus calcium, magnesium, and B-6. This should be side-effect free unless (a) the methylation is begun too abruptly or (b) the patient has a rare genetic enzyme disorder which disrupts the SAM cycle. We've found that direct methylation is usually more successful than tinkering with the SAM cycle. The primary way humans receive most of their methyl groups is from dietary methionine. It's often hard to improve on Mother Nature. (Jan 20, 2003)
SAMe is likely to cause great worsening of symptoms, including mania, if
given to an OVER-methylated person. The incidence of overmethylation in our
patient database of 1,500 bipolar cases is about 18%. Bipolar disorder is
not a single condition, but a collection of very different biochemical
disorders under the same umbrella diagnosis. SAMe works great for truly
undermethylated patients, but all hell breaks out if given to someone who is
overloaded (genetically) with methyl groups. The right way to do this
is to (a) first determine the person's innate methylation tendency &
then (b) act accordingly. (Jan 31, 2003)
Schizophrenia
Severe wheat gluten intolerance can cause classic symptoms of schizophrenia, and amounts to about 4% of all schizophrenia diagnoses in the U.S. These persons usually become quite normal when placed on a gluten-free diet.
I've done medical histories for more than 2,000 persons diagnosed with schizophrenia and have always been struck by the high frequency of schizophrenia in other relatives. Interestingly, the schizophrenia would often skip a generation. NIMH data suggests that the overall incidence of schizophrenia in the USA is between 1% and 4%, depending on the definitions. However, the incidence of schizophrenia for children who have a schizophrenic parent is about 16%. This number doesn't change much for children of schizophrenics adopted at birth. I don't think there is "a schizophrenia gene", partly because this is a garbage term which encompasses several completely different conditions. There are a number of biochemical ingredients which predispose to each phenotype of SZ..... these may be either genetic or acquired. However, I'm absolutely certain there is a genetic component in most cases.
Carl Pfeiffer was the first to develop meaningful chemical classifications of schizophrenia (and separate treatments for each phenotype). Carl Pfeiffer of Princeton, N.J. saw more than 20,000 schizophrenics in his lifetime. He found that 90% of all SZ patients could be classified into 3 large groups, with completely different etiologies & treatment approaches. These he termed "histapenia", "histadelia", and "pyroluria". The remaining 10% fit into several splinter groups. One of the splinter groups was gluten intolerance, which
represents 4% (1 case in 25). This is a rare form of schizophrenia, but if you've got it, it's everything!
Multiple food & chemical sensitivities are also associated with histapenia (low histamine, overmethylation), the largest of all SZ groups, amounting to about 48% of all cases. For this group, SZ symptoms often worsen if exposed to the offending substances, & nice improvements often occur if they are identified & avoided. However, the food sensitivities usually disappear after about 1 year of aggressive Folate/B-12/B-3 treatment, which is the primary route to a normal life for these patients.
We've known for
more than 20 years that the metallothionein protein system
does not perform well in most ADHD patients. About 68% of them
exhibit very poor control of Cu & Zn, based on lab data
from more than 6,000 patients diagnosed with ADD/ADHD. Autism
is different in that about 90% of patients exhibit Cu/Zn
imbalances that are generally much more severe than in ADHD.
For several months, we have extended our metallothionein-promotion
protocol to ADHD, behavior, depression, and schizophrenic
patients who exhibit Cu/Zn imbalance. The informal results so
far are very encouraging. However, we've not yet done a formal
outcome study for these populations, and thus have no
statistics yet.
We are considering applying MT-Promotion to Alzheimers &
Parkinsons patients in the near future. Both disorders involve
serious oxidative stress and abnormal trace metal levels. In
addition, recent research has revealed a striking
metallothionein deficiency in the brains of Alzheimers
patients. (Feb 25, 2003)
I've evaluated more than 3,500
patients with a diagnosis of bipolar or schizophrenia. The
predominance of auditory hallucinations, serious self abuse,
aggressiveness, inability to continue school, and social
isolation...... all point in the direction of classic
"paranoid schizophrenia", although many of these
patients are labeled "bipolar disorder with psychotic
features". Most severely mentally ill persons with a
history of exceptional artistic or musical talent test as
overmethylated. The biochemical recipe for these
patients usually consists of (1) overmethylation, (2) low
folate levels, and (3) elevated blood copper levels. All three
of these chemical imbalances impact dopamine and
norepinephrine in the brain, and together can cause rather
extraordinary abnormalities in these important
neurotransmitters. In my opinion, the key to successful
treatment is biochemical treatment to overcome these chemical
imbalances...... fortunately this can be accomplished using
aggressive therapy with nutrients to normalize the chemical
factors.
Most mental breakdowns are triggered by severe stress, but the
underlying cause is genetic and involves brain chemistry. Many
persons self-medicate with alcohol, marijuana, or other
illegal drugs in a desperate attempt to feel better. Many
patients and their families erroneously believe that the EtOH
or drug experiences were the underlying cause of the
condition. They are wrong! This adult-onset condition will
strike eventually in most cases, even if substance abuse never
occurs.
Traditional medicine can provide medication support which can
usually eliminate (temporarily) most/all psychosis symptoms.
However, these patients are usually plagued by drug side
effects and are a mere shadow of their original selves. Common
side effects are (a) fatigue, (b) inability to
focus/concentrate for more than a few minutes, (c) change in
personality, (d) massive weight gain, etc. The most popular
drugs for these patients are Zyprexa, Seroquil, Risperdal,
Geodon, and Clozaril..... the so-called atypical
antipsychotics. Since most patients hate these medications,
poor compliance is a major problem.
I've seen many young schizophrenics and bipolar patients
achieve complete recoveries through biochemical (nutrient)
therapy. This rarely occurs with traditional medication
therapy. (May 12, 2003)
Some of schizophrenics who spontaneously get better are those
who experience a toxic psychosis. I have a friend who had a
toxic psychosis after an accidental overdose of a medication
during childbirth. For 6 hours she was a full blown paranoid
schizophrenic..... No symptoms in the following 20 years.
Also, schizophrenia comes in mild, moderate, and severe
versions. Many persons with a very mild genetic tendency for
SZ can experience an environmental insult which pushes them
into a temporary mental illness. Most will become quite ok
with or without therapy.
The real problem is the millions of SZ persons who have
moderate to severe SZ which does not go away easily.
(May 27, 2003)
Taurine
Yes, I've read a
few articles and a book that talked about Taurine's slow
metabolism and tendency to build up over time. Because of
this, I've believed that high doses of Taurine (1,000 to 2,000
mg/day) are ok in the beginning..... but that the dosages need
to be reduced within 2 weeks to about 400 to 500 mg/day.....
to achieve the same effect.
I believe that Taurine is especially effective for (1)
combating seizure tendency and (2) reducing liver stress in
processing fats. There have been several reports of
intolerances and side effects from use of Taurine, and I feel
that indiscriminant high doses are unwise.
About 12 months ago, there was a fad among several alternative
practitioners in which high doses of Taurine were given to
every autistic patient. One of the reasons given was "to
assist the liver cope with stresses associated with toxic
metal overload". This seems to be a poor reason, since
Taurine's action in the liver appears to be limited to fat
metabolism, and most autistics are slender malabsorbers with
low lipid levels. (June 24, 2003)
Womb Trauma
There is an
exquisite and fragile biological/biochemical process during
gestation in which short, dense immature brain cells are
pruned, grow into fully-developed brain cells, and then
(remarkably) experience growth inhibition to complete the
process. The molecular biology of this process is becoming
very well defined, and it is clear that many environmental
events can hinder or disrupt early brain development. The
primary culprits are oxidative stress, teratological
chemicals, and infections. The least appreciated of these
harmful factors is oxidative stress which can deplete key
proteins and enzymes required for normal brain development.
Environmental harm to a developing fetus can result from (a)
biochemical inadequacies of the mother, and (b) external
environmental insults. We're all familiar with birth defects
that can result from Thalidomide, Thorazine, Prolixin, Haldol,
and other psychiatric medications. Also the dangers of
mercury, lead, and other toxics are well established, and we
know that a mother's improper diet (e.g. inadequate folic
acid) can be harmful. Although lower on the radar screen,
fetal oxidative stresses can be equally devastating.
What I'm leading up to.... is the scientific fact that serious
emotional or physical stresses experienced by the mother can
impair early brain development, especially if the mother is
not biochemically intact. For example high emotional stresses
or physical trauma to the mother will weaken the activity of
metallothionein (MT) and glutathione (GSH) proteins, and
increase oxidative stress in the brain. MT-1 and MT-2 are
directly involved in growth of immature brain cells. MT-3 is a
key protein required for pruning and growth inhibition. These
proteins also have the job of defending against oxidative
stress in the brain and are consumed in the process. Maternal
emotional stresses and psychic traumae deplete the embryonic
brain of MT proteins and can compromise brain development.
Womb trauma is real and the concept of "a cry so
deep" is not psycho-babble guesswork. Rather, it is
solidly supported by scientific fields such as embryology and
molecular biology. (Aug 1, 2003)
If fetal or early infant traumae have resulted in a brain that
hasn't completely matured..... therapies to promote MT and GSH
appear very promising..... especially in tandem with
behavioral therapies which stimulate the development of new
brain cells.
If the net result of the traumae is biochemical or
neurotransmitter differences, then biochemical therapy aimed
at normalizing brain chemistry would be indicated.
If the traumae resulted in diminished ability to tolerate
environmental toxins (for example an incompetent blood-brain
barrier), then avoidance of such toxins would be an important
aspect of treatment.
If the traumae resulted in an innate inability to cope with
emotional stresses, then counseling or other psychological
services could be very beneficial.
If the traumae resulted in a brain that is structurally
different, this may represent "brain damage" that
may be refractory to all treatments. (Aug 1, 2003)
Zinc
There have been
several recent published articles which indicate that zinc and
zinc metallothionein proteins (1) tend to prevent brain
strokes, (2) tend to assist brain recovery after strokes, and
(3) that deficiency of Zn or Zn-MT is associated with
increased stroke likelihood. An occasional test for plasma Zn
could help identify the proper dosage. Most adults can safely
start with 25 to 50 mg/day of Zn. Without indication of B-6
deficiency, it might be a good idea to limit pyridoxine
hydrochloride (usual form of B-6) to about 200 mg/day. B-6 is
very helpful in enhancing the utilization of Zn.
After use of these nutrients with thousands of persons, I'm
not aware of a single case of harm. However, it is a good idea
to introduce zinc gradually & to take Zn during the PM
only. (June 3, 2003
Every 5 years or
so, the zinc experts of the world convene for a symposium in which they share new advances in Zn technogy
& research..... It's usually headed up by the eminent Prof.
Prasad.
One of the topics is laboratory testing to indicate an
individual's Zn status. They consider about 10 different methods including
packed cells, taste tests, etc...... The last two symposia resulted in the
consensus that none of the testing options is wonderful, but that the
best of the commercially available tests is plasma zinc. Taste tests
didn't make the top three methods.
However the Zn experts also stated that the most definitive determination of zinc depletion is the presence of symptoms of
Zn depletion which disappear after Zn supplementation.
My organization has evaluated the Zn status of 18,000 patients
and we've tried all of these methods. Our standard protocol involves
plasma Zn, being careful to use acid-etched, trace-metal-free tubes.
We find that virtually all treatment-naive ASD persons are
very Zn depleted and overloaded in "free" (unbound
by ceruloplasmin)copper. Our patient population for ASD is
2,800. Our database of 5,600 ADHD patients indicates that
about 75% are depleted in Zn. The remaining 25% have problems
associated with pyrrole disorders, methylation disorders, EFA disorders, toxic overloads, etc. (July 22, 2003)
The high level of zinc depletion in ASD appears to stem from a
genetic weakness in the metallothionein protein system.
Cu/Zn ratios in hair are very helpful in ADHD and behavior
disorders..... but far less useful in ASD, depression, and
schizophrenia. Tracking plasma Zn, serum Cu and serum
ceruloplasmin levels can be very helpful in guiding dosages
aimed at normalizing Zn. Management of Zn & Cu levels is a challenging problem in
ASD. Sometimes rather extraordinary Zn dosages are required to
normalize blood Zn levels.
Virtually all ASD persons are Zn depleted., but not all
exhibit an elevated Cu/Zn ratio. A minority of ASD patients
exhibit normal or low Cu levels in serum, but have vastly
inadequate levles of ceruloplasmin. Thus, the level of
"unbound" Cu can be very high, even though all
standard measures of Cu appear to be low. Some of these
patients seem to have a mild version of Wilson's Disesase.
(July 24, 2003)
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