Printer Friendly

Diet and schizophrenia.


Most of the research on treating psychiatric disease has been directed at neurotransmitters. Although there has been some success with this approach, long-term prognosis with this approach is less than desirable. A growing body of data suggests that more natural approaches to schizophrenia, bipolar disorder, and severe depression deserve further investigation and consideration. The orthodox mindset has searched (in vain) for the anatomical and physiological basis of schizophrenia, but to date, no theoretical models really provide meaningful insight (or effective treatment). (1) The search for an anatomical basis for schizophrenia has engendered an enormous, almost indigestible, mass of data. No "common" genetic, morphological or microscopic abnormality has been found that is either necessary or sufficient for the diagnosis (except for ventricle enlargement, which is a non-specific finding).

This has led many to believe that schizophrenia has less to do with genetic or anatomical factors, and more to do with dietary and environmental ones. The relationship of food to mental illness is at the top of the list of items that are particularly inflammatory to the orthodox medicine paradigm of mental illness. (2) But is it really that simple? This article will review four major dietary and nutritional considerations that are linked to schizophrenia. These are 1) casein and wheat (gluten) allergy (more correctly termed hypersensitivity); 2) essential fatty acid deficiency; 3) niacin deficiency; and 4) glutamic acid and glycine supplementation. In addition, a few general/miscellaneous factors will be considered.

The study of micronutrients and mental health is known as orthomolecular psychiatry, a term coined by two-time Nobel laureate, Linus Pauling in a controversial 1968 essay. Pauling wrote that nutritional supplements, unlike psychotherapy or drugs, represent a way to provide "the optimum molecular environment for the mind." Varying the concentrations of substances normally present in the human body, he wrote, may control mental disease even better than conventional treatments. Today the Society for Orthomolecular Health Medicine counts about 200 American members. One of the foremost practitioners, the Canadian psychiatrist Abram Hoffer, claims to have successfully treated thousands of schizophrenics with massive doses of vitamin C and niacin.

Casein, Gluten, and Schizophrenia

Casein is a protein found in milk, especially high in cow's cheese and milk. Gluten is a protein found in grains, and is especially high in common wheat. It is interesting to note that the two predominantly used grains (wheat and barley) in this country are genetically engineered and have five times the gluten content and only one-third the protein content of the original wheat from which they were derived. This high gluten content is thought to be the culprit in allergic reactions, food intolerance, malabsorption, indigestion, mood disorders, arthritis, and a host of other symptoms and diseases. When scholars have studied disease patterns and the decline of various civilizations, many of the degenerative diseases developed when cultivation of these grains became a major part of their diet.

One consistent dietary factor linked to schizophrenia is an allergy or sensitivity to wheat (specifically the wheat protein gluten). (3) Epidemiologic data illustrate that the incidence of schizophrenia is much less in societies that eat no wheat or rye but do eat other cereal grains (e.g., maize and millet). (4) Historical and anthropological studies have shown a strong association between wheat consumption and the incidence of schizophrenia. (5) For example, in Finland and Sweden during World War II, these countries faced severe shortages of wheat and rye. During that time, the incidence of new cases of schizophrenics declined acutely, while in countries that did not face such shortages, it remained the same or increased. Also, schizophrenia is extremely rare in cultures that traditionally eat wheat-free diets (e.g., South Pacific inhabitants of New Guinea and Micronesia). However, when these cultures, under Western influence, convert to a high-grain diet, the incidence of schizophrenia rises sharply (about a 65% increase) to match that of other Western or modernized nations.

Schizophrenia is also more prevalent (about three times) (6) in celiac sprue (a gluten allergy that causes gastrointestinal, neurological and immunological problems). (7,8,9) Studies have shown that schizophrenics who are put on an exorphin-free or low-exorphin diet are able to reduce their need for medications. (10) And double-blind challenges of introducing or removing exorphins from the diet of schizophrenics show a remarkable correlation between behavior and symptoms (improving when exorphins are removed or limited). (11) Furthermore, schizophrenics who are assigned a lower gluten diet are discharged twice as quickly as those who are given a higher gluten diet.

One hypothesis to explain how gluten can cause behavioral changes (gluten is also implicated in attention deficit, hyperactivity, and autism) is what I call the Exorphin Dysfunction Hypothesis. Exorphin means endorphins and enkephalins that come from outside the body (exogenous). If you remember, endorphins and enkephalins are substances created within the body (endogenous) that have morphine-like pain-killing effects (and euphoric mood effects). (A detailed review of endorphins and enkephalins are beyond the scope of this article.)

When cereal proteins (grains) are ingested, gluten fragments enter the bloodstream. These gluten fragments have a very similar shape to the body's own endorphins (including enkephalin peptides). These gluten fragments, therefore, can act upon endorphin receptors in the brain, which are heavily clustered in the frontal lobes and the lower limbic regions of the brain (the same regions implicated in schizophrenia according to the dopamine hypothesis). This can lead to mood disturbances, euphoria, dysphoria (disturbed or altered mood), irritation, perceptual distortions, and even psychosis. Further lending credence to the exorphin dysfunction hypothesis are studies using "mixed agonist/antagonists" drugs (e.g., cyclazocine and nalorphine) that artificially stimulate and suppress the body's endorphin receptors and have been known to produce profound dysphoria bordering on psychosis in patients.

Gluten therefore, by its "molecular mimicry" of endorphins (and enkephalins) reacts with the brain's endorphin receptors in the same deleterious way as cyclazocine or nalorphine. Casein proteins in dairy products are also thought to have similar amino acid sequences to enkephalin, thus also capable of interacting with brain receptors.

It is interesting to note that the degree to which this occurs is highly individual along a spectrum from no disturbance to severe sensitivity. The factors that make a person more susceptible to exorphin dysfunction are not fully known, but hypothesized to be genetic, environmental, nutritional, bacterial (e.g., alternations in gut flora or infections), viral, and structural (e.g., alterations in the gut barrier integrity). Furthermore, some schizophrenics appear more sensitive to exorphins than others, with research showing 20% being severely sensitive to even minute amounts of exorphins in the diet.

From the above studies it would seem reasonable to assume that gluten and casein have a negative effect on some individuals with schizophrenia, which is reversible upon instituting a wheat and dairy-free diet. This is one of many examples of illness being the result of individual maladaptation to certain foods which are nonpathogenic in the majority of the population. Elimination diets should be a valuable adjunct in ruling out cryptic gluten sensitivity in schizophrenia. (12)

Essential Fatty Acids and Schizophrenia

Over the past 100 years a dramatic change in our diet has occurred. We have invented an industry of prepared foods made in factories and shipped to consumers via supermarkets. With this "invention," shelf-life became a premium. EFAs, on the other hand, kill shelf-life because they have a tendency to go rancid when exposed to heat, light, and oxygen. At the same time, large commercial oil manufacturers began producing the refined vegetable oils we are now so familiar with. Currently, four oils (soybean, cottonseed, corn, and canola) account for 96% of vegetable oil use in the US. The omega-6:omega-3 ratio of these combined oils is between 12:1 and 25:1. An estimate of the omega-6:omega-3 ratio in our diet 100 years ago is between 3:1 and 5:1. This dramatic shift toward omega-6 oil consumption, coupled with the alteration of the fats via hydrogenation and oxidation is thought to be one of the leading factors in the rise of chronic illnesses. (13)

Another consistent dietary factor linked to schizophrenia is the under-consumption of (or increased need for) essential fatty acids (aka the "good" fats). (14,15,16) Fatty acid deficiency has been linked to a variety of mental disorders, such as schizophrenia, bipolar disorder, and depression. Among criminals (who have a higher incidence of mental illness), treatment with essential fatty acids decreases behavior problems in prison by one-third or more. (18,19)

"Some researchers suspect that even mild deficiencies can affect the psyche long before any physical symptoms appear. Stephen Schoenthaler, a sociologist at California State University at Stanislaus, has been exploring the link between nutrients and mental health by giving basic vitamin and mineral supplements to prison inmates and juvenile detainees. Again and again, since the early 1980s, Schoenthaler has found that when inmate nutrition improves, the number of fights, infractions, and other antisocial behavior drops by about 40%. In each case, he has found, the calmer atmosphere can be traced to the mellower moods of just a few hotheads. The inmates most likely to throw a punch, he has discovered, are the ones with the least nutritious diets and the lowest levels of critical nutrients ... In the late 1990s, an Oxford University physiologist named Bernard Gesch decided to put the theories to a more rigorous test. Gesch divided 231 prisoners in one of Britain's toughest prisons into two groups. Half were given a standard vitamin and mineral supplement each day as well as fish-oil capsules and omega-6 oil from evening primrose. The other half received placebos. The results, published in 2002, in The British Journal of Psychiatry, drew headlines on both sides of the Atlantic. They were also almost identical to Schoenthaler's. Over the course of approximately nine months, inmates taking supplements committed about 35% fewer antisocial acts than the group taking placebos. A few weeks after the study started, the prison warden told Gesch that the administrative report that month showed no violent incidents had occurred. As far as he was aware, this had never happened in the history of the institution." (20)

The exact mechanism of the role of essential fatty acids in these disorders is not fully known, but can be hypothesized to be: 1) disruption of prostaglandins (local hormone-like messengers); 2) changes in cell membrane structures and neurotransmitter receptor shape; 3) changes in intracellular transport (e.g., the influx of calcium into the cell); and 4) changes in cell electrical charge or conductance. Researchers have suggested that present-day refining and food selection patterns have led to widespread deficiencies of omega-3 fatty acids in some industrialized countries, with a consequent increase in the incidence and prevalence of many medical and psychiatric disorders. (21) The hypothesis that changes in essential fatty acid metabolism and/or availability being responsible for schizophrenia is known as the "membrane phospholipids" model of schizophrenia and may provide a unifying conceptual framework for not only understanding schizophrenia but also bipolar disorder, dyslexia, schizotypal personality disorder, other schizophrenia-like syndromes, and possibly other psychiatric disorders. (22,23)

"Early in life, an out-of-kilter stress response could cause healthy tissue in the body to break down over time, initiating chronic inflammatory reactions. Since certain inflammatory cells depend on high amounts of omega-3 fatty acids, shortages of these nutrients could arise. Without sufficient fatty acids, cell membranes (including those of brain neurons) may form defective structures, triggering a vulnerability to develop chronic psychiatric diseases such as schizophrenia, dyslexia, autism, and depression ... This chain of events would help explain why a chronic maladaptive stress response and omega-3 fatty acid deficiency are common findings in individuals with these conditions." (24,25)

Studies over the last 20 years and thousands of research articles have demonstrated the essential role of the omega-3, omega-6, and omega-9 fatty acids. Since the brain tissue is primarily composed of fatty acids, it makes sense to consider its fatty acid make-up when examining affective disorders. (Of particular interest is the fact that the brain is 70% fat by dry weight.)

All cell membranes, particularly neuronal membranes, are made up of a high percentage of phospholipids (fats). The membranes of dendrite and synapses are 80% lipids by weight. Neurotransmitters, and indeed all substances which are expressed, reabsorbed at the synapse, or move within the neurons, must cross these membranes. This is true of the excitatory amino acid systems as well as dopamine, serotonin, acetylcholine, and norepinephrine.

The treatment of psychiatric patients (schizophrenia, bipolar, depression, ADHD) with essential fatty acids has resulted in significant reduction in symptoms, and sometimes complete remission of symptoms--without drugs. In a landmark 1999 study, Harvard psychiatrist Andrew Stoll found that bipolar patients who were given large doses of omega-3s did significantly better and resisted relapse longer than a matched group of patients who were given placebos. Case studies and double-blind studies have consistently demonstrated sustained improvement of both positive and negative symptoms in patients with chronic schizophrenia consuming certain fatty acids and not being treated concurrently with conventional antipsychotic medications. (26,27)

It is interesting to note that the onset of mental illness or psychotic episodes can be brought on by dieting (calorie restriction) and more important food avoidance (the limitation or avoidance of fats). Without sufficient fatty acids, cell membranes (including those of brain neurons) may form defective structures, triggering a "vulnerability to develop chronic psychiatric diseases such as schizophrenia, dyslexia, autism, and depression," the researchers explained. (28)

Essential fatty acids actually work by turning on health-promoting genes and interacting with receptors that can only be stimulated by these types of fats. The wrong types of fat either can't turn on the right genes, turn on the wrong genes, or cause the signaling of the wrong messages. (29) The demonization of all fats is not only misguided, but extremely harmful to our health as different fats have different personalities. It is important not to stereotype all fat as "bad" so that we do not under-consume the "good" fats that are some of the most versa-tile and powerful health promoting substances ever discovered. Essential fatty acids are an essential component of anyone's diet who wishes to be and remain healthy. (30)

In summary, recent studies are showing excellent treatment results of psychiatric conditions through the use of essential fatty acids. (31,32) It is almost unbelievable that the treatment of these conditions, so long resistant to other forms of treatment, can be managed with the help of a simple, available, and inexpensive nutritional supplement. (33) In addition, sometimes patients will present with an essential fatty acid deficiency, but may be suffering from a single or multi-nutritional deficiency, either solely or concurrently. This is because certain nutrients are necessary for the processing of essential fatty acids, especially nicotinic acid (niacin, vitamin [B.sub.3]), antioxidants (also vitamin E and C), magnesium, and zinc (part of the desaturaze enzyme necessary to break down fatty acids). Deficiency of any one of these nutrients (or a combination of) can manifest as an essential fatty acid deficiency and as mental disorders.

Nicotinic Acid (Niacin)

Nicotinic acid functions in over 50 known metabolic reactions, most of which are enzymatic. Its bioactive forms--NAD+, NADH, NADP, and NADPH--play important roles as catalysts in the energy production process in the cells, the breakdown of proteins and fatty acids, the synthesis of fatty acids, and the formation of steroid hormones and red blood cells. (34) Niacin for the treatment of schizophrenia is derived from the hypothesis that metabolites of adrenaline and noradrenaline are toxic and have neuro-mental consequences and that niacin helps metabolize these. In addition, niacin is thought to be beneficial through its role in energy production, nitric oxide modulation, and essential fatty acid metabolism. (35)

One of the first associations between nicotinic acid and mental illness was its link to the disorder of pellagra in the early 1900s. Pellagra is a disorder of the four Ds--dermatitis, diarrhea, dementia, and death. However, pellagra (like all diseases) can occur along a spectrum of symptoms and docs not always appear in the "textbook" style so often quoted. The disease can consist of any of the following: bilateral, symmetrical skin lesions; hyper pigmentation of the skin; thickening of the skin; inflammation of the tongue and mouth; indigestion; anorexia; neurasthenia; diarrhea; irritability; amnesia and delirium (and mood disturbances). (36,37) Pellagra was at epidemic proportions in the early part of the century and its cause was unknown. A member of the US Public Health Service, Joseph Goldberger, MD, researched the crisis and noticed that poorer people were more likely to get the disease, as were people in prisons, asylums and orphanages, where there was a limited diet (this same association is seen in schizophrenia). Goldberger began experiments on prison inmate volunteers, giving them the poor diet he associated with pellagra. Within months many developed the disease. The symptoms were reversed when foods rich in vitamin [B.sub.3] were added to the diet. Nicotinic acid (niacin), when its use was introduced, cured hundreds of thousands of pellagra patients of their psychoses (dementia) as well as of the other physical manifestations of their disease (diarrhea and dermatitis).

It is interesting to note that nicotinic acid was once considered a standard treatment for mental disorders, a fact made evident by Dr. William Kaufman's inadvertent discovery in 1951 that 758 psychotic patients treated with nicotinic acid had the added benefit of greatly improving the symptoms of all forms of arthritis and degenerative joint disease (DJD)--even partially or fully reversing ankylosed joints. (38) Recent research has confirmed a powerful role of nicotinic acid in treating joint pain, inflammation and lipid disorders (high cholesterol, low HDL, high LDL, and high Lipoprotein(a)). (39)

Niacinamide's primary mechanism of action is through its inhibition of PARS and tumor necrosis factor-[alpha] (TNF-[alpha]). Because inhibition of PARS suppresses inducible nitric oxide (NO) synthase, which reduces the generation of NO and peroxynitrite, niacinamide is able to interrupt this self-amplifying, positive feed-forward cycle. Reactive oxygen species (ROS), most notably peroxynitrite and hydroxyl radicals, induce DNA strand breaks that lead to the activation of the repair enzyme PARS. Unfortunately, PARS activation triggers a futile energy-consuming cycle, resulting in massive depletion of cellular NAD and ATP, leading to functional alterations of the cell and eventual cell death. PARS also regulates the expression of a number of genes, including the gene for collagenase and inducible NO synthase. Thus, PARS activation is inversely associated with joint tissue integrity. A related chain of events involves the activation of TNF-[alpha], a cytokine that produces higher amounts of ROS (which further activates PARS); stimulates production of other cytokines; and inhibits the synthesis of cartilage matrix and contributes to cartilage loss. Not surprisingly, high levels of TNF-[alpha] are found in the synovial fluid and joints of certain individuals.

Mohler has reported: "Nicotinamide has properties in common with benzodiazepines (and barbiturates) in its action on spinal cord activity, and its anticonflict, anticonvulsant, antiaggressive, muscle relaxant, and hypnotic action." Kennedy (3) reported: "This drug (niacinamide) has a qualitatively similar effect to diazepam on the turnover of serotonin, nor adrenaline, dopamine and GABA in those areas of the brain that are thought to be deranged in anxiety". (40,41)

As early as 1940, researchers reported treating dozens of patients successfully with moderately large doses of niacinamide (0.5-1.5 g). None of these patients, interestingly, had any overt signs or symptoms of pellagra (niacinamide deficiency) or any other vitamin deficiency.

More recently many other investigators have reported on the use of nicotinic acid and nicotinamide for the treatment of mental disease. In several studies collectively involving over approximately several hundred psychiatric patients, it was found that those who received niacinamide were less likely to be readmitted after discharge, and spend only half the time hospitalized. Hoffer and Osmond, have advocated and used nicotinic acid in large doses, in addition to the conventional therapy, for the treatment of schizophrenia since 1952. Hoffer has collected data on more than a 1,000 patients treated with this approach. (42) The dosage recommended by Hoffer is 3-18 g/day, as determined by the response of the patient, of either nicotinic acid or nicotinamide, together with 3 g/day of ascorbic acid. Hoffer contends the vitamins neutralize an oxidized compound that causes hallucinations when it accumulates in the brains of patients.

Niacinamide is tolerated well by schizophrenic patients and is safe. Some patients experience the "niacin flush;" however, within several days, the flush is no longer evident. Furthermore, new forms of niacinamide, such as sustained release and inositol hexanicotinate, have eliminated this problem. Sedatives and tranquilizers can be used with niacin, but the effect of phenothiazines may be potentiated. (43,44)

Glutamic Acid (Glutamine) and Glycine

Glutamine is an amino acid that is present at rather high concentration in brain and nerve tissue and plays an essential role in the functioning of these tissues. Research has implicated dysfunction of glutamatergic neurotransmission in the pathophysiology of schizophrenia. Dysfunction of glutamatergic neurotransmission (through N-methyl-D-aspartate (NMDA) receptors) may play an important role in the pathophysiology of schizophrenia, especially of the negative symptoms and cognitive impairments associated with the disorder, and is a promising target for drug development. (45) Glutamatergic neurons are the major excitatory pathways linking the cortex, limbic system (emotional centers), and thalamus, regions that have been implicated in schizophrenia. Further lending credence to the glutamate hypothesis of Schizophrenia is that the illicit drug PCP ("angel dust") induces psychotic effects in humans that closely resemble positive, negative, and cognitive symptoms of schizophrenia and behavior effects of PCP can be reversed by glycine. (46)

Glycine, a small nonessential amino acid, functions as an obligatory coagonist at NMDA active symptoms of schizophrenia. In one double-blind, placebo-controlled study of 22 treatment-resistant schizophrenic patients, treatment glycine administration resulted in a 30% reduction in negative symptoms. These findings support hypoglutamatergic hypotheses of schizophrenia and suggest a novel approach for the pharmacotherapy of negative symptoms associated with this illness. (47) Other studies have repeatedly confirmed these results. (48-51)

General Nutritional Factors

Other vitamins and substances influence the functioning of the brain. Beyond the nutrients already discussed, strongly associated with schizophrenia are deficiencies or increased need for magnesium, vitamin C, B vitamins (e.g., thiamine, folic acid, [B.sub.12], riboflavin), zinc, and the amino acid glycine. (52-58)

Magnesium: Although the evidence is inconsistent, some studies have found magnesium deficiencies in depressed patients. In addition, the mineral may work by enhancing the efficacy of other mood-stabilizing drugs.

B Vitamins: Folic acid is a B vitamin essential to mood regulation and the development of the nervous system. Patients deficient in these appear to respond poorly to antidepressants. In one 2000 British study, 127 patients taking Prozac were also given either 500 [micro]g of folic acid a day or a placebo. The folic acid group did significantly better, in particular the women, who fared 30% better than the placebo group. Plasma folate levels below the 10th percentile of controls was associated with a 4- to 7-fold increased risk of having schizophrenia. There was a significant dose-response relationship between plasma folate concentrations and the risk for schizophrenia, and a protective effect by high plasma folate levels. (59) Vitamin [B.sub.12] is another vitamin strongly associated with mental illness, especially dementia and psychosis. Numerous researchers and dozens of articles have shown a higher incidence of low [B.sub.12] concentrations in the blood of mental patients than in the population as a whole. (60,61)

In a personal dialogue with Dr. John Vlok Dommisse, one of the world's foremost experts on vitamin [B.sub.12] and mental illness, he writes: "1 have published a long paper, a chapter in a book on anti-aging medicine, and a long letter on the psychiatric manifestations of vitamin [B.sub.12] deficiency (1991, 1996a & b) and was the published 'expert' in a long 'The expert speaks' interview published in the March 1998 issue of Clinical Pearls News, a nutritional and preventive medicine abstracts journal. (Dommisse) In all these publications I mention the review article from St. Louis that shows which are the commonest psychiatric syndromes caused by this vitamin deficiency: mood disorders, dementia, paranoid psychosis, and violent behavior (Zucker, et al, 1981). Various authors have documented the psychotic (Hart/ McCurdy), depressive (MacCallum), and consecutive affective and psychotic conditions in the same patient (Verbanck/LeBon). Doctors Levitt and Joffe, working at the Clarke Institute of Psychiatry in Toronto (where I trained, years earlier), published a report about vitamin [B.sub.12] deficiency causing the psychotic form of depression, in the British Journal of Psychiatry in 1988 (Levitt/Joffe). They also reviewed the medical literature and found that psychotic depression is more often caused by [B.sub.12] deficiency than by any other known or unknown cause [emphasis author's]. This fact is hardly ever borne in mind when psychiatrists confront a case of psychotic depression and, when they do think of it and order a serum [B.sub.12] level, they will more often than not still miss the deficiency because the lab 'normal range' is so low that their patient's [B.sub.12] level almost always appears to be in the 'normal range.' At least six neurological and psychiatric papers, in top medical journals, have shown that the normal range should be regarded as at least 500-1,300 pg/ml (rather than 200-1,100), since the cerebrospinal fluid level can be deficient when the serum level drops below 500, and neuropsychiatric symptoms often occur at serum levels between 200 and 500 pg/ml (VanTiggelen, et al; Lindenbaum, et al; Mitsuyama, Kogoh, Nijst, et al; Ikeda, et al; Regland). As for the still-held misconception that the neuropsychiatric effects of [B.sub.12] deficiency are always accompanied by a macrocytic anemia, it is humbling to know that this notion was already debunked in 1905 (Langdon)! Since then, many papers have stressed this point, including those by Strachan and Henderson (1965), Evans, et al (1983), and Lindenbaum, et al (1988)."

Vitamin C: Vitamin C deficiency (even sub-clinical) can manifest symptoms of mental illness. In 1957, Akerfeldt reported that the serum of schizophrenics had been found to have greater power of oxidizing N,N dimethyl-p-phenylenediamine than that of other persons. Several investigators then reported that this difference is due to a smaller concentration of ascorbic acid in the serum of schizophrenics than of other persons. This difference has been attributed to the poor diet and increased tendency to chronic infectious disease of the patients, and has also been interpreted as showing an increased rate of metabolism of ascorbic acid by the patients. It may be that schizophrenics have an increased metabolism of ascorbic acid, presumably genetic in origin, and that the ingestion of massive amounts of ascorbic acid has some value in treating mental disease.

Inositol: This sugar molecule appears to make the brain's receptors more sensitive to serotonin, one of the chemical messengers that mediate mood. In a series of short-term, placebo-controlled trials, researchers at Ben Gurion University of the Negev in Israel found that large doses of inositol (12-18 g/day) helped alleviate depression, panic disorder, and obsessive-compulsive disorder.


More and more data is suggesting a role of nutrition in the cause, prevention, and treatment of mental illness. If one eliminates milk/cheese, wheat, caffeine, alcohol and sweets, it would make a big difference on the symptoms of chronically, mentally ill patients. In addition, palliative or curative effects may be possible by consuming a multi-vitamin/multi-mineral (with a good amount of B vitamins) and adding a supplement program consisting of the following:

** Fish Oil* (EPA/DHA): 3-6 g/day (The author recommends Kirunal, an EPA enhanced fish oil which provides an EPA to DHA ratio of 3:1 which is the ratio shown beneficial in studies. Standard fish oil supplements provide a 2:1 ratio of EPA to DHA.)

** GLA* (essential fatty acid): 250 mg day

** Niacinamide*: 1-6 g/day

** Vitamin C: 1-5 g/day

** Glycine: 10-60 g/day

** L-Glutaminc: 3-10 g/day

** Inositol: 3-18 g/day

This is a pretty "hefty" supplement program, and the doses here are doses consistent with studies. No study to date has seen if there is a "synergistic" effect between these supplements, thus allowing one to take less of each. In my experience, many patients often achieve clinical results with less than the above, especially when doing all the above. Start with the low dose and increase each until clinical response. The absolutely most essential parts of the program are indicated by an asterisk.

In my experience, the presence of skin lesions, joint problems, gastrointestinal disturbances and concurrent mood disturbances strongly suggest a nutritional component to the disease. What is also of concern in mental illness is that these patients tend to self-medicate with illicit drugs, especially alcohol. The problem with drugs and alcohol is they further interfere with the nutritional process by affecting digestion, storage, utilization, and excretion of nutrients. (62)

Of course, not everyone with a vitamin deficiency grows violent or sinks into a clinical depression. So why might a nutritional supplement help only some people? Possible explanations include "inborn errors of metabolism" (genes that require a person get more than the "average" of nutrients for proper function), changes in the blood-brain barrier permeability, frank or subclinical (aka sub-optimal) nutrient deficiency and toxins.

Nobel Prize winner, Linus Pauling said, "The methods principally used now for treating patients with mental disease are psychotherapy, chemotherapy, and convulsive or shock therapy." However, we have seen that perhaps a more "natural" approach can complement or replace these invasive approaches, which are often marked with numerous side-effects and poor compliance.

About the Author

Nicholas Calvino is a chiropractic physician and Master Herbalist candidate. He is the co-author of an upcoming book, Eat This! An Introduction To The New World Food Order and in private practice in Southern Arizona. He can be reached through his virtual practice at


1) Stevens J. "Anatomy of schizophrenia revisited." Schizophrenia Bulletin, 1997; 23(3):373-383.

2) Hoffer A. "The vitamin paradigm wars." Townsend Letters for Doctors and Patients, June, 1996; 56-60.

3) Dohan FC. "Schizophrenia, cereal grains, and celiac disease." Del Med J, 1973;45(10):303-4; Pfeiffer CC. "Schizophrenia and wheat gluten enteropathy." Biol Psychiatry, 1984; 19(3):279-80; Singh MM and Kay SR. "Wheat gluten as a pathogenic factor in schizophrenia." Science, 1976; 191(4225):401-2; Horrobin DF. "What should be done about schizophrenia?" J R Soc Med, 1981; 74(3):180-2; Lindsay JS. "Probability and schizophrenia." Br J Med Psychol, 1966; 39(2): 145-56; Lemperiere T, Dureau F, and Laberge P. "Etiology and pathogenesis of schizophrenia." Rev Prat, 1965; 15(25):3311-22; Dohan FC, Harper EH, Clark MH, et al. "Is schizophrenia rare if grain is rare?" Biol Psychiatry, 1984; 19(3):385-99.

4) Dohan FC and Grasberger JC. "Relapsed schizophrenics: Earlier discharge from the hospital after cereal-free, milk-free diet." Am J Psychiatry, 1973; 130(6):685-688.

5) Dohan FC and Grasberger JC. "Relapsed schizophrenics: Earlier discharge from the hospital after cereal-free, milk-free diet." Am J Psychiatry, 1973; 130(6):685-688.

6) "Lead, celiac disease linked to schizophrenia." Autism Res Rev Int, 2004; 18(1):4; Eaton W, Mortensen PB, et al. BMJ, 2004; 328:438-439.

7) Walsh D. "Coeliac disease and schizophrenia." BMJ, 1973; 2 (860):242; Ross-Smith P and Jenner FA. "Diet (gluten) and schizophrenia." J Hum Nutr, 1980; 34(2):07-12; Dohan FC. "Is celiac disease a clue to the pathogenesis of schizophrenia?" Ment Hyg, 1969; 53(4):525-9.

8) Singh MM and Kay SR. "Wheat gluten as a pathogenic factor in schizophrenia." Science, 1976; 191(4225):401-2.

9) Zioudrou C, Streaty RA, and Klee WA. "Opioid peptides derived from food proteins: The exorphins." J Biol Chem, 1979; 254(7):2446-2449.

10) Zioudrou C, Streaty RA, and Klee WA. "Opioid peptides derived from food proteins: The exorphins." J Biol Chem, 1979; 254(7):2446-2449.

11) Singh MM and Kay SR. "Wheat gluten as a pathogenic factor in schizophrenia." Science, 1976; 191(4225):401-2.

12) Klee W, Zioudrou C, et al. "Exorphins: Peptides with opioid activity isolated from wheat gluten, and their possible role in the etiology of schizophrenia." In: Endorphins in Mental Health Research. Uspin E, Bunney WE, and Kline N, editors. 1977; 209-218; Dohan FC, et al. "Is schizophrenia rare if grain is rare?" Biological Psychiatry, 1984; 19:385-399; Dohan FC. "Schizophrenia: Possible relationship to cereal grains and celiac disease." In: Schizophrenia: Current Concepts and Research. Sankar S, editor. PDJ Publishing, New York, 1969; 539-551; Singh MM and Kay SR. "Wheat gluten as a pathogenic factor in schizophrenia." Science, 1976; 191(4225):401-2; Rice JR, Ham CH, et al. "Another look at gluten in schizophrenia." Am J Psychiatry, 1978; 135:1417-1419.

13) Guilliams T. "Fatty acids: Essential ... therapeutic." The Standard. May/June 2000. PO Box 1060, Stevens Point, WI 54481.

14) Assies J, Lieverse R, Vreken P, et al. "Significantly reduced docosahexaenoic and docosapentaenoic acid concentrations in erythrocyte membranes from schizophrenic patients compared with a carefully matched control group." Biol Psychiatry, 2001; 49:510-522; Peet M, Brind J, Ramchand CN, et al. "Two double-blind placebo-controlled pilot studies of eicosapentaenoic acid in the treatment of schizophrenia." Schizophr Res, 2001; 49(3):243-51.

15) Su KP, Shen WW, and Huang SY. "Omega-3 fatty acids as a psychotherapeutic agent for a pregnant schizophrenic patient." Eur Neuropsychopharmacol, 2001; 11(4):295-299.

16) Vaddadi KS. "Penicillin and essential fatty acid supplementation in schizophrenia." Prostglandins Med, 1979; 2:77-80.

17) Stoll A, et al. "Omega-3 fatty acids in bipolar disorder. A preliminary double-blind, placebo-controlled trial." Arch Gen Psychiatry, 1999; 56:407-412

18) Ness C. "Can vitamins, omega fats improve behavior? Study links diet to mental health." San Francisco Chronicle, January 15, 2003.

19) Gesch CB, et al. "Influence of supplementary vitamins, minerals and essential fatty acids on the antisocial behavior of young adult prisoners. Randomised, placebo-controlled trial." British Journal of Pyschiatry, 2002; 181:22-28.

20) Freinkel S. "Vitamin cure: Can common nutrients curb violent tendencies and dispel clinical depression?" Discover, May 2005; 26(5).

21) Rudin DO. "The dominant diseases of modernized societies as omega-3 essential fatty acid deficiency syndrome: substrate beriberi." Med Hypotheses, 1982; 8(1):17-47; Rudin DO. "The major psychoses and neuroses as omega-3 essential fatty acid deficiency syndrome: substrate pellagra." Biol Psychiatry, 1981; 16(9):837-850.

22) Horrobin DF. "The membrane hypothesis of schizophrenia." Schizophr Res, 1998; 30(3):193-208; Horrobin DF. "Schizophrenia as a membrane lipid disorder, which is expressed throughout the body." Prostaglandins, Leukot Essent Fatty Acids, 1996; 55(1-2):3-7; Horrobin DF and Bennett CN. "Depression and bipolar disorder: relationships to impaired fatty acid and phospholipid metabolism and to diabetes, cardiovascular disease, immunological abnormalities, cancer, ageing and osteoporosis. Possible candidate genes." Prostaglandins, Leukot Essent Fatty Acids, 1999; 60(4):217-234; Horrobin DF, Glen AI, and Hudson CJ. "Possible relevance of phospholipid abnormalities and genetic interactions in psychiatric disorders: the relationship between dyslexia and schizophrenia." Med Hypotheses, 1995; 45(6):605-613; Horrobin DF, Glen AI, and Vaddadi K. "The membrane hypothesis of schizophrenia." Schizophr Res, 1994; 13(3):193-207.

23) Haag M. "Essential fatty acids and the brain." Can J Psychiatry, 2003; 48(3):195-203.

24) Assies J, Lieverse R, Vreken P, et al. "Significantly reduced docosahexaenoic and docosapentaenoic acid concentrations in erythrocyte membranes from schizophrenic patients compared with a carefully matched control group." Biol Psychiatry, 2001; 49:510-522.

25) Bell JG, Sargent JR, et al. "Red blood cell fatty acid compositions in a patient with autistic spectrum disorder: a characteristic abnormality in neurodevelopmental disorders?" Prostaglandins, Leukot Essent Fatty Acids, 2000; 63(1/2):21-25.

26) Puri BK, Counsell SJ, et al. "Eicosapentaenoic acid in treatment-resistant depression." Arch Gen Psychiatry, 2002; 59(1):91-92 [letter]; Puri BK, Richardson AJ, et al. "Eicosapentaenoic acid treatment in schizophrenia associated with symptom remission, normalization of blood fatty acids, reduced neuronal membrane phospholipid turnover and structural brain changes." Int J Clin Pract, 2000; 54(1):57-63; Laugharne JD, Mellor JE, and Peet M. "Fatty acids and schizophrenia." Lipids, 1996; 31(suppl):S163-S165; Mellor JE, Laugharne JD, and Peet M. "Schizophrenic symptoms and dietary intake of n-3 fatty acids." Schizophr Res, 1995; 18(1):85-86; Peet M, Brind J, et al. "Two double-blind placebocontrolled pilot studies of eicosapentaenoic acid in the treatment ofschiozophrenia. Schizophr Res, 2001; 49(3):243-251; Phospholipid Spectrum Disorder in Psychiatry. Peet M, Glen I, and Horrobin D, editors. Marius Press, Carnforth, UK, 1999; Peet M, Laugharne JD, et al. "Essential fatty acid deficiency in erythrocyte membranes from chronic schizophrenic patients, and the clinical effects of dietary supplementation." Prostaglandins, Leukot Essent Fatty Acids, 1996; 55(1-2):71-75.

27) Wright J. "Treatment of chronic anxiety and associated physical complaints with niacinamide and essential fatty acids: Two cases." Journal of Orthomolecular Medicine, 1995; 7(3).

28) Assies J, Lieverse R, Vreken P, et al. "Significantly reduced docosahexaenoic and docosapentaenoic acid concentrations in erythrocyte membranes from schizophrenic patients compared with a carefully matched control group." Biol Psychiatry, 2001; 49:510-522.

29) Raclot T, et al. "Site-specific regulation of gene expression by n-3 polyunsaturated fatty acids in rat white adipose tissues." Journal of Lipid Research; 38:1963-1972.

30) Calvino N. Modern Foods Solution: How To Achieve Vibrant Health In A Toxic World! CenterPoint Press, Scottsdale, AZ, 2004.

31) Vaddadi KS. "Penicillin and essential fatty acid supplementation in schizophrenia." Prostglandins Med, 1979; 2:77-80.

32) Peet M, Brind J, et al. "Two double-blind placebo-controlled pilot studies of eicosapentaenoic acid in the treatment ofschiozophrenia. Schizophr Res, 2001; 49:243-251.

33) Horrobin, DF. "The membrane phospholipid hypothesis as a biochemical basis for the neurodevelopmental concept of schizophrenia." Schizophr Res, 1998; 30:193-208; Ward PE, Sutherland J, et al. "Niacin skin flush in schizophrenia: a preliminary report." Schizophr Res, 1998; 29:269-274; Horrobin DF and Bennett CN. "Depression and bipolar disorder: relationships to impaired fatty acid and phospholipid metabolism and to diabetes, cardiovascular disease, immunological abnormalities, cancer, ageing and osteoporosis." Prostaglandins, Leukotrienes and Essential Fatty Acids, 1999; 60(4):217-234; Horrobin DF and Bennett CN. "New gene targets related to schizophrenia and other psychiatric disorder: enzymes, binding proteins and transport proteins involved in phospholipid and fatty acid metabolism." Prostaglandins, Leukotrienes and Essential Fatty Acids, 1999; 60(3):141-167; Stoll AL, et al. "Omega-3 fatty acids in bipolar disease: A preliminary double-blind, placebocontrolled trial." Arch Gen Psychiatry, 1999; 56:407-412; Peet M, Murphy B, et al. "Depletion of omega-3 fatty acid levels in red blood cell membranes of depressive patients." Biol Psychiatry, 1998; 43:315-319; Edwards R, Peet M, et al. "Omega-3 polyunsaturated fatty acid levels in the diet and in red blood cell membranes of depressed patients." J of Affective Disorders, 1998; 48:149-155; Stevens LJ, et al. "Omega-3 fatty acids in boys with behavior, learning, and health problems." Physiology & Behavior, 1996; 59(4/5):915-920; Mellor JE and Peet M. "Double-blind, placebo-controlled, trial of omega-3 fatty acids as an adjunct to the treatment of schizophrenia." Presented at the Winter Schizophrenia Workshop, Davos, Feb 17-23, 1998. Submitted for publication.

34) "Niacinamide: Monograph." Alternative Medicine Review, 2002; 7(6):525-529.

35) Wittenborn JR. "Niacin in the long-term treatment of schizophrenia." Arch Gen Psychiatry, 1973; 28:308-315.

36) "Niacinamide: Monograph." Alternative Medicine Review, 2002; 7(6):525-529.

37) Green RG. "Subclinical pellagra: Its diagnosis and treatment." Schizophrenia, 1970; 2:70-79.

38) Kaufman W. "Niacinamide therapy for joint mobility: There-apuetic reversal of a common clinical manifestation of the normal aging process." Connecticut State Medical Journal, 1951; 3252(28):584-589.

39) Jonas W. "The effect of niacinamide on osteoarthritis: A pilot study." Inflamm Res, 1996; 45:330-334.

40) Mohler H, et al. "Nicotinamide is a brain constituent with benzodiazepine-like actions." Nature, 1979; 278:563.

41) "Niacinamide: Monograph." Alternative Medicine Review, 2002; 7(6):525-529.

42) "Niacinamide: Monograph." Alternative Medicine Review, 2002; 7(6):525-529.

43) Osmond H and Hoffer A. "Massive niacin treatment in schizophrenia: Review of a nine-year study." Lancet, February 10, 1962; 316-320.

44) Parsons WB. "Introduction of niacin as the first successful treatment for cholesterol control. A reminiscence." J Orthomolecular Med, 2000; 15(3):121-126.

45) Goff DC and Coyle JT. The Emerging Role of Glutamate in the Pathophysiology and Treatment of Schizophrenia.

46) Javitt DC, Balla A, et al. "Reversal of phencyclidine-induced effects by glycine and glycine transport inhibitors." Biol Psychiatry, 1999; 45(6):668-79.

47) Heresco-Levy U, Javitt DC, et al. "Efficacy of high-dose glycine in the treatment of enduring negative symptoms of schizophrenia." Arch Gen Psychiatry, 1999; 56(1):29-36.

48) "Double-blind, placebo-controlled, crossover trial of glycine adjuvant therapy for treatment-resistant schizophrenia." Br J Psychiatry, 1996; 169(5):610-7.

49) Heresco-Levy U, Silipo G, and Javitt DC. "Glycinergic augmentation of NMDA receptor-mediated neurotransmission in the treatment of schizophrenia." Psychopharmacol Bull, 1996; 32(4):731-40.

50) Javitt DC, Zylberman I, et al. "Amelioration of negative symptoms in schizophrenia by glycine." Am J Psychiatry, 1994; 151(8):1234-6.

51) Javitt DC, Zylberman I, et al. "Amelioration of negative symptoms in schizophrenia by glycine." Am J Psychiatry, 1994; 151(8):1234-6.

52) Nechifor M, Vaideanu C, et al. "The influence of some antipsychotics on erythrocyte magnesium and plasma magnesium, calcium, copper and zinc in patients with paranoid schizophrenia." J Am Coll Nutr, 2004; 23(5):549S-551S.

53) Muntjewerff JW, van der Put N, et al. "Homocysteine metabolism and B vitamins in schizophrenic patients: Low plasma folate as a possible independent risk factor for schizophrenia." Psychiatry Res, 2003; 121:1-9.

54) Tokdemir M, Polat SA, et al. "Blood zinc and copper concentrations in criminal and noncriminal schizophrenic men." Arch Androl, 2003; 49:365-368.

55) Prakash R and Petrie WM. "Psychiatric changes associated with an excess of folic acid." Am J Psychiatry, 1982; 139(9):1192-1193.

56) Peet M, Brind J, et al. "Two double-blind placebo-controlled pilot studies of eicosapentaenoic acid in the treatment ofschiozophrenia. Schizophr Res, 2001; 49:243-251.

57) Bucci L. "Pyridoxine and schizophrenia," Br J Psychiatry, 1973; 122:240.

58) Carney MWP, Ravindran A, et al. "Thiamine, riboflavin and pyridoxine deficiency in psychiatric in-patients." Br J Psychiatr, 1982; 141:271-272.

59) Muntjewerff JW, van der Put N, et al. "Homocysteine metabolism and B vitamins in schizophrenic patients: Low plasma folate as a possible independent risk factor for schizophrenia." Psychiatry Res, 2003; 121:1-9.

60) T Ran, OJ Rafaelson, P Rodbro, Laurel 1966-II. 965. (1966). "Report serum Br concentration below 150 pg/ml in 13 of I" consecutive patients admitted to a Copenhagen psychiatric clinic."

61) Edwin R, Holten K, et al. Act Med Scand, 1965; 171:689.

62) Lieber CS. "The influence of alcohol on nutritional status." Nutrition Reviews, 1988; 46(7):241-254.

by Nicholas Calvino, DC, MHC
COPYRIGHT 2006 Original Internist, Inc.
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2006 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Title Annotation:diet relevance to mental illness
Author:Calvino, Nicholas
Publication:Original Internist
Geographic Code:1USA
Date:Mar 22, 2006
Previous Article:The history of iodine in medicine Part I: from discovery to essentiality.
Next Article:Personal exposure to the pollution controversy.

Terms of use | Privacy policy | Copyright © 2022 Farlex, Inc. | Feedback | For webmasters |