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The use of nutritional supplements in psychiatry has had a
controversial history. It is the experience of most psychiatrists
that powerful medications are commonly needed to curb
psychotic behavior, manic episodes, suicidality, and other
dramatic manifestations they are asked to treat. It hardly seems
reasonable that a vitamin or mineral would have much beneficial
effect. The usual response of most phsicians, when asked about
nutritional supplements, is that they likely won’t help but they
probably won’t hurt.
But as studies now show, there is a place for nutritional
treatments in mental health treatment. Some patients, due to
poor diets or metabolic abnormalities, have unusually high
needs for some nutrients—biochemicals that are required for
normal physiological function. Supplementation can sometimes
fully or partially restore neurological activity that has gone
awry. Additionally, some supplements—as lithium has for
decades—have a palliative effect on symptoms and, in moderate
doses, can improve the patient’s condition with few or no side
effects.
controversial history. It is the experience of most psychiatrists
that powerful medications are commonly needed to curb
psychotic behavior, manic episodes, suicidality, and other
dramatic manifestations they are asked to treat. It hardly seems
reasonable that a vitamin or mineral would have much beneficial
effect. The usual response of most phsicians, when asked about
nutritional supplements, is that they likely won’t help but they
probably won’t hurt.
But as studies now show, there is a place for nutritional
treatments in mental health treatment. Some patients, due to
poor diets or metabolic abnormalities, have unusually high
needs for some nutrients—biochemicals that are required for
normal physiological function. Supplementation can sometimes
fully or partially restore neurological activity that has gone
awry. Additionally, some supplements—as lithium has for
decades—have a palliative effect on symptoms and, in moderate
doses, can improve the patient’s condition with few or no side
effects.
A Brief History
What we now call nutritional or “orthomolecular” psychiatry
began in a university laboratory in the early 1950s in Saskatoon,
Saskatchewan, Canada. At that time Abram Hoffer, M.D., Ph.D.,
and his colleague Humphry Osmond, M.D., (who coined the term
“psychedelic”) along with another physician, John Smythies,
M.D., hypothesized that the origins of schizophrenia could be
related to an abnormality of adrenaline metabolism, creating
hallucinogenic metabolites which could be alleviated with niacin
(vitamin B3). Hoffer, with his background in animal husbandry
and biochemistry, undertook what is believed to be the first
double blind studies in psychiatry. (In the interest of full
disclosure, one of the writers—Vickar—is Dr. Hoffer’s nephew.)
Numerous studies were published in the 1950s as the work
unfolded (Agnew 1955, Hoffer 1957). Publishing the results of a
nine-year study in the Lancet, Hoffer continued to find that those
patients blinded to placebo versus niacin or niacinamide showed
significant improvement only to the vitamin and definitely
separation from placebo (Hoffer 1962). The results were exciting
to them during a time when the only treatments were
barbiturates, ECT, insulin shock therapy, and restraints.
However, at the same time chlorpromazine had been introduced
by Heinz Leiman in Montreal and the results were so dramatic
that the idea that a vitamin could do something paled in
comparison and did not gain traction.
In the 1960s, two-time Nobel laureate Linus Pauling, who had
been doing his own research on Vitamin C and the common cold,
was attracted to Hoffer’s work and joined Hoffer and likeminded
scientists in advancing the cause. In listing the available
psychiatric treatments of the period, Pauling remarked, “I have
reached the conclusion that another general method of
treatment, which may be called orthomolecular therapy, may be
found to be of great value, and may turn out to be the best
method of treatment for many patients.” Pauling defined
What we now call nutritional or “orthomolecular” psychiatry
began in a university laboratory in the early 1950s in Saskatoon,
Saskatchewan, Canada. At that time Abram Hoffer, M.D., Ph.D.,
and his colleague Humphry Osmond, M.D., (who coined the term
“psychedelic”) along with another physician, John Smythies,
M.D., hypothesized that the origins of schizophrenia could be
related to an abnormality of adrenaline metabolism, creating
hallucinogenic metabolites which could be alleviated with niacin
(vitamin B3). Hoffer, with his background in animal husbandry
and biochemistry, undertook what is believed to be the first
double blind studies in psychiatry. (In the interest of full
disclosure, one of the writers—Vickar—is Dr. Hoffer’s nephew.)
Numerous studies were published in the 1950s as the work
unfolded (Agnew 1955, Hoffer 1957). Publishing the results of a
nine-year study in the Lancet, Hoffer continued to find that those
patients blinded to placebo versus niacin or niacinamide showed
significant improvement only to the vitamin and definitely
separation from placebo (Hoffer 1962). The results were exciting
to them during a time when the only treatments were
barbiturates, ECT, insulin shock therapy, and restraints.
However, at the same time chlorpromazine had been introduced
by Heinz Leiman in Montreal and the results were so dramatic
that the idea that a vitamin could do something paled in
comparison and did not gain traction.
In the 1960s, two-time Nobel laureate Linus Pauling, who had
been doing his own research on Vitamin C and the common cold,
was attracted to Hoffer’s work and joined Hoffer and likeminded
scientists in advancing the cause. In listing the available
psychiatric treatments of the period, Pauling remarked, “I have
reached the conclusion that another general method of
treatment, which may be called orthomolecular therapy, may be
found to be of great value, and may turn out to be the best
method of treatment for many patients.” Pauling defined
“orthomolecular” as “optimum molecular environment.”
(Pauling 1968)
As medical science has progressed, nutrients have been
subjected to continued rigorous study as psychiatric treatments.
Biochemical pathways of neurotransmitters and other
neurochemicals have been mapped, showing the roles of
vitamins, minerals, enzymes, amino acids, and other
contributors to healthy neurochemistry.
Niacin has now been found to possibly be helpful with
Alzheimer’s disease (AD). A study on Alzheimer’s Disease
Transgenic Mice concluded: “...these results suggest that
nicotinamide [a form of B3] may also be effective against other
tauopathies, which share many common pathological features
with the tau pathology seen both in AD and in the 3xTg-AD mice.
In summary, the results presented here suggest that
nicotinamide has potential as a novel, safe, and inexpensive AD
therapy, either alone or in combination with AB [amyloid-beta]-
lowering therapies.” (Green 2008)
Also, a study of the nutritional habits of 4000 people aged 65
and older, who had no Alzheimer’s disease at the start of the
project, found: “Dietary niacin may protect against AD and age
related cognitive decline.” (Morris 2004)
The Methylation Cycle
While nutritional supplementation may seem, at first glance,
unlikely to impact mental function as significantly as
pharmaceuticals, the picture becomes clearer when we take a
look at some of the biochemical pathways that affect psychiatric
symptoms. Here we see that nutrients are the building blocks of
normal cerebral activity and, without them, necessary neural
processes cannot occur.
One example of such biochemical activity is the methylation
cycle (Figure 4.1). Methylation refers to the transfer of methyl
groups (CH3—a carbon atom bonded to three hydrogen atoms) to
and from organic molecules, a process that occurs billions of
48 | Complementary and Alternative Medicine Treatments in Psychiatry
(Pauling 1968)
As medical science has progressed, nutrients have been
subjected to continued rigorous study as psychiatric treatments.
Biochemical pathways of neurotransmitters and other
neurochemicals have been mapped, showing the roles of
vitamins, minerals, enzymes, amino acids, and other
contributors to healthy neurochemistry.
Niacin has now been found to possibly be helpful with
Alzheimer’s disease (AD). A study on Alzheimer’s Disease
Transgenic Mice concluded: “...these results suggest that
nicotinamide [a form of B3] may also be effective against other
tauopathies, which share many common pathological features
with the tau pathology seen both in AD and in the 3xTg-AD mice.
In summary, the results presented here suggest that
nicotinamide has potential as a novel, safe, and inexpensive AD
therapy, either alone or in combination with AB [amyloid-beta]-
lowering therapies.” (Green 2008)
Also, a study of the nutritional habits of 4000 people aged 65
and older, who had no Alzheimer’s disease at the start of the
project, found: “Dietary niacin may protect against AD and age
related cognitive decline.” (Morris 2004)
The Methylation Cycle
While nutritional supplementation may seem, at first glance,
unlikely to impact mental function as significantly as
pharmaceuticals, the picture becomes clearer when we take a
look at some of the biochemical pathways that affect psychiatric
symptoms. Here we see that nutrients are the building blocks of
normal cerebral activity and, without them, necessary neural
processes cannot occur.
One example of such biochemical activity is the methylation
cycle (Figure 4.1). Methylation refers to the transfer of methyl
groups (CH3—a carbon atom bonded to three hydrogen atoms) to
and from organic molecules, a process that occurs billions of
48 | Complementary and Alternative Medicine Treatments in Psychiatry
times in the body each day. This process impacts a broad range
of physiological and psychiatric issues. Methylation deactivates
noradrenalin, for example, a neurotransmitter associated with
cortisol and the stress response. Methylation acts on dopamine,
norepinephrine and serotonin to impact, among other things,
mood, memory, concentration and sleep.
For the methylation cycle to work properly, the correct
substrates, or materials, must be available. Nutrients involved in
this activity include folic acid (noted by its derivative
tetrahydrofolate, or THF, in Figure 4.1), B6, B12, and SAM-e
(shown as SAM in Figure 4.1). As expected, supplementation with
each of these nutrients has been found to have some psychiatric
benefit and deficiencies have been seen to affect brain
performance.
of physiological and psychiatric issues. Methylation deactivates
noradrenalin, for example, a neurotransmitter associated with
cortisol and the stress response. Methylation acts on dopamine,
norepinephrine and serotonin to impact, among other things,
mood, memory, concentration and sleep.
For the methylation cycle to work properly, the correct
substrates, or materials, must be available. Nutrients involved in
this activity include folic acid (noted by its derivative
tetrahydrofolate, or THF, in Figure 4.1), B6, B12, and SAM-e
(shown as SAM in Figure 4.1). As expected, supplementation with
each of these nutrients has been found to have some psychiatric
benefit and deficiencies have been seen to affect brain
performance.
A lack of B vitamins has been found to cause cognitive
dysfunction and reductions in brain capillary length and density
in mice. Test animals fed a B-deficient diet were found to have
seven times the homocysteine levels of controls (Troen 2008).
Folate: Vitamin B9
A clear relationship has been established between B12 and folate
deficiencies and depressive disorders in the elderly (Tiemeier
2002). Researchers report that low folate and B12 status has been
found in depressed patients in general, along with increased
homocysteine levels (see Figure 4.1), a common metabolic result
of low B vitamins that has a wide range of negative health
ramifications. Low plasma or serum folate has also been found in
patients with recurrent mood disorders treated by lithium. In
one review of the evidence of B vitamin influence on mood, the
authors concluded, “On the basis of current data, we suggest that
oral doses of both folic acid (800 microg daily) and vitamin B12 (1
mg daily) should be tried to improve treatment outcome in
depression.” (Coppen 2005)
Serum folate levels have also been found to be low in
schizophrenia patients and supplementation significantly
improves negative symptoms in a specific genotype: MTHFR
status (see Figure 4.1—MTHFR is in sequence C) significantly
moderated the relationship between change in serum folate and
change in negative symptoms (Hill 2011).
MTHFR refers to the enzyme methylenetetrahydrofolate
reductase and the gene that regulates it. The MTHFR gene has
been found to have a large number of mutations. One particular
form—C677T—is found in significantly higher numbers in
psychiatric populations. MTHFR-C677T reduces MTHFR enzyme
activity to 30–65%, thus affecting the processing of folate and
other nutrients. A meta-analysis of research on the MTHFR gene
and psychiatric sequelae found “an association between the
MTHFR C677T variant and depression, schizophrenia, and
dysfunction and reductions in brain capillary length and density
in mice. Test animals fed a B-deficient diet were found to have
seven times the homocysteine levels of controls (Troen 2008).
Folate: Vitamin B9
A clear relationship has been established between B12 and folate
deficiencies and depressive disorders in the elderly (Tiemeier
2002). Researchers report that low folate and B12 status has been
found in depressed patients in general, along with increased
homocysteine levels (see Figure 4.1), a common metabolic result
of low B vitamins that has a wide range of negative health
ramifications. Low plasma or serum folate has also been found in
patients with recurrent mood disorders treated by lithium. In
one review of the evidence of B vitamin influence on mood, the
authors concluded, “On the basis of current data, we suggest that
oral doses of both folic acid (800 microg daily) and vitamin B12 (1
mg daily) should be tried to improve treatment outcome in
depression.” (Coppen 2005)
Serum folate levels have also been found to be low in
schizophrenia patients and supplementation significantly
improves negative symptoms in a specific genotype: MTHFR
status (see Figure 4.1—MTHFR is in sequence C) significantly
moderated the relationship between change in serum folate and
change in negative symptoms (Hill 2011).
MTHFR refers to the enzyme methylenetetrahydrofolate
reductase and the gene that regulates it. The MTHFR gene has
been found to have a large number of mutations. One particular
form—C677T—is found in significantly higher numbers in
psychiatric populations. MTHFR-C677T reduces MTHFR enzyme
activity to 30–65%, thus affecting the processing of folate and
other nutrients. A meta-analysis of research on the MTHFR gene
and psychiatric sequelae found “an association between the
MTHFR C677T variant and depression, schizophrenia, and
bipolar disorder, raising the possibility of the use of folate in
treatment and prevention.” (Gilbody 2007)
Vitamin B12
Cobalamin, commonly known as vitamin B12, is another link in
the methylation cycle. Psychiatric signs of deficiency include
concentration difficulties, confusion, irritation, impaired
memory, dementia, irritability, depression, personality changes,
and psychosis.
Psychiatric symptoms may exist despite the absence of typical
blood or neurologic symptoms common with B12 deficiency.
Psychosis may respond to supplementation, even after a
prolonged period of cobalamin deficiency. B12-related mental
disorders can manifest even with low-to-moderate B12 serum
levels. If homocysteine or methylmalonic acid levels are
elevated, despite “normal” B12 levels, a deficiency could be
indicated. This is a particular issue with the elderly, who
commonly experience B12 deficiency, in part due to a scarcity of
intrinsic factor, a glycoprotein that aids in B12 absorption
(Sabeen 2009). For these patients, injected B12 may prove more
effective than supplements taken orally. It should be noted that
some non-elderly also do not produce sufficient intrinsic factor
and are at risk for psychiatric symptoms due to B12 deficiency,
as are vegans and vegetarians.
Recent research suggests that B12 supplementation may reduce
the risk of Alzheimer’s disease. In Finland 271 people, age 65 to
79, were selected who did not have dementia at the start of the
study. Over a seven-year span, 17 people developed AD.
Researchers found that, as homocysteine levels rose (a factor of
B12 deficiency), the likelihood of AD increased. The same was
true as B12 levels dropped (Hooshmand 2010).
B12 has been found as a marker of how well people will respond
to treatment for depression. In another Finnish study,
researchers monitored 115 patients suffering from depression
over a six-month period and grouped them according to how
Nutritional
treatment and prevention.” (Gilbody 2007)
Vitamin B12
Cobalamin, commonly known as vitamin B12, is another link in
the methylation cycle. Psychiatric signs of deficiency include
concentration difficulties, confusion, irritation, impaired
memory, dementia, irritability, depression, personality changes,
and psychosis.
Psychiatric symptoms may exist despite the absence of typical
blood or neurologic symptoms common with B12 deficiency.
Psychosis may respond to supplementation, even after a
prolonged period of cobalamin deficiency. B12-related mental
disorders can manifest even with low-to-moderate B12 serum
levels. If homocysteine or methylmalonic acid levels are
elevated, despite “normal” B12 levels, a deficiency could be
indicated. This is a particular issue with the elderly, who
commonly experience B12 deficiency, in part due to a scarcity of
intrinsic factor, a glycoprotein that aids in B12 absorption
(Sabeen 2009). For these patients, injected B12 may prove more
effective than supplements taken orally. It should be noted that
some non-elderly also do not produce sufficient intrinsic factor
and are at risk for psychiatric symptoms due to B12 deficiency,
as are vegans and vegetarians.
Recent research suggests that B12 supplementation may reduce
the risk of Alzheimer’s disease. In Finland 271 people, age 65 to
79, were selected who did not have dementia at the start of the
study. Over a seven-year span, 17 people developed AD.
Researchers found that, as homocysteine levels rose (a factor of
B12 deficiency), the likelihood of AD increased. The same was
true as B12 levels dropped (Hooshmand 2010).
B12 has been found as a marker of how well people will respond
to treatment for depression. In another Finnish study,
researchers monitored 115 patients suffering from depression
over a six-month period and grouped them according to how
Nutritional
well they responded to treatment. The patients who responded
fully to treatment had higher concentrations of vitamin B12 in
their blood at both the start and the end of the study than those
for whom treatment was less effective. Results confirmed the
conclusions of a similar study on elderly patients (Hintikka
2003). These observations suggest that B12 can be a helpful
complement to any treatment regimen for depression.
Vitamin B6
Vitamin B6, or pyridoxine, is another critical element of the
methylation cycle. One of its many tasks is to convert
tryptophan to serotonin and to assist in the making of
norepinephrine and melatonin. A lack of B6 or a metabolic
failure to process it correctly can cause nervousness, irritability,
depression, difficulty concentrating, and short-term memory
loss.
B6 has been found in a multitude of studies to be twice as
effective as placebo in improving symptoms of premenstrual
syndrome when taken in doses of 50-100 mg per day. Higher
doses were not found to increase effectiveness (Wyatt 1999).
Pyridoxine may also be helpful in autism and related disorders,
many studies suggest. It’s been found that when 100 mg of B6 is
administered daily for two weeks, then twice a day after that,
children with pervasive developmental disorder see an 11.2-
point increase in verbal IQ in 4 weeks (Kuriyama 2002).
SAM-e
SAM-e (S-adenosyl methionine), though not among the B
vitamins, is also a critical part of the methylation cycle. As a
result, supplementation with this nutrient has been found
helpful for depression when taken alone or as an adjunct to
medication. A more recent study found that on a dose of 800 mg
twice daily, twice as many participants taking SAM-e along with
medication improved compared to controls. Additionally, 26% of
fully to treatment had higher concentrations of vitamin B12 in
their blood at both the start and the end of the study than those
for whom treatment was less effective. Results confirmed the
conclusions of a similar study on elderly patients (Hintikka
2003). These observations suggest that B12 can be a helpful
complement to any treatment regimen for depression.
Vitamin B6
Vitamin B6, or pyridoxine, is another critical element of the
methylation cycle. One of its many tasks is to convert
tryptophan to serotonin and to assist in the making of
norepinephrine and melatonin. A lack of B6 or a metabolic
failure to process it correctly can cause nervousness, irritability,
depression, difficulty concentrating, and short-term memory
loss.
B6 has been found in a multitude of studies to be twice as
effective as placebo in improving symptoms of premenstrual
syndrome when taken in doses of 50-100 mg per day. Higher
doses were not found to increase effectiveness (Wyatt 1999).
Pyridoxine may also be helpful in autism and related disorders,
many studies suggest. It’s been found that when 100 mg of B6 is
administered daily for two weeks, then twice a day after that,
children with pervasive developmental disorder see an 11.2-
point increase in verbal IQ in 4 weeks (Kuriyama 2002).
SAM-e
SAM-e (S-adenosyl methionine), though not among the B
vitamins, is also a critical part of the methylation cycle. As a
result, supplementation with this nutrient has been found
helpful for depression when taken alone or as an adjunct to
medication. A more recent study found that on a dose of 800 mg
twice daily, twice as many participants taking SAM-e along with
medication improved compared to controls. Additionally, 26% of
the SAM-e group experience complete remission, compared to
12% of controls (Papakostas 2010).
An Italian study comparing the effects of imipramine versus
SAM-e found they proved equally effective against depression in
a four-week trial, with SAM-e, at a dose of 400 mg/day
intramuscularly, causing significantly fewer side effects
(Pancheri 2002).
Of course, all of these studies supplemented elements of the
methylation cycle—B12, B6, SAM-e, etc.—in isolation, providing
an increased dose of a single nutrient. Many CAM practitioners,
working with the structure of the methylation cycle, often
supplement with multiple elements simultaneously—such as B6,
methionine, calcium, magnesium, SAM-e, inositol (a B vitamin),
vitamin C, and others—to provide more substrate materials for
the cells, thus hopefully enriching the functionability of the
methylation pathway and obtaining a more therapeutic
response.
Not all patients, however, are deficient in methylation, so one
has to be alert to a negative response to methylation
supplementation and discontinue supplementation if necessary.
Fatty Acids
In the past decade we have seen a plethora of studies showing
the effectiveness of fatty acids in the treatment of a range of
mental disorders. Like the elements of the methylation cycle,
fatty acids have their own chemical pathway, which also
requires specific substrate materials which must be in adequate
supply for normal physiological response to occur.
Of particular interest to mental health professionals has been
the omega-3 fatty acids—so-called because the molecule has 3
hydrogen atoms at the end of a carbon chain. Note that this
makes CH3, a methyl group. Omega-3 fatty acids include alpha
linolenic acid (ALA), eicosapentaenoic acid (EPA), and
docosahexaenoic acid (DHA). These are found in fish oil, flax
seed oil and other sources.
12% of controls (Papakostas 2010).
An Italian study comparing the effects of imipramine versus
SAM-e found they proved equally effective against depression in
a four-week trial, with SAM-e, at a dose of 400 mg/day
intramuscularly, causing significantly fewer side effects
(Pancheri 2002).
Of course, all of these studies supplemented elements of the
methylation cycle—B12, B6, SAM-e, etc.—in isolation, providing
an increased dose of a single nutrient. Many CAM practitioners,
working with the structure of the methylation cycle, often
supplement with multiple elements simultaneously—such as B6,
methionine, calcium, magnesium, SAM-e, inositol (a B vitamin),
vitamin C, and others—to provide more substrate materials for
the cells, thus hopefully enriching the functionability of the
methylation pathway and obtaining a more therapeutic
response.
Not all patients, however, are deficient in methylation, so one
has to be alert to a negative response to methylation
supplementation and discontinue supplementation if necessary.
Fatty Acids
In the past decade we have seen a plethora of studies showing
the effectiveness of fatty acids in the treatment of a range of
mental disorders. Like the elements of the methylation cycle,
fatty acids have their own chemical pathway, which also
requires specific substrate materials which must be in adequate
supply for normal physiological response to occur.
Of particular interest to mental health professionals has been
the omega-3 fatty acids—so-called because the molecule has 3
hydrogen atoms at the end of a carbon chain. Note that this
makes CH3, a methyl group. Omega-3 fatty acids include alpha
linolenic acid (ALA), eicosapentaenoic acid (EPA), and
docosahexaenoic acid (DHA). These are found in fish oil, flax
seed oil and other sources.
As examples of how fatty acids impact mental health, EPA is
converted to leukotrienes and prostaglandins, both of which
help reduce inflammation. Inflammation has been repeatedly
associated with depression. Also DHA is critical for adequate
functioning of embedded proteins in postsynaptic receptors for
neurotransmission.
Omega 3s and Psychotic Disorders
One of the landmark studies of essential fatty acids (EFAs) in
psychiatry—a Harvard-based clinical trial that sparked many
follow-up studies for numerous mental disorders—was a doubleblind
study of patients with bipolar disorder. Treated with
9.6g/day of omega-3 EFAs (current psychiatric studies generally
use lower dosages in the 1-4 gram range), after 4 months, the
EFA group not only had a significantly longer period of
remission, but for nearly every other outcome measure, they
performed better than the placebo group (Stoll 1999).
Omega-3 EFAs have shown promise as a treatment for
schizophrenia. One reason for this is that the neuronal
membranes of the brain are rich in EFAs which impact neural
receptor function. A review of the literature finds ample
evidence of therapeutic response from EFAs. An epidemiological
study found improved outcomes for schizophrenia patients in
countries where diets are high in unsaturated fatty acids. Trials
of EPA versus placebo have found significant benefit on positive
and negative symptoms. One study found EPA as a monotherapy
to have some antipsychotic qualities (Emsley 2003).
A review of 18,411 women in Sweden found that those who ate
fish 3–4 times per week were 53% as likely to experience highlevel
psychotic symptoms as women who ate no fish at all. The
risk was also lower for women with a high intake of omega-3 and
omega-6 fatty acids compared to women with a lower intake
(Hedelin 2010).
While omega-3 EFAs appear to improve symptomology in
psychotic disorders, their greater value may lie in their
converted to leukotrienes and prostaglandins, both of which
help reduce inflammation. Inflammation has been repeatedly
associated with depression. Also DHA is critical for adequate
functioning of embedded proteins in postsynaptic receptors for
neurotransmission.
Omega 3s and Psychotic Disorders
One of the landmark studies of essential fatty acids (EFAs) in
psychiatry—a Harvard-based clinical trial that sparked many
follow-up studies for numerous mental disorders—was a doubleblind
study of patients with bipolar disorder. Treated with
9.6g/day of omega-3 EFAs (current psychiatric studies generally
use lower dosages in the 1-4 gram range), after 4 months, the
EFA group not only had a significantly longer period of
remission, but for nearly every other outcome measure, they
performed better than the placebo group (Stoll 1999).
Omega-3 EFAs have shown promise as a treatment for
schizophrenia. One reason for this is that the neuronal
membranes of the brain are rich in EFAs which impact neural
receptor function. A review of the literature finds ample
evidence of therapeutic response from EFAs. An epidemiological
study found improved outcomes for schizophrenia patients in
countries where diets are high in unsaturated fatty acids. Trials
of EPA versus placebo have found significant benefit on positive
and negative symptoms. One study found EPA as a monotherapy
to have some antipsychotic qualities (Emsley 2003).
A review of 18,411 women in Sweden found that those who ate
fish 3–4 times per week were 53% as likely to experience highlevel
psychotic symptoms as women who ate no fish at all. The
risk was also lower for women with a high intake of omega-3 and
omega-6 fatty acids compared to women with a lower intake
(Hedelin 2010).
While omega-3 EFAs appear to improve symptomology in
psychotic disorders, their greater value may lie in their
prophylactic effect against psychosis. Researchers in Austria
treated young patients, aged 13 to 25, who were at ultra-high
risk for psychotic disorder, in a twelve-week, double-blind study.
This was followed by a 40-week monitoring period. The EFA
group received 1.2 grams a day of omega-3 fatty acids. At the end
of the study, among the EFA group only 2 of 41 individuals had
transitioned to psychotic disorder compared to 11 of 40 in the
placebo group (Amminger 2010).
Fatty Acids and Depression
As good as the news has been with EFA treatment of psychotic
disorders, a stream of studies has consistently shown the
effectiveness of omega-3s in the treatment of depression, so
much so that it has become a mainstay therapy in many private
practices and hospitals.
As an example of the effectiveness of EFAs in a broad range of
depressive clients, researchers in Israel reviewed three clinical
trials carried out on a variety of patient populations at Beer
Sheva Mental Health Center. The first tested EPA versus placebo
on 20 unipolar clients with major depression as an adjunct to
antidepressant therapy. The second study treated 28 children,
ages 6–12, with a monotherapy of EPA or placebo. The third
study treated 12 bipolar patients with an open-label, add-on trial
of 1.5 to 2 grams per day of EPA for up to 6 months.
Results were very good across the board. The unipolar group
showed “highly significant benefits” by week three. The child
study showed, again, “highly significant effects of omega-3” on
each of the three rating scales. Of the participants in the bipolar
study, 8 of 10 who completed at least one month of follow-up
achieved a 50% or greater reduction in Hamilton depression
scores within one month. No significant side effects were
reported in any of the studies (Osher 2009).
treated young patients, aged 13 to 25, who were at ultra-high
risk for psychotic disorder, in a twelve-week, double-blind study.
This was followed by a 40-week monitoring period. The EFA
group received 1.2 grams a day of omega-3 fatty acids. At the end
of the study, among the EFA group only 2 of 41 individuals had
transitioned to psychotic disorder compared to 11 of 40 in the
placebo group (Amminger 2010).
Fatty Acids and Depression
As good as the news has been with EFA treatment of psychotic
disorders, a stream of studies has consistently shown the
effectiveness of omega-3s in the treatment of depression, so
much so that it has become a mainstay therapy in many private
practices and hospitals.
As an example of the effectiveness of EFAs in a broad range of
depressive clients, researchers in Israel reviewed three clinical
trials carried out on a variety of patient populations at Beer
Sheva Mental Health Center. The first tested EPA versus placebo
on 20 unipolar clients with major depression as an adjunct to
antidepressant therapy. The second study treated 28 children,
ages 6–12, with a monotherapy of EPA or placebo. The third
study treated 12 bipolar patients with an open-label, add-on trial
of 1.5 to 2 grams per day of EPA for up to 6 months.
Results were very good across the board. The unipolar group
showed “highly significant benefits” by week three. The child
study showed, again, “highly significant effects of omega-3” on
each of the three rating scales. Of the participants in the bipolar
study, 8 of 10 who completed at least one month of follow-up
achieved a 50% or greater reduction in Hamilton depression
scores within one month. No significant side effects were
reported in any of the studies (Osher 2009).
Vitamin D
The role of Vitamin D in mental health is just beginning to
unfold. Generated primarily by the body through sun and light
exposure, this nutrient, among other things, plays a role in
stress mediation through the regulation of dopamine and
cortisol. Although clinical studies are few, epidemiological
studies show remarkable associations between low Vitamin D
and psychiatric disorders, including depression and bipolar
disorder. A review of 250 publications found that patients with
either schizophrenia or bipolar disorder are more frequently
born in winter or spring. These same periods have the largest
maternal decline in plasma concentrations of vitamin D
(Ashkanian 2010).
A previously-cited study of 18,411 women found that those in
the highest quartile of Vitamin D consumption had a 37% lower
risk of psychotic-like behavior than women in the lowest
quartile (Hedelin 2010).
Consistent with a number of studies, an examination of the
Vitamin D levels of 2070 participants over the age of 65 in
England found that low D serum levels were clearly associated
with depressive symptoms (Stewart 2010).
Given Vitamin D‘s broad impact on health in general and poor
diet and lack of sun exposure commonly found in psychiatric
patients, testing for serum D levels and correcting them is an
inexpensive but effective way of protecting and improving a
patient’s mental and physical health.
Minerals
Like vitamins, minerals of all kinds are needed for normal
physical and cerebral function. A lack of one or more minerals or
a metabolic failure to correctly process minerals can create
deficiency states that negatively impact mental activity,
emotion, and/or behavior.
The role of Vitamin D in mental health is just beginning to
unfold. Generated primarily by the body through sun and light
exposure, this nutrient, among other things, plays a role in
stress mediation through the regulation of dopamine and
cortisol. Although clinical studies are few, epidemiological
studies show remarkable associations between low Vitamin D
and psychiatric disorders, including depression and bipolar
disorder. A review of 250 publications found that patients with
either schizophrenia or bipolar disorder are more frequently
born in winter or spring. These same periods have the largest
maternal decline in plasma concentrations of vitamin D
(Ashkanian 2010).
A previously-cited study of 18,411 women found that those in
the highest quartile of Vitamin D consumption had a 37% lower
risk of psychotic-like behavior than women in the lowest
quartile (Hedelin 2010).
Consistent with a number of studies, an examination of the
Vitamin D levels of 2070 participants over the age of 65 in
England found that low D serum levels were clearly associated
with depressive symptoms (Stewart 2010).
Given Vitamin D‘s broad impact on health in general and poor
diet and lack of sun exposure commonly found in psychiatric
patients, testing for serum D levels and correcting them is an
inexpensive but effective way of protecting and improving a
patient’s mental and physical health.
Minerals
Like vitamins, minerals of all kinds are needed for normal
physical and cerebral function. A lack of one or more minerals or
a metabolic failure to correctly process minerals can create
deficiency states that negatively impact mental activity,
emotion, and/or behavior.
Zinc
Zinc has been studied as a treatment for a number of psychiatric
issues. Zinc deficiencies—commonly recognized by white spots
or lines on the fingernails—create symptoms such as behavioral
disturbances, depression, and confusion. Amongst other roles,
zinc regulates copper levels in the body as evidenced in the
treatment of Wilson’s Disease, a liver disorder that causes copper
to accumulate to toxic levels. Psychiatric sequelae such as
psychosis, anxiety, and depression are common in Wilson’s
sufferers, and a typical treatment to avoid symptoms and
maintain normal copper levels is zinc supplementation.
For some, depression may respond to zinc treatment. A review
of all zinc research for depression—covering six databases—
concluded: “Evidence suggests potential benefits of zinc
supplementation as a stand-alone intervention or as an adjunct
to conventional antidepressant drug therapy for depression.”
(Lai 2011)
Zinc has also been shown to increase mental and physical
resiliency. Rats placed on zinc supplementation for 4 weeks, then
administered a moderately severe traumatic brain injury, were
found to have reduced depression-like behaviors and improved
cognitive behavior compared to controls. Additionally, they
showed no significant difference from non-injured controls at
any point in the 10-day trial when required to swim a water
maze (Cope 2011).
Since lack of appetite is another symptom of low zinc, the
mineral has been seen to be helpful in the treatment of anorexia
nervosa. Approximately half of anorexics tested are low in zinc
and supplementation has been shown to increase weight gain in
these patients (Shay 2000).
Calcium and Magnesium
Calcium and magnesium are biochemical partners in the human
body. Deficiencies in these two minerals are actually quite
common and often overlooked in medical settings (Olinger 1989).
Zinc has been studied as a treatment for a number of psychiatric
issues. Zinc deficiencies—commonly recognized by white spots
or lines on the fingernails—create symptoms such as behavioral
disturbances, depression, and confusion. Amongst other roles,
zinc regulates copper levels in the body as evidenced in the
treatment of Wilson’s Disease, a liver disorder that causes copper
to accumulate to toxic levels. Psychiatric sequelae such as
psychosis, anxiety, and depression are common in Wilson’s
sufferers, and a typical treatment to avoid symptoms and
maintain normal copper levels is zinc supplementation.
For some, depression may respond to zinc treatment. A review
of all zinc research for depression—covering six databases—
concluded: “Evidence suggests potential benefits of zinc
supplementation as a stand-alone intervention or as an adjunct
to conventional antidepressant drug therapy for depression.”
(Lai 2011)
Zinc has also been shown to increase mental and physical
resiliency. Rats placed on zinc supplementation for 4 weeks, then
administered a moderately severe traumatic brain injury, were
found to have reduced depression-like behaviors and improved
cognitive behavior compared to controls. Additionally, they
showed no significant difference from non-injured controls at
any point in the 10-day trial when required to swim a water
maze (Cope 2011).
Since lack of appetite is another symptom of low zinc, the
mineral has been seen to be helpful in the treatment of anorexia
nervosa. Approximately half of anorexics tested are low in zinc
and supplementation has been shown to increase weight gain in
these patients (Shay 2000).
Calcium and Magnesium
Calcium and magnesium are biochemical partners in the human
body. Deficiencies in these two minerals are actually quite
common and often overlooked in medical settings (Olinger 1989).
Digestive disorders, such as Crohn’s Disease, that inhibit
nutritional absorption, can contribute to a deficiency state in
these and other nutrients. Low magnesium can cause depressive
symptoms, confusion, anxiety, and hallucinations; calcium
deficiency can lead to nervousness, apprehension, and
numbness. Often supplemented together in approximately a 2:1
calcium-magnesium ratio, this combination is well-known in the
CAM world as a calmant and muscle relaxer.
Magnesium deficiency has been linked to depression and other
psychiatric disorders (Barbagallo 2009). A study of older diabetic
patients found that the prevalence of low serum magnesium was
3.5 times higher amongst depressed individuals compared to
controls (Barragan-Rodríguez 2007). Follow-up research by the
same team showed that magnesium treatment of depression in
elderly diabetics was as effective as imipramine therapy
(Barragan-Rodríguez 2008).
Calcium carbonate supplementation, in the form of 1200 mg of
elemental calcium daily, was given to 497 women between the
ages of 18 and over a range of three menstrual cycles. The
researchers concluded: “Calcium supplementation is a simple
and effective treatment in premenstrual syndrome, resulting in
a major reduction in overall luteal phase symptoms.” (Thys-
Jacobs 1998)
Summary
Nutritional psychiatry has come a long way since Hoffer and
Osmond’s first double-blind studies in the 1950s. Through the
extensive research of neurochemistry and related fields over the
past decades and ample clinical evidence, the logic behind the
therapeutic use of vitamins, minerals, and other nutrients has
become clear. Hopefully, it is also evident that, for many
patients, psychiatric symptoms are warning signs of nutritional
deficiency that impact physical status as well. Failure to address
these nutritional deficits may not only result in little or no
change in the patient’s complaints but, as when any medical
nutritional absorption, can contribute to a deficiency state in
these and other nutrients. Low magnesium can cause depressive
symptoms, confusion, anxiety, and hallucinations; calcium
deficiency can lead to nervousness, apprehension, and
numbness. Often supplemented together in approximately a 2:1
calcium-magnesium ratio, this combination is well-known in the
CAM world as a calmant and muscle relaxer.
Magnesium deficiency has been linked to depression and other
psychiatric disorders (Barbagallo 2009). A study of older diabetic
patients found that the prevalence of low serum magnesium was
3.5 times higher amongst depressed individuals compared to
controls (Barragan-Rodríguez 2007). Follow-up research by the
same team showed that magnesium treatment of depression in
elderly diabetics was as effective as imipramine therapy
(Barragan-Rodríguez 2008).
Calcium carbonate supplementation, in the form of 1200 mg of
elemental calcium daily, was given to 497 women between the
ages of 18 and over a range of three menstrual cycles. The
researchers concluded: “Calcium supplementation is a simple
and effective treatment in premenstrual syndrome, resulting in
a major reduction in overall luteal phase symptoms.” (Thys-
Jacobs 1998)
Summary
Nutritional psychiatry has come a long way since Hoffer and
Osmond’s first double-blind studies in the 1950s. Through the
extensive research of neurochemistry and related fields over the
past decades and ample clinical evidence, the logic behind the
therapeutic use of vitamins, minerals, and other nutrients has
become clear. Hopefully, it is also evident that, for many
patients, psychiatric symptoms are warning signs of nutritional
deficiency that impact physical status as well. Failure to address
these nutritional deficits may not only result in little or no
change in the patient’s complaints but, as when any medical
anomaly is ignored, may lead to worse symptoms as time goes on
and even physical deterioration and early death.
CAM physicians well versed in nutritional tools often find great
intrigue in their work. Each patient is uniquely different.
Through lab work and clinical observation, nutrient needs are
uncovered and remedied, bringing each to a more normalized
state, usually with resulting improvement in patient physical
and mental well-being.
We have only scratched the surface in this chapter and have
not even touched upon amino acids, probiotics, other vitamins
and minerals, and other supplements that have been shown to
be helpful in the treatment of psychiatric disorders. A great
many resources exist to further the practitioner’s knowledge.
and even physical deterioration and early death.
CAM physicians well versed in nutritional tools often find great
intrigue in their work. Each patient is uniquely different.
Through lab work and clinical observation, nutrient needs are
uncovered and remedied, bringing each to a more normalized
state, usually with resulting improvement in patient physical
and mental well-being.
We have only scratched the surface in this chapter and have
not even touched upon amino acids, probiotics, other vitamins
and minerals, and other supplements that have been shown to
be helpful in the treatment of psychiatric disorders. A great
many resources exist to further the practitioner’s knowledge.
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