The
Orthomolecular
Treatment of
Schizophrenia:
A Primer for Clinicians
Introduction
Schizophrenia affects one to
two percent of the population.
This disease is characterized by a
combination of perceptual changes
(e.g., hallucinations) and thought
disorder (e.g., delusions).' These
aberrant mental states, which can
lead to psychotic behavior, cause
a tremendous amount of emotional
and psychological suffering.
The cause of schizophrenia is
the subject of much debate. It is
considered a biochemical disease,
although certain genetic factors
most certainly play a role.
The majority of scientists
and psychiatrists subscribe to
the dopamine excess theory of
schizophrenia - that too much
dopamine is largely responsible
for the symptoms of psychosis.
However, since 1952, Dr. Abram
Hoffer, the founding father of
orthomolecular medicine, has
researched, published, and
expanded upon the adrenochrome
theory of schizophrenia.'- He and
his colleagues, Drs. Osmond and
Smythies, came to this theory by
studyingand researching the effects
of substances such as mescaline,
lysergic acid diethylamide (LSD),
and amphetamines - all of which
by Jonathan E. Prousky, ND, FRSH
The Canadian College of Naturopathic Medicine
can cause a clinical syndrome in
normal individuals that would be
clinically indistinguishable from
schizophrenia.
Hoffer noticed that mescaline
had a similar chemical structure
to that of adrenaline, and since
both can be converted to
indoles in the body, the potential
schizophrenic toxin might be an
indole derivative of adrenaline
with similar neurochemical
properties to that of mescaline or
LSD. He eventually deduced that
the schizophrenic toxin was an
oxidized derivative of adrenaline
known as adrenochrome. Since the
early 1950s. Hoffer's adrenochrome
theory has been validated due to
the following findings:
• that adrenochrome and its close
relatives - dopaminochrome
(from dopamine) and
noradrenochrome (from
noradrenaline) - are present in
the human brain,'^
• that these compounds probably
induce a combination of
neurotoxic and mind-mood-
altering effect, and' •'
• that reducing adrenochrome
and its close relatives is
therapeutic for the treatment of
schizophrenia.''
TOWNSEND LETTER - FEBRUARY/MARCH 200
The majority of schizophrenic
patients (about 90%) who receive
mainstream treatments remain
unwell and nonfunctional for
the rest of their lives despite
receiving the most advanced drugs
and social services currently
available.' Estimates of first
episode schizophrenics are a little
more optimistic, reporting that of
five recently diagnosed patients,
one will recover sufficiently to
live an almost normal life without
medication or with very low doses
of medication.*" The economic
costs of schizophrenia to society
are enormous, amounting to
approximately two million dollars
for each schizophrenic patient over
a 40-year course of the illness.^
In a recent publication
examining the economic burden
of schizophrenia in Canada, the
direct and non-direct heath care
costs associated with this disease
were estimated to be 2.02 billion
Canadian dollars in 2004.'" In
addition, when these figures were
added to the high unemployment
rate with additional productivity,
morbidity, and mortality losses,
the estimate reached 4.83 billion
Canadian dollars, for a total cost
estimate of 6.85 billion Canadian
dollars in 2004. The authors of
this report arrived at the following
conclusion: "Despite significant
improvements in the past decade
in pharmacotherapy, programs,
and services available for patients
with schizophrenia, the economic
burden of schizophrenia in Canada
remains high."
The purpose of the report is to
highlight the problems with the
standard medical treatment of
schizophrenia and to demonstrate
that the addition of orthomolecuiar
medicine provides patients with
the best opportunity of living a
reasonable quality of life. Common
orthomolecular treatments are
reviewed, including summaries
of relevant clinical studies and
prescribing information. Four
patient cases are described to
show the reader the potential
benefits of this approach, as well as
the difficulties with this approach
when certain essential treatment
components are lacking.
Standard Medical Treatment of
Schizophrenia
Schizophrenic patients will
remain ill and less capable of
engaging in a normal quality of life
as long as their treatments involve
only standard medical treatments.
Standard treatments use powerful
atypical anti psychotic drugs (APDs)
such as aripiprazole, clozapine,
olanzapine. quetiapine, and
risperidone. These drugs primarily
act on dopamine receptors within
the central nervous system and
reduce symptoms of the disease
by about 15-20%." Additional
medications are often prescribed
to control the Parkinsonian/
extrapyramidal symptoms (e.g.,
involuntary movements, tremors,
and rigidity) that can result from
their use.
When they were first introduced,
the atypical APDs were thought
to produce less Parkinsonian
symptoms. However, recent
research has demonstrated that,
at high dosages, the atypical
WNSENO LETTER - FEBRUARY/MARCH 2007
APDs pose the same risks for the
development of Parkinsonian
symptoms as do the older APDs."
The majority of schizophrenic
patients are also provided
with a supplementary cocktail
of medications consisting of
benzodiazepines, antidepressants,
and, sometimes, additional atypical
APDs.
Schizophrenic patients taking
one or two of the atypical APDs
are at high risk for brain damage,
cardiac arrhythmias, diabetes
mellitus, sedation, sexual
dysfunction, akathisia, and weight
gain.'- Often patients experience
a vague dysphoria from their
medications, a sense of unease
that something isn't quite right.**
Hoffer has written extensively
about the side effects caused
by the atypical APDs, which he
calls the "tranquilizer psychosis."
This occurs when patients are
taken from a psychotic state (with
symptoms that are best described
as "hot") to a new medicated
psychotic state (where they now
display symptoms that are best
described as "cold").'-'
Hot symptoms denote extreme
changes in personality (e.g.,
paranoid delusions, auditory
and/or visual hallucinations) and
behavior (e.g., agitation and/or
suicidal tendencies) that attract the
attention of friends, relatives, and/
or coworkers. Patients displaying
hot symptoms typically receive the
medical care they need because
their symptoms are so obvious
and abnormal. Cold symptoms
are a medicated and dampened
version of the hot symptoms. Even
though schizophrenic patients are
easier to manage while on atypical
APDs, when their symptoms
become cold, they fare no better.
They remain debilitated by this
tranquilizer psychosis and will be
unable to live a normal quality of
life unless they are lucky enough to
receive adjunctive orthomolecular
treatments.
Orthomolecular Treatment of
Schizophrenia
Orthomolecular substances are
found naturally in the human body
and include amino acids, essentUii
fatty acids, minerals, and vitamins.
To effectively use orthomoleculai
substances, it is necessary that
they be prescribed in the correct
amounts, which typically means
the use of optimum therapeutic
dosages that are individualized to
suit each schizophrenic patient.
The main orthomolecular strategies
that are required for the effective
treatment of schizophrenia
include; (1) dietary and lifestyle
adjustments; (2) vitamin B3 (niacin
or niacinamide); (3) vitamin C
(ascorbic acid); (4) zinc and vitamin
B6 (pyridoxine); (5) selenium: and
(6) omega-3 essential fatty acids.
Dietary and Lifestyle
Adjustments
All processed foods, refined
sugars, and stimulants (e.g., caffeine
and black tea) should be avoided
Strict avoidance of common food
allergens (e.g., milk, dairy, wheat
corn, and eggs) should be highly
considered since about 50% of all
chronic cases of schizophrenia
are caused by unrecognized food
allergies.'^ A combination of a bad
diet, poor lifestyle behaviors, and
common food allergens increase.s
the production of adrenaline
and consequently increases thi
production of adrenochrome iii
schizophrenic patients.'^"'
The ideal diet for the majorit\
of schizophrenic patients should
be high in protein and fat and low
in carbohydrates. Such a diet has
been clinically proven to correct
hypoglycemia, increase the
therapeutic effectiveness of vltamiii
B3, and reduce schizophreni(
symptoms.'' Cigarette smokinij,
alcohol consumption, and the use
of mind-altering substances (e.g..
hashish and marijuana) must be
avoided. Continued use of such
substances will significantly
interfere with the effectiveness ol
this approach. >
 Schizophrenia and NADH are available, then the
oxidized adrenaline is reconverted
to adrenaline. These back-and-
Vitamin B3 forth processes continue to occur
(Niacin or Niacinamide) in the presence of sufficient vitamin
B3 coenzymes. However, in the
To reduce the production
absence of enough NAD and NADH,
of adrenochrome, Hoffer and his
the oxidized adrenaline loses an
team decided upon the methyl
additional electron and becomes
acceptor vitamin B3 (either
adrenochrome. This last reaction is
niacin or niacinamide). This
irreversible and presumably occurs
vitamin had previously been used
in much greater concentrations in
in to treat pellagra (a disease
the schizophrenic brain.
clinically indistinguishable from
Another potential mechanism
schizophrenia), and it had relevant
for Vitamin B3 has to do with
biochemical properties.'- Hoffer
and his team researched the recent postmortem findings of
metabolism of adrenaline. They schizophrenic brain tissues."*
knew that the reaction involving In this report, an upregulation
noradrenaline to adrenaline of the enzyme tryptophan 2,3
required the addition of one dioxygenase (TD02) was found
methyl group. Vitamin B3 was among schizophrenic patients but
known to function as a methyl not among the controls who were
acceptor. Hoffer's team thought examined. The brain tissues of the
that an optimum dose of niacin schizophrenic patients showed
might decrease the amount of significant elevations of kynurenine
noradrenaline that would be (1.9 fold, p = 0.02), TD02 mRNA (1.7
converted to adrenaline. Since fold, p^O.049), and the density of
adrenochrome was thought to be an TD02-positive white matter glial
oxidized derivative of adrenaline, cells (p=0.01). In schizophrenia,
vitamin B3 could help to reduce the TD02 enzyme was found
the quantity of adrenochrome to be upregulated, causing an
by limiting the production of over-production of pathway
adrenaline. intermediates (e.g., kynurenine).
This upregulation might be
Hoffer and his team also responsible for the evolution of
discovered an additional bio- some schizophrenic symptoms.
chemical property of vitamin Instead of linking this upregulation
B3 that would help to explain its to some defective factor in the
therapeutic efficacy. Vitamin B3 Is a TD02 gene, the authors suggested
precursor to nicotinamide adenine that it might be due to a diminished
dinucleotide, which is present in niacin effect - possibly the result of
both oxidized (NAD) and reduced depressed production or reduced
forms (NADH) in the body. In the signal transduction via the niacin
brain, adrenaline becomes oxidized receptor. They recommended
and loses one electron to become that niacin or its congeners are
oxidized adrenaline. If enough NAD
Table 1. Summary of the First Clinical Study Using Vitamin B3
Number on Number Sent
Days in Eiectroconvulsive to Weyburn
Treatment Number Hospital Treatment (ECT) (Mental Hospitai)
Placebo 9 63 6 0
Niacin 10 60 7 1
Niacinamide 11 72 7 2
(Adapted from; Hoffer A. Vitamin 8-3 & Schizophrenia. Discovery. Recovery. Controversy. Kingston, Ontario:
Quarry Press. Inc,;1998:51, These findings were first reported in: Hoffer A. Osmond H, Callbeck MJ. Kahan 1.
Treatment of schizophrenia with nicolinic acid and Nicotinamide, J Ctin Exp Psychopath. 1957:18 131-158. 1
necessary regulators of this
biochemical pathway and should bi
capable of restoring homeostasis
Although these findings are ver>
important and relevant, they are ntii
novel. In 1973, Hoffer hypothesize(i
that there are defects in thf
metabolism of tryptophan and tha!
such defects or deficiencies in tht
ensuing reactions would cause <i
back-up of indole metabolites in
the precursor chain.'^ He further
hypothesized that such defects
would lead to an underproduction
of NAD.
The first report on thi
therapeutic use of vitamin B3 for
schizophrenia was presented in 19.SL'
at the Saskatchewan Committei
on Schizophrenia. At this meetins^
eight cases were presented, eacli
demonstrating favorable effect .^
from giving one to ten grams (g) ol
vitamin B3 and, in the majority <n
cases, equal amounts of vitamin C,
After a more involved pilot stud>
of 29 patients also demonstrated
excellent therapeutic responses t(>
vitamin B3,' the first double-blind
placebo-controlled experiment
in psychiatry was undertakeii
to assess whether or not this
vitamin was effective. The stud>
which began in 1952 but was noi
published until 1957, involved 'M^
acute schizophrenic patients who
were each randomized to placebo
niacinamide, or niacin.'- They werr
given 1 g three times daily for 3ii
days, and then followed for om
year. After the year, the patients
given vitamin B3 with the standarii
treatments at that time had mon
than double the recovery ratr
(80%) compared to patients in
the placebo group (33%). Table 1
summarizes the findings from this
initial clinical study.
Other clinical studies sooi i
Number followed that involved more patients
Well and longer treatment durations
3 The goals were to validate the initia I
8 findings and ascertain if there wen
other benefits and therapeutic
9
effects from the administration
of vitamin B3. In 1955, Hoffer and
his team reported on their results
TOWNSEND LETTER - FEBRUARY MARCH 2
involving 171 patients: 73 patients
received vitamin treatment with
niacin or niacinamide and were
compared to 98 patients having
received standard treatment (i.e.,
a combination of ECT. insulin
subcoma, and psychotherapy).'
(Table 2 summarizes these
findings.) They concluded, "When
used in adequate dosages, nicotinlc
acid and nicotinamide materially
contributed to the recovery of
schizophrenic patients." Vitamin
B3 reduced the number of suicides
to zero and imposed much less
of a burden upon the health care
system, since less patients in the
vitamin group were sent to the
mental hospital and subsequently
spent less time in the mental
hospital upon admission.
In their second double-blind,
placebo-controlled experiment,
Hoffer and his team used only niacin
and placebo.'^" The study lasted 33
days and involved 82 patients (43
in the placebo group and 39 in the
niacin group). (The results of this
study are summarized in Table 3.)
As can be seen, vitamin B3 once
again contributed significantly to
the recovery of acute schizophrenic
patients.
Other parameters were
evaluated and reported by Hoffer
and his team including the number
of patients readmitted, the number
of readmissions, the number of
patients well or much improved,
and the number of patients who
were considered cured.''" This
Group Number
Treatment 73
Comparison 98
(Adapted from: Hoffer A. Niacin Therapy In Psychiatry. Springfield, IL: Charles C Thomas: 1962:108.)
Table 3. Results from the Second Double-Blind, Controllec1 Experiment
Group Number
Placebo 43
Niacin 39
(Adapted from: Hoffer A. Niacin Therapy In Psychiatry. Springfield, IL: Charles C Thomas; 1962:42-46.)
WNSEND LETTER - FEBRUARY/MARCH 2007
data involved the following groups
of patients: (1) those who only took
vitamin B3 while in the hospital and
not in the community; (2) patients
who did not take vitamin B3 when
in the hospital but did take the
vitamin when in the community; (3)
patients who took vitamin B3 when
in the hospital and community; and
(4) patients who never took vitamin
The results of this review demonstrated
that patients who had taken vitamin B3
fared much better than patients who were
not given the vitamin.
B3. The results demonstrated that
patients in the community who
were taking niacin (groups 2 and
3) had more community years that
were free of readmissions compared
to patients not taking vitamin B3
(groups 1 and 4): 91% versus 62%
of the community years free of
readmissions. The entire niacin
group (group 3) was readmitted 38
times for 67 readmissions (average
was 64 days per patient), and this
was much better than the placebo/
non-niacin group (group 4) that
was readmitted 36 times for 81
readmissions (average was 147 days
per patient), Once all the data was
combined, the results revealed that
the most five-year cures and best
treatment responses were among
the patients who took vitamin B3
Table 2. Effects of Vitamin 63 Against Standard Treatment
Mean Days Number Sent to Mental Hospitai
in Hospital After Treatment
63 7 234
50 47
Mean Number that Mean Number of Days
Age Received ECT in the Hospital
31.9 21 73.8
30.3 15 72
Schizophrenia
when in the hospital and in the
community.
Hoffer followed patients from
1953 to 1960 and published a total
of six double-blind, randomized
controlled clinical trials. All these
trials confirmed the positive effects
that vitamin B3 had upon the
recovery of acute schizophrenic
patients and verified that the use of
this vitamin substantially reduced
patients' reliance upon the health
care system.- Hoffer even followed
patients who were being treated by
other psychiatrists from October
1. 1955 to December 31. 1962.' The
results of this review demonstrated
that patients who had taken
vitamin B3 fared much better than
patients who were not given the
vitamin. The patients on vitamin B3
had fewer hospital readmissions,
required hospitalization for fewer
days, and had no suicides.
In terms of treating chronic
schizophrenic patients, Hoffer's
early studies did not show a
Mean Days Number of
in Mental Hospitall Suicides
0
319 4
Not Improved
Improved (Percentage Improved)
25 18(41.9%)
8 31 (79.5%)
 Schizophrenia
favorable response among chronic
schizophrenic patients who were
ill longer than one year. However,
when Hoffer reviewed this problem
more substantially, he discovered
that the treatment duration was
not long enough to have produced
adequate results. Chronic patients
required vitamin B3 treatment for
five or more years in order to derive
observable benefits.' -' In one study
involving 32 chronic patients,
all the patients failed to respond
to vitamin B3 after two years
of use. Nineteen of the patients
discontinued the vitamin, and the
remaining 13 patients continued
with the vitamin treatment. Data
was obtained for the years, 1956-
1957, 1958-1959. 1960-1961, 1962-
1963. and 1964.' Of the patients
not on niacin, the mean number
of days spent in hospital were 691
compared to 79 in the niacin group.
Also, the proportion of time spent
in the hospital was substantially
less for the chronic patients who
remained on the vitamin.
In a more recent analysis of 27
chronic schizophrenic patients who
had been under treatment for at
least ten years, consistent treatment
with vitamin B3 produced the
following results: 11 patients were
able to work: two patients were
able to marry and look after their
families and homes; two patients
were single mothers able to take
care of their children; and three
patients were able to manage their
own businesses.-' These results are
remarkable when one considers
the state of these patients prior
to receiving orthomolecular care.
The average age of these patients
was 40. The majority of them had
been ill for seven years before
they sought treatment from Hoffer,
and all had been unresponsive to
previous treatments.
If one is to look at the enormity
of this data, as I have, the only
reasonable conclusion to be made
is that all schizophrenic patients.
BEST OF NATUROPATHIC MEDICINE
including both acute and chronic
patients, need to be treated with
vitamin B3 as quickly as possible
and for the duration of their
lives. Vitamin B3 treatment offers
significant hope of a reasonable
quality of life among patients
who would otherwise remain
incapacitated and in and out of
hospitals for the remainder of their
lives.
The starting dose of niacin for
adults is 1000 milligrams (mg) three
times daily. In my opinion, the daily
dose needs to be slowly increased
to 4,500-18,000 mg to achieve the
best possible outcome. Patients
need to be educated about the
flushing, heat, itchiness, pruritis,
redness, and tingling that they
will transiently experience. These
benign cutaneous reactions usually
begin 15 minutes after taking
niacin for the first time, and are
first noticed around the forehead,
then descend to the thorax, and
sometimes to the feet. These
reactions typically abate in one to
two hours following the ingestion
of niacin. Niacin causes these
cutaneous reactions by inducing the
production of prostaglandin D^ in
the skin, leading to vasodilation and
a marked increase of its metabolite,
9a, UP-PGF2. in the plasma.-^ Niacin
is its own anti-flushing agent, and
taking it regularly depletes the skin
of prostagiandin D2 and prevents
subsequent cutaneous reactions. At
3,000 mg daily, the flush and other
symptoms will cease to be an issue
following the first two to three days
of treatment and will practically
disappear thereafter. If patients
are not consistently taking these
high-milligram doses throughout
the day, they will continually
re-experience these cutaneous
reactions. The concern over liver
toxicity is very minor if immediate-
release niacin preparations
are used.-'-"' Sustained-release
preparations (and likely other
preparations such as timed- or
slow-release ones) can cause liver
toxicity and are not recommended
for schizophrenic patients unless
under close supervision.^^ [n my
clinical experience, niacin is more
effective and better-tolerated than
niacinamide for schizophrenia.
Some patients prefer niacinamide,
since it does not cause flushing
as well as the other cutaneous
reactions. Nausea and dry mouth
are much more common with
the use of niacinamide than with
niacin. The daily dosages of
niacinamide should not exceed
6,000 mg, since the likelihood of
nausea accompanied with vomiting
is much greater.-'*
Vitamin C (Ascorbic Acid)
In their early pilot and
controlled clinicai studies. Hoffer
and his team also used vitamin
C since its powerful antioxidant
properties would also diminish
the double oxidation of adrenalin
to adrenochrome and prevent its
auto-oxidation in critical brain
areas.--' This vitamin is also an
effective anti-stress nutrient that
helps schizophrenic patients
cope more effectively.-' There is
recent evidence that high-dose
vitamin C (3,000 mg of sustained-
release daily) is indeed an anti-
stress nutrient, since it was able to
subjectively reduce psychological
stress, decrease blood pressure,
and lower cortisol levels in healthy
men after 14 days of use.-" A report
by Smythies described additional
roles that vitamin C has upon
the brain including the following:
(1) its ability to protect NMDA
receptors from glutamate toxicity
within the brain; (2) its antagonism
of the effects of amphetamines;
(3) its enhancement of older
APDs like haloperidol; and (4)
its ability to prevent the auto-
oxidation of dopamine to its toxic
derivatives.^^ Vitamin C also
conserves intracellular glutathione
and is likely a redox glutathione
cofactor.^" This is important since
glutathione S-transferases are
important enzymes that facilitate
the conjugation of glutathione to
adrenochrome. dopaminochrome,
and noradrenochrome and render
Y/MARCH
these toxic metabolites non-toxic
by the production of unreactive
glutathione conjugates.^' The gene
for glutathione S-transferase is
defective in schizophrenia.^ I believe
that this defect might be partially
remedied by supplementation with
high dosages of vitamin C, which
would preserve glutathione in its
reduced state and increase the
amount of available glutathione
that could be used for the synthesis
of the glutathione S-transferase
enzyme.
Vitamin C should be prescribed
at 1,000 mg three times daily and
then eventually increased to the
sub-laxative dose. There are reports
suggesting that acute and chronic
schizophrenic patients require
more of it. In one study, the fraction
of urinary vitamin C was evaluated
in 44 recently hospitalized acute
schizophrenic patients and was
compared to 44 other subjects
serving as the control group.-'-
All the subjects were given 1.76
g of vitamin C orally and had
their urinary levels of vitamin C
measured every two hours during
a six-hour collection period. The
schizophrenic patients differed
significantly from the control group
in their elimination of ascorbic
acid. Seventy-six percent of the
schizophrenic subjects were low
excretors, which means that less
than 17% of the administered oral
dose of vitamin C was recovered
in their urine samples. This result
was 2.5 times the incidence of the
control group, which demonstrated
that only 30% from this group were
low excretors.
In this same study, the low
excretors of both groups were
given additional vitamin C for
seven days (approximately 10
g), and urine samples were
collected on the eighth day. In the
control group, the low excretor
group went from 7/16 to 5/16 and
remained essentially unchanged.
In the schizophrenic group, the
low excretors decreased from 9/11
to 3/11, a substantial change. The
authors of this study concluded
OWNSEND LETTER - FEBRUARY/MARCH 2007
that a combination of genetic and
nutritional-environmental factors
cause a higher degree of "tissue
unsaturation" among the acute
schizophrenic patients.
In another study using chronic
schizophrenic patients, the plasma
and urinary vitamin C levels of
35 schizophrenic patients were
compared to an equal number of
controls.'' All subjects were given
the same hospital diet and 70 mg
of vitamin C daily for four weeks.
Baseline plasma vitamin C values
were lower in the schizophrenic
patients (p < 0.05), but normalized
to be approximately the same as
the control group values after
the four weeks of treatment. The
mean vitamin C levels as measured
in a six-hour urine collection
were different among the low
excretors of both groups, and
this difference reached statistical
significance (p<0.05) - 15.9 mg for
schizophrenics and 39.5 mg for the
controls, When all theschizophrenic
and control subjects were given a
loading test of 1 g of vitamin C after
the four weeks of 70 mg of oral
vitamin C daily, the schizophrenic
patients continued to excrete lower
amounts of vitamin C in their urine
compared to the control values.
After the loading test, the plasma
levels of vitamin C were different,
with the schizophrenic patients
having a lower mean value than
the controls (p<0.05). After one
month of supplementation with 1
g of vitamin C, the plasma levels of
each group equalized, as did their
six-hour urinary excretion rates.
The authors of this study were in
agreement with the hypothesis that
Table 4. Psychiatric and Non-Psychiatric Groups with
Abnormal Urine Levels of Kryptopyrrole
Group
Acute schizophrenics
Chronic schizophrenics
All non-psychotics
Physically ill patients
Normal subjects
Recovered schizophrenics
Schizophrenia
"schizophrenic patients require
higher levels of vitamin C than the
suggested optimal ascorbic acid
requirement for healthy humans."
Vitamin B6 (Pyridoxine) and
Zinc
Many schizophrenic patients test
positive in the urine for a compound
known as kryptopyrrole, which is
associated with physiological and/
or psychological stress.''' Hoffer
compiled data from thousands of
patients and found abnormal levels
of kryptopyrrole in the urine of
different types of psychiatric and
non-psychiatric disorders (Table
4).'
Kryptopyrrole combines ir-
reversibly with pyridoxine and
then with zinc, and this creates a
combined deficiency syndrome.^^'
Some common clinical symptoms
of patients having high amounts
of kryptopyrrole in their system
are white areas in the fingernails,
stretch marks on the body, and
female premenstrual syndrome."
Many of the clinical features of
patients excreting high amounts
of kryptopyrrole resemble those of
schizophrenia.'^ Even though it is
possible to test for this compound,
I choose not to do so, and I
prescribe these nutrients to all of
my schizophrenic patients. They
are relatively free of side effects
and often help to reduce symptoms.
The daily dosages that 1 routinely
prescribe are 250 mg of pyridoxine
and 50 mg of zinc. ^
Percentage with Abnormal Urine Levels
75
50
25
5
0
 Schizophrenia
Selenium
I recommend that all
schizophrenic patients take 200-
400 micrograms (meg) of selenium
daily. Several published reports
indicate a potential need for this
trace mineral among schizophrenic
patients. In one report. Brown
and Foster linked a deficiency of
this trace mineral to an increased
Regardless of when the orthomolecular
treatments begin to demonstrate their
effectiveness, it Is paramount that,
once initiated, they are never discontinued.
prevalence of schizophrenia in
regions of the United States where
fodder crops had the lowest levels
of selenium.-"' They calculated the
selenium-related relative risk to
be 1.77:1 in these areas. According
to these authors, some of the
biological consequences ol selen-
ium deficiency (i.e., prostaglandin
imbalances, viral mutation,
excess 12-HPETE production, and
decreased glutathione peroxidase
activity) might be related to the
etiopathology of schizophrenia.
They also reviewed additional
evidence of a negative correlation
in schizophrenic patients between
glutathione peroxidase activity
and brain damage (i.e., brain
atrophy and increased ventricle-
brain ratios), which was not found
among a group of controls. In
another report, Foster suggested
that selenium might be tried as
a treatment for schizophrenia
since it protects against free
radical damage and is probably
antagonistic to adrenaline and
therefore to adrenochrome." He
also hypothesized that, when
supplementing with essential
fatty acids, selenium is essential,
as it would prevent the excessive
oxidation of the fatty acids, restore
glutathione peroxidase activity,
and ensure the proper production
and action of prostaglandins. In
that same report, Foster discussed
the relationship between niacin
and selenium, in that niacin being
a methyl acceptor might slow
down the metabolism of selenium
(since its metabolism involves
methylation) and prolong its action
in the body. Berry was the first to
report on the potential relationship
between selenium and niacin.'* He
reported that a certain sub-type
of schizophrenia might be due to
a defective selenium transport
protein and to low levels of this
trace mineral in the body. Niacin's
antipsychotic properties, according
to Berry, are possibly due to its
prolongation of selenium within the
body, which would correct both
the defective transport protein and
its deficiency.
Foster also reported on an
additional reason why selenium
would appear to be useful for the
treatment of schizophrenia.•'•' He
noted some evidence that showed
that the desiccated or pure form of
thyroid hormone achieved better
cure rates for schizophrenia when
compared to untreated patients
and to patients receiving standard
tranquilizers. He suggested that
the triiodothyronine component
accounted for the favorable
clinical results, as this hormone
would reverse the toxic effects of
excess adrenochrome. Since the
deiodinase enzyme that converts
thyroxine to triiodothyronine
requires selenium, he hypothesized
that an effective treatment protocol
should include both selenium and
thyroid hormone.
TOWMSEND LETTER - FEBRUARY/MARCH 2007
Omega-3 Essential Fatty Acids
from Fish - Docosahexaenoic
Acid and Eicosapentaenoic Acid
Schizophrenia is characterized
by lipid membrane abnormalities
(a.k.a., the phospholipid membrane
hypothesis) that include
abnormal brain phospholipid
turnover, increased levels of
phospholipase A2, reduced niacin
skin flush response, abnormal
electroretinogram, and reduced
cell membrane levels of omega-3
and omega-6 polyunsaturated fatty
acids.^"^' Fish oils, particularly
the eicosapentaenoic acid (EPA)
content (as opposed to the
docosahexaenoic acid [DHA]), have
been shown to help with both the
positive (e.g., hallucinations and
delusions) and negative symptoms
(e.g., flat affect, depression, and
isolation) of schizophrenia when
used as an adjunct to standard
treatment.'- The optimal daily dose
should provide at least 2 g of EPA.
Treatment Strategies
Even though all the nutrients
just described are essential, the
most important are vitamins B3
and C. I recommend that these
particular vitamins be given to
schizophrenic patients initially,
and the others then added over
several months. Of course, success
is invariably dependent on the
patient's willingness to comply and
the skill of the prescribing clinician.
Compliance is a significant issue
with all schizophrenic patients.
At the beginning of this report. I
mentioned that one out of five first-
episode schizophrenic patients
have a chance at living a near-
normal existence. Of the remaining
four, only one patient will comply
with his medications; one patient
will not take his medications
continuously due to side effects:
and the remaining two patients
will be lost to follow-up.^ They
need to be informed that their
orthomolecular treatments are
equally as important as are their
antipsychotic medications. Results
are sometimes seen after the first
 two months," and sometimes three
to six months are necessary before
clinical benefits are observed.*'
For chronic patients having had
schizophrenia for five or more
years, the necessary treatment
time is at least five years before
benefits are noticed. Regardless
of when the orthomolecular
treatments begin to demonstrate
their effectiveness, it is paramount
that, once initiated, they are never
discontinued. Medications should
likewise not be discontinued but,
with the cooperation of the patient's
psychiatrist, can be reduced very
slowly over the course of many
months to several years once
the orthomolecular treatments
are helping. Abrupt cessation of
atypical APDs will cause a relapse,
as will too much of a decrease
or too early of a decrease in
medication. The orthomolecular
approach requires a tremendous
amount of patience from the
prescribing clinician, since results
take a long time to materialize.
Likewise, schizophrenic patients
and their respective families and/
or caregivers need to have the
necessary patience and motivation
to stay the course.
Measuring Patient Progress and
Prognosis
Once orthomolecular treatments
are started, how is the clinician
able to monitor his/her patients'
progress? Hoffer has published
a practical system that can be
used to determine how a patient
is responding to orthomolecular
treatments.-' He has four measures
of recovery:
Table 5. Expected Results from Orthomolecular Treatments
Group
Sick one year, or in second or third relapse
Sick two to five years
Sick over five years, but out of mental hospital
Sick over five years and in mental hospital
TOWNSENO LETTER - FEBRUARY/MARCH 2007
1. Freedom from signs and
symptoms (1 point)
2. Ability to get on reasonably well
with family (1 point)
3. Ability to get on reasonably well
with the community (1 point)
4. The ability to work at a job or
to be productive in the same
manner as before the illness
struck
Patients who have never been
engaged in some type of job or
productive work can be judged
by their ability to perform any
useful work. (1 point)
Patients are categorized as
"well" if they have achieved 4
points, "much improved" if they
achieved 3 points, "improved"
when they have achieved 2 points,
and "not improved" if they only
acquired 1 point. I also use a
questionnaire, known as the HOD
test (Hoffer-Osmond Diagnostic
test for schizophrenia), to monitor
and evaluate my patients. This
true/false test assesses the
overall intensity of the disease by
providing a total score (TS). The
HOD test also provides scores for
common schizophrenic symptoms
of perception (PerS), paranoia
(PS), and depression (DS). If a
patient achieves a high TS (>30)
or a high score (>3) in any of the
individual categories, this would
indicate pronounced illness. Once
orthomolecular treatments begin
to show effectiveness, the scores
decrease. This test has been shown
to be valid in terms of its ability to
detect (diagnose) schizophrenia
and to assess the severity of the
In terms of prognosis, if the
orthomolecular program is started
early in the course of the patients'
Duration of Treatment
Up to one year
Up to five years
Five or more years
Five or more years 25%
Schizophrenia
disease, they will have greater
chances of recovering. According
to Hoffer's eariy placebo-controllec!
clinical trials and his many
published clinical reports spanning
more than 50 years, patients can I
expect certain prognoses once
orthomolecular treatments are
initiated.'^ Table 5 indicates the
expected results from the addition
of orthomolecular treatments to
the standard approach.
Schizophrenic Cases
I have chosen four cases from
my naturopathic medical practice.
The first two cases represent the
effectiveness of this approach. The
latter two cases demonstrate the
difficulties that patients and their
families have with this approach,
especially when necessary
treatment components are missing
or not sufficiently followed.
Case#l
This 24-year-old female first
presented to my private practice on
October 1, 2005. She was formally
diagnosed with schizophrenia
in March 2005 when she was
hospitalized for two-and-a-half
months due to paranoid ideation
that involved worries about
being poisoned, social isolation
and withdrawal, and significant
impairments in maintaining
healthy relationships. Prior to her
formal diagnosis, she reported
several years of intermittent
paranoid ideation; she had abused
drugs such as cocaine, heroin,
and methamphetamine, felt that
certain noises were causing her
to be crazy, thought she could
I
Well and Much Improved
90%
73%
50%
 Schizophrenia
read people's minds, and felt
unable to hold down jobs. During
the previous six years, she was
enrolled in a geography program
at Carleton University in Ottawa,
but had to drop out since she could
not handle the course load. She
had some boyfriends while living
in Ottawa, but the relationships
failed since she became very
suspicious of each boyfriend and
thought he was trying to poison
her. She also thought her family
members were out to poison her
and that her mother wanted her
dead because she was not Jewish
enough. In November 200,5. she
was hospitalized a second time for
severe auditory hallucinations, but
only for the night and was then
discharged the next day. At the time
of my initial consultation, she was
unemployed and unable to pay for
her rent and other living expenses.
She was living part of the time with
her mother, but would also live in
an apartment that was financed by
her mother. Although she was not
acutely psychotic, she continued
to exhibit schizophrenic symptoms
such as social isolation and
frequent auditory hallucinations.
She was taking 1 mg of risperidone
and 30 mg of olanzapine at that
time. Table 6 sumnfiarizes the
patient's response to the adjunctive
orthomolecular treatments.
This patient has continued
to do exceptionally well. In June
2006, I wrote to her family doctor
about the benefits of thyroid
medication for the treatment of
schizophrenia (Hoffer, 2001b). The
patient was prescribed desiccated
thyroid and has been taking it
daily. I also corresponded with her
psychiatrist, and in early June 2006
her olanzapine was reduced to 20
mg daily. As of my last visit with
her. August 20. 2006, she remained
well and free of all schizophrenic
symptoms. Even though her initial
HOD scores were within normal
limits, they must have been

Table 6. Case #1: Patient's Response to Adjunctive Orthomolecular Treatments

Consultation Dates October 1, 2005 November 26. 2005 January 21, 2006 May 27, 2006

Clinical Presentation Regularly hearing More engaged with her Psychiatrist approved Working at a major
voices, unable to attend family. Heard voices the reduction in meds. Montreal hotel and has
University full-time one to two nights Patient no longer gained acceptance to a
(taking one course), during the past month. hearing any voices. community college for
antisocial behavior. Continues to watch lots is full of energy and hotel management. No
watching lots of TV, and of TV, but wants to start is exercising three schizophrenic
sleeping more than 11 volunteering next week. times each week. symptoms.
hours each night. In the last month, had Quit smoking since
pizza once, avoided November. Received a
all alcohol, and only B+ last semester and
smoked two to three is enrolled in another
cigarettes. course.

Current Psychiatric 1 mg of risperidone and Same. 1 mg of risperidone and 1 mg of risperidone and

Medications 30 mg of olanzapine 25 mg of olanzapine 25 mg of olanzapine
daily daily. daily.

Orthomolecular 3 g of niacin, 3 g of Increased niacin to 2,000 Added 200 mg daily of Plan was modified to
Treatments & Plan vitamin C, 250 mg of mg three times daily. Ginkgo biloba extract. include 500 meg of
pyridoxine, 50 mg of Added a caffeine-free Instructed patient to chromium twice daily.
zinc, 2 teaspoons of extract of green tea to continue with the current and herniacin was
highly concentrated help with acne. Letter program. Discontinued increased to 6,500 mg
fish oil, and 5 mg of sent to psychiatrist about the methylcobalamin daily
methylcobalamin. Patient reducing olanzapine to due to acne.
advised to quit smoking 25 mg daily.
and cut out all dairy,
wheat, and alcohol.

HOD Results Not Assessed.

TS (normal <30) 27 13 3
PerS (normal <3) 4 4 4
PS (normal <3) 2 0 2
DS (normal <3) 0 0 0
Category of Recovery Not improved. Improved. Well. Well.

TOWNSEND LETTER - FEBRUARY/MARCH 200

 abnormal for her, since she was
very symptomatic, and her clinical
picture improved dramatically as
these scores decreased. In August
2006, I spoke with the patient's
mother about her daughter's
progress. The mother said that
the "orthomolecular treatments
have given her daughter back
her life." Per her mother's report,
the patient is a lot slimmer, had a
boyfriend during the summer, and
is working every day and paying all
of her expenses including rent and
groceries. She is looking forward
to starting a community college
program in the fall of 2006. and her
disease is clinically in remission.
I instructed her to remain on
the current program and to not
change anything without first
consulting me. She will still have
regular visits with me, but not as
frequently. I expect her to remain
well, for she has not had a relapse
since commencing treatment. She
has many of the essentials of good
response, which include a strong
desire to get well, the cooperation
of an open-minded psychiatrist,
and a very supportive and caring
family.
Schizophrenia
Case#2
This 36-year-old male patient
presented to the Robert Schad
Naturopathic Clinic on May 23.
2006 with a chief complaint
of schizophrenia. I supervise
naturopathic interns on this clinical
shift, so a fourth-year clinical
Intern and myself evaluated thi.s
patient. The patient's goal was to
eventually get off his medication
due to troublesome side effects
of fatigue and weight gain. Since
January 2006, the patient was

Table 7. Case #2: Patient's Response to Adjunctive Orthomolecular Treatments

Consultation Dates May 23, 2006 May 30. 2006 July 25, 2006 August 15, 2006

Clinical Presentation Very talkative. Expressed strong Hearing fewer voices Continues to experience
disorganized speech, desire to get off his than the previous visits. fatigue. His voices are
and thought blocking. medications. Very Continues to be tired still present, but remain
Described his drowsy and sleeping and fatigued most of the as per the last visit.
schizophrenia as some ten to 12 hours each time, which he feels is Continues to be very
type of gift from God. day. Complained of due to the medication. Is interactive with coherent
Also believed that there muscular contractions sleeping ten to 12 hours speech and less thought
were supernatural around his head, which each day. More coherent blocking.
beings and angels he felt was due to the speech and less thought
following him and medication. Believed blocking.
looking after his that he has clairvoyant
well-being. Described abilities.
various instances of
seeing supernatural
beings that no one else
could see.

Current Psychiatric 450 mg of clozapine Same. Same Same.

Medications daily.

Orthomolecutar None prescribed. 1,000 mg of both niacin 2,000 mg of niacin Given an intramuscular
Treatments & Plan and vitamin C three three times daiiy. injection of vitamin
times daiiy. Omega-3 Vitamin C the same as B12 (1,000 meg). Letter

I
fatty acids providing before. Ginkgo biioba sent to patient's
a daily dose of 3,600 extract at 240 mg psychiatrist requesting
mg of EPA and 1,800 daily. Added 250 mg of a minor decrease in his
mg of DHA. Given an pyridoxine and 50 mg medication to 425 mg
intramuscular injection of zinc. daily.
of vitamin B12 (5,000
meg).

HOD Results Not assessed. Not assessed.

TS (normal <30) 32 5
PerS (normal <3) 11 1
PS (normal <3) 2 0
DS (normal <3) 2 1

Category of Recovery Improved. Improved. Improved. Improved.

TOWNSEND LETTER - FEBRUARY/MARCH 2007

 Schizophrenia
on clozapine at a daily dose of
450 mg. He was required to get
blood tests every two weeks due
to the potentially life-threatening
agranulocytosis. Previously, he
had been resistant to a number
of antipsychotic medications that
included loxapine, quetiapine,
olanzapine, and risperidone. He
was also given lorazepam in the
past, but was no longer taking it.
His most recent hospitalizations
were in January and March of
2006. He was considered a chronic
patient since his schizophrenia
had lasted more than five years,
but the year of his initial diagnosis
could not be ascertained due to the
patient's difficulties with timelines.
During the initial interview, he was
very talkative, had disorganized
speech, and demonstrated
thought blocking. He described his
schizophrenia as some type of gift
from God. He also believed that
there were supernatural beings
and angels (which he could see)

Table 8. Case 3: Patient's Response to Adjunctive Orthomolecular Treatments

Consultation Dates August 30, 2004 September 18. 2004 October 16. 2004 November 13, 2004

Clinical Presentation Thought blocking, Patient was more Auditory hallucinations Patient reported
difficulty concentrating. positive and motivated have stopped smoking less. Living
difficulty answering compared to the - no longer hearing in new group home,
routine questions, initial visit. Reported death threats in his and has more privacy.
and comprehension some muscle tension head. Reduced the Is volunteering as a
problems. Reported in his neck. Was niacinamide to 1,500 salesperson. Auditory
constant auditory encouraged to remain mg daily. Anxiety hallucinations continue
hallucinations, on all the prescribed has decreased, and to be absent. Anxiety
and some visual supplements. patient exhibited better and diaphoresis have
hallucinations. Very eye contact. Less not worsened since the
anxious, restless and diaphoretic than the last visit.
visibly diaphoretic initial visit.

Current Psychiatric 20 mg of olanzapine Same. Same. 1 mg of risperidone at

Medications daily, 0.5 mg of bedtime in addition to
clonazepam twice daily, the other medications.
1 mg of apobenztropine
daily, 37.5 mg of
venlafaxine, and an
injection of 40 mg
flupenthixol every 2
weeks.

Orthomolecular 1,000 mg of Niacinamide was Patient instructed to Niacinamide was

Treatments & Plan niacinamide three reduced to 1,000 mg stay on all supplements. discontinued. 1.000 mg
times daily, 1,000 mg of twice daily. Was also Was given an of niacin three times
vitamin C three times prescribed 500 meg of intramuscular injection daily was prescribed.
daily, 2 teaspoons of chromium three times of 5 mg of folic acid and Given an intramuscular
liquid fish oil (2,100 daily, to help with the 1,500 meg of vitamin injection of 5 mg of folio
mg of EPA and 1,500 hypertriglyceridemia. B12. acid and 1.500 meg of
mg of DHA), 50 mg of weight gain, and vitamin B12.
zinc, and 250 mg of dysinsulinemia
pyridoxine. associated with the
use of atypical APDs.
He was given an
intramuscular injection
of 5 mg of folic acid and
1,500 meg of vitamin
B12.

HOD Results Not assessed. Not assessed.

TS (normal <30) 50 36
PerS (normal <3) 10 6
PS (normal <3) 10 4
DS (normal <3) 1 5

Category of Recovery Not improved. Not improved. Not improved. Improved.

TOWNSEND LETTER- FEBRUARY/MARCH

 following him and looking after
his well-being. He lived with his
parents who were doing whatever
they could to make his life as
productive and comfortable as
possible. Table 7 summarizes the
patient's response to the adjunctive
orthomolecular treatments.
This patient has not been on the
orthomolecular program for a long
time. Since my initial consultation,
he has shown a positive response
by having fewer auditory
hallucinations. This change was also
reflected by the decreases in his
TS and PerS HOD scores. To derive
the most benefits, he will need
to remain on the orthomolecular
program for at least five years, but
the duration of his life would be
preferable. Although his "Category
of Recovery" did not change in
this short time, he showed modest
improvements and was able to
complete his examination for a
plumbing license. I believe he has
a very good chance of recovering
since he has the necessary
components for favorable response
(e.g., a supportive and caring
family, proper psychiatric care, and
orthomolecular treatment).
Case#3
This 30-year-oId male patient
presented to my office on August
30, 2004. He reported that his
schizophrenic symptoms began
when he was 15 years old. At that
time, he was having paranoid
thoughts that involved abduction
and death threats. For the next
eight years, his symptoms
progressively worsened, and by
1997. he was having constant visual
hallucinations. In that same year, he
had a difficult time dealing with the
end of a relationship with a woman.
He was hospitalized in December
of 1997 and has been hospitalized
15 additional times, with the latest
one occurring in March 2004. In
1998, the patient was formally
diagnosed with schizophrenia. At
my initial consultation, he reported
having trouble thinking clearly
and difficulty an.swering routine
TOWNSEND LETTER - FEBRUARY/MARCH 2007
questions. He sweated profusely Schizophrenia
during the visit and frequently
drank water from a large water he was finally able to engage
bottle. He was having constant in some type of regular work.
auditory hallucinations and His HOD scores reflected these
occasional visual hallucinations. He clinical improvements as well. His
described himself as an antisocial "Category of Recovery" went from
person. He was living in a group "not improved" to "improved" in
home for mentally ill patients, under three months of treatment.
but purposely kept his distance Sadly, from the early part of
from the other residents. He was December to February 2005, the
The orthomolecular approach requires a tremendous
amount of patience from the prescribing clinician,
since results take a long time to materialize. Likewise,
schizophrenic patients and their respective families and/
or caregivers need to have the necessary patience and
motivation to stay the course.
not exercising regularly and was patient was very inconsistent with
smoking 12-15 cigarettes daily. He the orthomolecular treatments
was last employed in 2000 as a and even did some drugs for a
bus boy, which involved washing few weeks during the Christmas
dishes and cleaning up, but this holidays. He had a significant
only lasted a few months. His relapse that caused a return of his
goals were to eventually get off his previous symptoms, including the
medications, to experience fewer constant auditory hallucinations.
side effects, to live independently, In each visit with me, the
and to work. He also reported patient expressed a dislike for his
having anxiety, difficulty breathing, living situation. He lived in three
light sensitivity, a feeling of not different residences during the six
being grounded, and problems with months of active orthomolecular
involuntary movements. Table 8 treatment. On numerous occasions,
summarizes the patient's response I expressed concern about his
to the adjunctive orthomolecular living situation with each of his
treatments. parents. I explained to his parents
On November 25, 2004, a that this treatment would work
letter was sent to the patient's best if their son were provided
psychiatrist. After reviewing the with a decent place to live, privacy,
letter, the psychiatrist discontinued security, and encouragement to
the antipsychotic injection, the follow through with the treatments.
risperidone, and the venlafaxine. I recommended that the patient live
with one of them for at least three
The patient remained on the same
doses of apobenztropine and to six months, after which, he would
likely learn to comply on his own.
clonazepam, but the olanzapine
was increased to 30 mg daily. Neither parent would allow him to
live at their respective places of
He was also prescribed 50 mg of
fluvoxamine daily. Overall, the residence. I also discussed the
relationship between nicotine and
addition of the orthomolecular
treatments allowed this patient to vitamin B3, in that smoking reduces
the clinical effectiveness of the
be more positive and motivated,
vitamin. Unfortunately, the patient
to be less anxious, and to exude
was unwilling to quit smoking
more confidence. His auditory
hallucinations disappeared, and
 in an adult learning program so did not control her symptoms
Schizophrenia that she would not need to attend Her psychiatrist then prescribed
classes during the day. Then she 10 mg of olanzapine and 1 niL;
despite my encouragement. As began to isolate herself from her of apo-haloperidol daily. When
of August 2006, the patient is family. She even blasted the music she finally came to my office for
living in his fourth group home, on her portable headset so that a consultation, her medication
is unemployed, smokes at least she would be unable hear anyone. regiment had not changed, but
one-half a pack of cigarettes daily, She complained of bad thoughts neither had her symptoms. Sht
is symptomatic, and is no longer and started to hear voices from her continued to hear voices constantly,
mom's purse. She became paranoid had difficulty focusing and was
on any of the orthomolecular
that there were recorders and worried about being monitored
treatments that I prescribed.
monitoring devices documenting and followed all the time. She had
her every move. Finally, in June gained about 15 pounds since
Case #4 starting the medications. Table !'
A 17-year-old female presented 2005, she asked her mother for
help and was taken to the local summarizes the patient's response
to my office in January 2006 with a to the adjunctive orthomolecular
chief complaint of psychosis. Her hospital for evaluation. Although
the diagnosis of schizophrenia was treatments.
symptoms began in February 2005
when she refused to go to high never mentioned, she was told that One week after the March 4tli
school. She informed her parents she had had a psychotic episode. visit, her parents took her off both
that she had been the victim of She was placed on risperidone psychiatric medications despite m\
bullying and harassment from other and quetiapine, but discontinued instructions to the contrary. From
students. Her parents enrolled her these medications since they the second week in March to April,
the patient's condition continued
to decline. 1 spoke to the patients
Table 9. Case #4: Patient's Response to Adjunctive
father and reiterated to him that
Orthomolecular Treatments
not enough time had elapsed since
Consultation Dates January 7. 2006 March 4, 2006 commencing the orthomolecular
treatments. I explained to him
Clinical Presentation Auditory hallucinations, No change in symptoms. the connection between food
paranoid ideation, thought TSH normal. Serum vitamin allergies and schizophrenia
blocking, shaking, and B12was145pmol/L(in Since the patient had extreme
restlessness. the possibly B12 deficient sugar cravings and would eat as
range). much sugar as she could possibl>
consume, we decided to eliminate
Current Psychiatric 10 mg of olanzapine and 1 lOmgofolanzapineand 1 mg all sugar from her diet. A few days
Medications mg of apo-haloperidol of apo-haloperidol daily.
daily.
later, I received a telephone call
Her father was amazed. When
Orthomolecular 1,000 mg of niacinamide Niacinamide was the patient was off sugar, she was
Treatments & Plan three times daily. 1,000 discontinued. Switched to practically normal. The momenl
mg of vitamin C three 1,500 mg of niacin three she resumed eating sugar, all her
times daily. 2 teaspoons times daily. Added 2,500 mg psychotic symptoms returned
of liquid fish oil (2,100 mg of glycine at bedtime to help However, the patient was unwillinjj
of EPA and 1,500 mg of with sleep, 100 mg of B6, 50 to give up sugar and was unable
DHA), and 1,000 meg of mg of zinc, and 240 mg of to apprehend the connection
B12 sublingually daily. She Ginkgo biloba extract. between sugar elimination
was given an intramuscular
and less psychotic symptoms.
Injection of 5,000 meg of
B12. following blood serum
Eventually, she discontinue( i
B12 and TSH tests. Patient all the nutritional treatments
instructed to take the HOD and opted to try clozapine as n
test. last resort. As of April 2006, the
patient was started on clozapine
HOD Results Not assessed. and has done reasonably well.
TS (normal <30) 76 Although she continues to have
PerS (normal <3) 14 psychotic symptoms, the auditory
PS (normal <3) 10 hallucinations are much more
DS (normal <3) 5 tolerable than before. She is able
Not improved.
to attend a special high school
Category of Recovery Not improved.

TOWNSEND LETTER - FEBRUARY/MARCH 2

 each day and has even tnodified
her diet to include more fruits
and vegetables. 1 personally
worry about her future, since she
has opted to not resume any of
the adjunctive orthomolecular
treatments.
The patients cited in the first
two cases continue to do well since
they both have all the components
for a successful response to
treatment: (a) shelter; (b) decency,
understanding, support, safety, and
privacy; (c) psychiatric treatment;
and (d) orthomolecular treatment.'
All these components are equally
important. If one component is
missing, the chances of success
are diminished. In Case #3, the
patient did not have adequate
shelter and was not able to receive
support, safety, and privacy in
the various group homes in which
he lived. He lacked the guidance
from one caregiver to ensure that
he remained consistent with his
psychiatric and orthomolecular
medications. In Case #4, the patient
was not on the orthomolecular
approach for a sufficient period
of time. She was also unwilling to
give up refined sugar when I was
actively treating her, even though
her response to sugar significantly
contributed to her psychosis.
Thus, patients who are receiving
all of these necessary components
(Cases #1 and #2) show more
improvements than patients who
do not (Cases #3 and #4).
Conclusion
As clinicians we need to offer
restorative care to patients who
suffer with schizophrenia, a
severe and often chronic mental
illness. If the information in this
report is reviewed carefully
and implemented, I believe that
many schizophrenic patients will
improve substantially and achieve
a reasonable quality of life. Some
might improve so much that they
achieve clinical remission. Since
not enough clinicians utilize
orthomolecular treatments with
schizophrenic patients, this author
TOWNSEND LETTER - FEBRUARY/MARCH 2007
hopes that many of you will do Schizophrenia
so and continue the exceptional
and important work of Dr. Abram Notes
Hoffer. 1. Hofler A. Vitamin B-3 & Schizophrenia.
Discovery. Recovery, Controversy Kingston.
Ontario: Quarry Press, Inc., 1998;28-76.
Acknowledgements 2. Hoffer A. Adventures !n Psychiatry. The
Written consent was obtained from Scientific Memoirs of Dr. Abram Hoffer, KOS
the four patients for publication of Publishing Inc. Caledon. ON, 2005:50-99.
this report. The author would like to 3. Smythies .IR. Endogenous neuroloxlns
relevant to schizophrenia. J R Soc Med.
thank Dr. Abram Hoffer for reviewing 1996:89:679-680.
this report, Mrs. Erynn Marcus for her 4. Smythies JR. Oxidative reactions and
thorough editing, and Mr. Robert Sealey schizophrenia: a revlew-d[8cussion.5c/»zop/(j
for his expert editing and sui^jjestions. Res 1997:24:357-364.
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O I* I I M A I I K I I I <> N A I Si l» IM ) U
 2L Holfer A. Vitamin B-li and schizophrenia. .17, Foster HI). Schizophrenia, thyroid hormone
Schizophrenia Townsend Lett Doctors Patients. 2O0l;213:20-
23.
and selenium. J Orthomol Med. 2002:17:55-511
38. Fenton WS, Hibbelln J. Knable M. Essenti..
22. Paterson ET. Vitamin B3 and liver toxicity. fattyacids. lipid membrane abnormalitie.s,ani;

Smytliles JR. The adrenochrome hypothesis
of schizophrenia revisited. Neurotox Res.
6. Hoffer .\. The adrenochrome hypothesis and
psychiatry. yOr;/)omo/Aferf. 1999:14:49-62.
7. Hoffer A, Heatini) Scliizophrenia. Toronto.
Ontario: CCNM Press Inc. 2()(>4;7-21.
8. Horrnbii; D. The Madness of Adam and Eve.
Lotidrm. England: Corgi Books, 201)l;149-151.
9. Hoffer A. Treating chronic schizophrenic
patients. J Orthomol Med. 2002:17:25-41.
10. Goeree R, FarahatI F. Burke N, et ai. The
economic burden of schizophrenia in Canada
in 2004. Curr Med Res Opirt. 2005;2]:2017-
2028.
11 Rochnn PA, Stukel TA. Sykora K. et al. Atypical
antipsychotks and Parkinsonism. Arch Intern
Med 2005:165:1882-1888.
12 Prou.sky JE, Hayinan R, Orlhomolecular and
botanical treatments to help alleviate the
side effects o( alypicai antipsychotic dru^s. J
OrihomolMed 200(!: 21:17-3;).
13 Hoffer A. Atypical aiiti-psyctiotics create
dependency disorders. J Orthomol Med
2004:I9::!-iO.
M Hoffer A. Orlhoniolecuiar psychiatry In
theory and practice. Townsend LeII Doctors
15 Hoffer A. Of ambulant sciiizophrenics with
vitamin B3and relative hypoglycemic diet. J
Orf/jomo/,V/et/i<W9:14:23-27.
16 Miller CL, Llen.os IC. Dulay JR. Weis S.
Upreguiatlon of the initiating step of the
kynurenine pathway in postmortem anterior
ciitgulate cortex (rom individuals with
schizophrenia and bipolar disorder. Brain
Res. 2006:1(173-1074:25-37.
17. Hofler A. Mechanism of action ol nicotinic
acid and iiicotinamide In the treatment of
schizophrenia, in iiawitlns D. Pauling L, eds.
Orthomolecular Psydiialry. San Francisco, CA:
W.H. Freeman And Company; 1973:202-262.
18. Hoffer A. Niacin Therapy In Psychiutry.
Springfield, Illinois: Charles C Thomas.
1962:35-71.
19 Hoffer A. Chronic schizophrenic patients
treated ten years of more. J Orthomol Med
1994:9:7-37,
Morrow JD, Parsons WG. Roberts LJ.
20
Release o( markedly increased quantities
oi prostaHltindin U2 in vivo in humans
fuilowing the administration ot nicotinic acid.
Prostaglandins. 1989:38:263-274.
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Townsend Lett Doctors Patients. 2001:207:23. the diagnosis and treatment of schizophrenia,
Biol Psychiatry 2000:47:8-2!.
23. Mullen CE, Greenspan JK, Mitchell MC.
Fulminant hepatic faiiure after ingestion o\ 39. Peet M. Eicosapeiitaenoic acid In the
sustained-release nicotinic acid. Ann Intern treatmeni of schizophrenia and depression:
Med 1989:111:253.255. Rationale and preiiminary double-blind
clinicai trial results, Prostuitlandms Leukot
24. Hoffer A. Vitamin B-3: niacin and its amide.
Essent Fatty Acids. 2003:69:477-485.
Townsend Lett Doctors Patients. 1995:147:30-
39. 40. Emsley R. Oosthuizen P, van Rensburg b'
Clinical potential of oniega-3 (atty acids in
25. Hoffer A. Oxidation reduction and the brain. J
Orthomol Psychiatr 1983:12:292-301. the treatment of schizophrenia, CNS Drugs
2003:17:1081-1091.
26. Brody S. Preut R. Schornmer K, Schurmeyer
TH. A randomized controlled trial of high 41. Hawkins D, Orthomolecuiar psychiatry:
dose ascorbic acid for reduction of blood treatment of schizophrenia. In. eds. Hawkins
pressure, cortisol. and subjective responses D. Pauling L, Orthomolecular Psychiatry. San
to psycholoyical stress. Psychopharmacology. Francisco, CA: W.H. Freeman And Company:
CBerl) 2002:159:319.324. 1973:631-673.
27. Smythies JR. The role of ascorbate in brain: 42. Neziroglu F. The relationship amonu
the Hoffer-Osmond Diagnostic Test, tlv
Therapeutic implications. J R Soc Med,
i996:89:24I. Minnesota Multiphaslc Personality inventor\
and Independent clinical diagnoses. J Chn
28. Meister A. (JIutattiione, ascorbate, and cellular
protection. Cancer Res. l994:54:i969S-1975S. Psydwl. 197.5:31:430-433,
29. Baez S. Segura-Aguilar .1, Widerslen M, 43. Hoffer A, Healing Schizophrenia. Toronto.
Ontario: CCNM Press Inc. 2004:152-155.
Johansson A-S. Mannervik B. Glutathione
transferases catalyse the detoxification
o( oxidized metabolites (o-quinones)
of catecholaniines and may serve as an
antioxidant system preventing degenerative
cellular processes. Biochem J. 1997:324:25-28.
31). Pauling L, Robinson AB. Oxiey SS. et al.
Results of a loadinfj test of ascorbic acid,
niacinamide. and pyridoxine in schizophrenic
subjects and controls. In. eds. Hawkins I),
Pauling L. Orlhomolecular Psychiatry. San
Francisco, CA: W.H. Freeman And Company:
1973:18-34.
31. Suboticanec K, Fohiegovic-Smalc V.
Korbar M, ol al. Vitamin C status in chronic
schizophrenia. BinI Psychiatry. 1990:28:9.'J9-
966.
32. Jackson JA. Riordan HD. Neathery SS. Mayer
K. Urine pyrroles revisited, J Orthomol Med
2000:15:47-48.
33. PfeiKer C, l.aMola S. Zinc and manganese
In the schizophrenias. J Orthomol Med.
1999:14:28-48.
34. Brown JA. Foster HD. Schizophrenia: An
update of the selenium deficiency hypothesis.
JOrihomolMed 1996:11:211-222.
35. Foster HD. The biochemical treatment of
schizophrenia revisited. J Orthomol Med. Dr. Jonathan Prousky is the Chief
1999:14:110-112. Naturopathic Medical Officer of the
36. Berry T. An alternative e.'<planatlon of the Robert Schad Naturopathic Clinic,
psychotropic effect of niacin in schizophrenia.
J Orthomol Med. 1994;9:58. the teaching clinic of The Canadian
College of Naturopathic Medicine. In
addition, Dr. Prousky is an Associate
Professor of Ciinicai Nutrition and
teaches the third-year clinical
nutrition course at the college. He
also operates a private practice
specializing in the orthomolecular
treatment of mental health
disorders. In April 2006, CCNM
Press published Dr. Prousky's book,
Anxiety: Orthomolecular Diagnosis
and Treatment. Please send
correspondences to: J. Prousky,
ND. FRSH, CCNM, 1255 Sheppard
Ave. E., Toronto. Ontario.. M2K 1E2;
800-543-3026 email: jprousky@ccnm.edu.

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