Fatty acids, vitamins and minerals are major factors in brain neurotransmitter metabolism, and thus in most mental disorders.
One out of 100 people world-wide suffer from schizophrenia, a vaguely defined chronic mental condition with disabling multiple manifestations. As far as the outcome of treatment is concerned, there is an almost medieval attitude towards the condition, among the public, and the medical professionals as well.
All the symptoms of schizophrenia are common to other mental disorders such as Depression, bipolar disorder, post traumatic stress, obsessive compulsive disorders, phobias, Attention Deficit Disorder (ADD), and Wilson Disease (hallucinations). There is some recognition by the American Psychiatric Association (APA) that the diagnoses criteria for some of these diseases need some overhauling, yet there is a long way to go.
Schizophrenia is diagnosed when there is serious impairment in mood, emotion, sensory perception, cognitive skills and even movement. The schizophrenia patient may have hallucinations, may be mentally confused, and chronically depressed to the point of total apathy. His emotions may be reduced, absent altogether, or misplaced.
There is sometimes delusion as to one’s own identity and environment. The paranoid type may suffer with persecution syndrome, constantly seeing himself as a possible victim. Social alienation and withdrawal is common. About 10 percent of those diagnosed with schizophrenia end their own lives. In sum, schizophrenia is the jack-of-all-trades of mental diseases, and as such, is treated with a number of drugs that address the individual symptoms. Several hundreds of such drugs have been developed and are being used – without hope of a true cure.
However, an increasing body of evidence reveals that most mental diseases, those enumerated above, as well as others such as senility, Alzheimer’s and Parkinson’s are in fact nutritional diseases. At this time, there is enough evidence to propose that what is diagnosed as schizophrenia is in fact a number of conditions related to nutritional problems such as imbalance of fatty acids, vitamin and/or mineral deficiencies, faulty glucose metabolism, poor antioxidant load, and excess of toxic metals.
There are records of schizophrenia being cured or considerably improved, through megavitamins, fatty acids, minerals or combinations of these. In some clinical studies, various micronutrients were added with advantage to the pharmaceutical treatment, with reduction of drug dosages, and mitigation of adverse effects from the drugs.
While presenting a summary of the research agenda, part of which having been kicked off in 2002, Jeffrey D. Rediger, M.D., noted at this year’s APA symposium held in Toronto that “genetic studies, despite several decades of effort, have not yet identified with certainty any bona fide psychiatric disease gene, although the field is getting closer…”
Scientists found deviations, both structural and gene-related which they have linked with schizophrenia. However, studies with identical twins show that only half of the subjects develop the disease in pairs. This means the environmental factors of schizophrenia account for 50 to 100 percent (the 50 percent of those who developed the disease in pairs, could have experienced the same environmental triggering factors).
While genetic differences were found to characterize different schizophrenia subtypes, it does not follow that the disease itself is genetically inherited. The medical truth allows for a more optimistic view of those conditions. Firstly, some patients do not have those genetic characteristics, and still have the disease. Secondly, as it is often found in most so-called ‘genetic’ diseases, what the individual inherits is not the disease itself, but a tendency.
While in theory this distinction doesn’t seem much, in practice it makes all the difference. Gene variations have often been shown to mean simply a higher requirement for a certain nutrient or a missing enzyme that synthesizes a nutrient. A person for example may be unable to express a gene that synthesizes vitamin B12 in the intestines from meat, so this person will benefit from taking this vitamin as a supplement that melts under the tongue, or by injection.
While sophisticated brain imaging techniques can give us a good account, not only of brain structure, but even a live action sequence of it, and thus give much fodder to fatalistic views of brain diseases, the same techniques reveal that nutrients themselves can change the very structure of the brain. In one study, a brain that has been observed as ‘shrunk’ in an MRI, has returned to normal size after supplementation with omega 3 fatty acids and antioxidants. The brain is hopelessly complex and reassuringly plastic.
Four decades ago, two types of schizophrenia were distinguished on the basis of vitamins, minerals and immune system abnormality. The so-called ‘histapenic’ patients were those who had low histamine levels and high levels of the mineral copper, and the ‘pyroluric’ patients were deficient in vitamin B6 and the mineral Zinc. The two disease qualifiers have disappeared from the medical literature.
According to the APA, a categorization of the disease based on etiology (causes) is desirable and it would help research, however, admittedly it is far for being possible. The APA sees an etiology-based diagnostic in relation to genes, and not with nutrients. The hidden truth of genetic research is that it is a theoretical endeavor. There are so many genes affecting factors and co-factors involved in the brain neurotransmitter metabolism in one single symptom, that it will take centuries, or millennia to discover them all, and pinpoint their multiple actions.
Some forms of psychoses have been directly attributed to nutrient deficiency (one of the B complex vitamin, vitamin C, or an excess of the mineral copper) and these are completely cured with supplementation, or copper chelation, respectively, however, these forms are not considered schizophrenia proper by the APA. This distinction favors drug-related approaches to the detriment of further research on nutrition and supplementation.
Dopamine is one of the hormone/neurotransmitters in the brain that affects behavior, emotions, cognition, as well as motor function. Patients with schizophrenia were found to have high dopamine levels. Parkinson’s, on the other hand, is characterized by not enough dopamine neurons in a certain part of the brain. Ten percent of Parkinson’s patients on L-dopa, a precursors of dopamine, develop psychotic symptoms. Other brain neurotransmitters such as serotonin, norepinephrine, acetylcholine are more or less involved in the same functions.
Studies have linked disruption of dopamine metabolism with Parkinson’s, schizophrenia, as long as Depression, addictions and bi-polar disorder. Dopamine and serotonin exist in a metabolic seesaw, when one increases, the other decreases. This axial model characterizes the metabolism of most hormones. The two so-called catecholamines are also on the same metabolic path of most other major hormones in the body. Feedback loops inform their activity continuously and the complexity of this setup, with transporters, receptors, and inhibitors have made it difficult to diagnose mental diseases on the basis of what caused them, and even more difficult to treat.
Some pharmaceuticals are precursors of hormones, others bind to receptors and displace hormones, others yet antagonize receptors, others stimulate them, others antagonize natural inhibitors, or the neurotransmitter recycling process. The problem compounds when different parts of the brain are affected by the same neurotransmitter/hormone.
Low dopamine in one part of the brain affects movement and in another part of the brain affects cognitive function. After the failure of the past century’s antipsychotic drugs now called the ‘first generation’ or ‘atypical,’ new better-targeted, ‘typical’ drugs have been developed. These drugs are not cures, but temporary relief for one or a group of symptoms. Paradoxically, as theoretical knowledge advances the concepts behind drug development becomes more and more narrow, and the hope for true health, in the sense of achieving homeostasis, vanishes.
The ‘second generation’ of drugs are not as promising as one might have thought. For example, a group at the Department of Psychiatry at Yale University School of Medicine found that antidepressant drugs that treat Depression by targeting the amount of serotonin that is recycled in the brain (SSRIs, selective serotonin reuptake inhibitors), modify the dopamine balance of the patient (by enhancing the dopamine transporter factor). This occurs after only 6 weeks of treatment. The authors conclude that “This apparent SSRI-induced modulation of the dopamine system may be associated with some of the side effects of these agents, including sexual dysfunction.”
While, long term studies are hard to come by, theoretically, a chronic Depression treated with such drugs may turn into schizophrenia or other dopamine-related condition down the line. The SSRIs are becoming the number one mood altering drugs in this country, prescribed to children as well. These researchers found the drug effect on dopamine transporters “unexpected.” However, pharmaceuticals that modulate hormones have always turned out to have adverse effects; the body acts against them, and sometimes homeostasis is even further compromised. Thus, ten percent of Parkinson’s patients on L-Dopa develop psychotic symptoms. Most adverse effects are only known by patients, their families and their caretakers. There are no follow up on drug usage.
A comprehensive review of more than 2000 studies on 586 new antipsychotic drugs found most reporting of poor quality. The study, published this year in the Cochrane Database of Systematic Reviews characterizes the data regarding the ‘new generation’ of anti-psychotics drugs ‘inconclusive.’ According to these authors “There are no data at all on outcomes such as compliance, cost, social and cognitive functioning, relapse, rehospitalisation, or quality of life.” Also, the authors of this review contend, these studies are short term and there is no possibility for follow up.
Also, the reports are inconclusive as to whether or not the patients, on their own, stayed on medication longer than with the ‘first generation’ or ‘atypical’ drugs, which, due to adverse effects, are characterized by low compliance. The review reported 18 types of outcomes measured on 670 rating scales. Such huge number of rating scales suggests systemic incompetence as well, that is the medial research industry is not set up in a way that may help patients, the public, health providers, other researchers and the advancement of medicine.
To the question of why many thousands (most studies have multiple authors) of trained scientists would write incompetent/incomplete records of their studies, one cynic may answer: 1) because the authors were hiding the negative outcomes of the studies, and/or 2) because the studies themselves were set up to result in inconclusive data.
Status quo is the norm, and there is no incentive for change. A 1998 meta-analysis of 50 years of studies by the Cochrane Schizophrenia Group, Oxford, U.K., deemed them shoddily reported and found no improvement over the 50-year period.
Reviews of published drug studies found a bias against negative reports in studies funded by researchers working for profit (funded by the drug companies).
The conclusion is that patients and families ought to be mistrustful of pharmaceuticals.
In the 1960’s after more than a decade of research into the causes of psychiatric illness Linus Pauling coined the term ‘orthomolecular’ to denote a concept of disease and treatment that focused on discovering and returning to the body of those specific chemicals, in the specific amounts, that are missing from a malfunctioning metabolic gear. Pauling later extended his theory to the entire body. At that time, two Canadians, Abram Hoffer and Humphrey Osmond had published their clinical research according to which they successfully treated mentally ill patients with megavitamins among which niacin, vitamin B3. However, the Board of Directors of the Canadian Mental Health Association set up long term studies on niacin or nicotinamide (a form of niacin) megadozes (gradually up to 3 g daily and sometimes 8 g) which turned out negative.
A study by J.V Ananth and his colleagues published in the Canadian Psychiatric Association Journal in 1973 however shows that both nicotinic acid (niacin) and pyridoxine (B6) given individually over a period of 48 weeks, improved schizophrenia symptoms in hospitalized patients, although when the two were given together the anti-psychotic medication could be reduced.
Hoffer’s and Humphrey’s megavitamin studies cannot be discarded. Results of studies by physicians with intend to ‘cure’ cannot be duplicated by ‘studies for the sake of studies,’ for multiple reasons. Moreover, the same treatment doesn’t work for all patients.
Overdosing on niacin is dangerous. In at least one clinical case, a man took 11,000 mg (11 g) of the vitamin and ended up in the emergency department with dangerous Low Blood Pressure levels. Besides saline solutions needed to increase his Blood pressure, he required 12 hours of dopamine infusion.
Nicotinic acid (a form of niacin) in excess may have serious side effects, among which liver problems, Gout, high blood sugar, Vomiting, Diarrhea, high Blood pressure. Although high niacin dozes are prescribed in some cases to lower blood fats and Cholesterol, this has to be done under physician monitoring.
Unfortunately, as revealed by the APA’s stance and proposed research directions, most psychiatrists feel threatened by non-pharmaceutical approaches, and may have distorted the studies. In a 2-year study for example, 7 out of 19 patients from the vitamin group took the vitamin for only one year and one patient took the vitamin for only 2 weeks but they were all counted as undergoing a full 2-year treatment. With small total numbers, this is likely to skew the outcome. In these studies, the patients were given the vitamins together with their current drug therapies.
Whether or not micronutrient success studies were duplicated, the fact remains that the major element affecting directly the working of brain neurotransmitters is food. Food affects brain neurotransmitters at every step, by way of glucose metabolism, amino-acid and prostaglandin synthesis which are only possible in the presence of proper amounts of vitamins, minerals and fatty acids. Deficiencies of certain micronutrients such as folic acid, ascorbic acid, manganese and Zinc are known to cause psychotic behavior.
The synthesis of prostaglandins, those fugitive metabolic substances that are created in the body by way of essential fatty acids and contribute to the immune system, as well to the brain neurotransmitter synthesis need fatty acids and a host of minerals and vitamins, especially B-3, B-6, C, magnesium and Zinc.
The prostaglandins, like hormones, exist in pairs, are sensitive to balance, and are involved in practically all metabolic processes. Health in body and mind is not possible when various prostaglandins are not in balance.
A deficiency in Omega 3 fatty acids leads to deficiency in the E3 prostaglandins and this has often been correlated with mental problems. Numerous studies on Depression, bi-polar disorder, hyperactivity and aggression, schizophrenia and poor cognitive function have linked these conditions with low EFA’s status, particularly the DHA and EPA (two of the Omega 3 fatty acids).
The importance of essential fatty acids (EFAs) in health, including mental health is widely recognized. A large part of the brain is made of fatty acids, which have a role in the synthesis of neurotransmitters, as well as brain cell membrane activity and integrity, and cell connections (synapses).
The modern diet yielding a high ratio of the Omega 6 oils (derived from alpha-linoleic acids preponderant in corn, soy, sunflower and sesame oils) and the Omega 3 fatty acids (from alpha-linolenic acids, abundant in fish, flax, hemp, Walnut, and brazil nuts oils) has been implicated in most brain diseases (as well as other health problems). “Lipids, and especially omega-3 fatty acids, provided the first coherent experimental demonstration of the effect of diet (nutrients) on the structure and function of the brain.” Notes the French researcher Marie Bourre in the Journal of Nutrition on Health and Ageing.
In the journal Drugs, the U.K. psychiatrists M. Peet and C. Stokes note that “The evidence to date supports the adjunctive use of omega-3 fatty acids in the management of treatment of unresponsive Depression and schizophrenia.”
Some researchers believe the abnormal fat metabolism, or more specifically an EFAs deficiency, actually cause schizophrenia.
An U.K. study using advance high resolution 3D MRI cerebral imaging showed that “ in the year before EPA treatment, cerebral atrophy was taking place and that this atrophy was reversed by six month of EPA treatment. These results demonstrate that EPA can reverse both the phospholipids abnormalities previously described in schizophrenia and cerebral atrophy. They provide strong further evidence in support of the membrane phospholipid model of schizhophrenia.”
As pointed out earlier, there is more than one nutrient to brain metabolism. A study by researchers in the Netherlands found that a subgroup of schizophrenia patients had low essential fatty acids and vitamin B levels as well. Patients who were not taking any vitamins were found to have high homocysteine levels and low vitamin B 12.
The group could predict high homocysteine levels in males who did not east fish, while alcohol consumption was linked with low EFA status. The researchers noted that none of the patients were found to be malnourished by their clinicians, and concluded that “a subgroup of patients with schizophrenia has biochemical EFA deficiency, omega3/DHA marginality, moderate hyperhomocysteinemia, or combinations. Correction seems indicated in view of the possible relation of poor EFA and B-vitamin status with some of their psychiatric symptoms, but notably to reduce their high risk of cardiovascular disease.”
This group from the Netherlands found that differences in homocysteine levels were caused by folate deficiencies in both males and females, while low vitamin B12 and B6 explained high homocysteine levels in females. These researchers found a strong association between folate metabolism (low plasma and high red blood cell levels of folic acid, a B vitamin) and schizophrenia.
A pioneer in the field of EFA’s role in metabolism, Donald Rudin, M.D. studied, in a clinical environment, the effect of Omega-3 fatty acids in numerous health conditions. Rudin’s patients suffering from heart conditions, Arthritis, intractable skin diseases and Depression benefited from supplementation with B vitamins, antioxidants and Omega-3 fatty acids.
In one dramatic case which Rudin describes in his 1983 book, the Omega-3 Oils (which he co-authored with Berkeley nutritionist Clara Felix) Rudin relates the case of a psychotic woman who had been institutionalized for ten years, before she recovered fully with a program of flax seed oil devised by Dr. Rudin, mostly through trial and error. According to Rudin, every individual has his/her own Omega 3 fatty acids needs. Some studies showed that most people achieve a propitious fatty acid balance from fish oil, rather than vegetable sources such as flax, yet, at least one study with children with ADD (Attention Deficit Disorder) suggests some people do not metabolize fish oil efficiently and do better with flax oil, which contains the precursors of the fish EFAs.
Even if fatty acids are in correct balance, the vitamin C is needed to prevent brain damage due to oxidation of lipids and the free radicals created in the normal metabolic process. An increasing number of studies show that most brain diseases are characterized by high inflammation of the brain caused by oxidation. A high level of antioxidants prevent degenerative diseases of any kind, including brain diseases Ascorbic acid has other function in the brain as well. In fact at least one study suggests it modifies dopamine levels.
One of the side-effect of Scurvy, the disease of vitamin C deficiency, is schizophrenia. Scurvy is a rare disease in the modern world, however, studies show that schizophrenia patients are low in red blood cell vitamin C. At least one study shows that ascorbic acid alone is able to mediate dopamine release.
According to the conclusion of a study published in the British Journal of Psychiatry in 1963 “These findings suggest that chronic psychiatric pts maybe in a state of ‘subscurvy’ and thus could benefit from ascorbic acid supplementation.”
In an 1983 observational study published in the Human Nutrition: Clinical Nutrition researchers C.J. Schorah, D.B. Morgan, and R.P. Hullin noted that the average plasma levels of ascorbic acid in 885 psychiatric patients was much lower than that of healthy individuals and that 32% of them had levels at “the threshold which has been associated with detrimental effects on immune responses and behavior.” The psychiatric patients had an average ascorbic acid of 0.51/100 ml., while the mentally healthy individuals had an average of 0.87/100 ml.
Another study published in Acta Medica by researchers from former Yugoslavia also revealed that psychiatric patients had lower plasma vitamin C levels than other individuals.
A study with ascorbic acid in rats published in the journal Science in 1985 by G.V. Rebec, found that ascorbic acid was capable of modulating anti-psychotic drugs. The researcher concluded that ascorbic acid alone “could attenuate dopamine-mediated behaviors.”
Another condition that manifests itself with hallucinations, Wilson Disease, is characterized by abnormal deposits of the mineral copper in the tissue. Copper is part of the enzymatic path that produces dopamine, and an abnormal dopamine level is linked with hallucinations, as well as other psychiatric conditions.
Copper may be ingested in excess from cooking utensils, as well as from drinking water that has been ducted in dilapidated copper pipes. Toxic schizophrenia may result from such conditions. It turns out however that some schizophrenic persons, according to researchers from the Department of Psychiatry, University of Michigan Medical School, Ann Arbor, manifest a condition in which the level of an enzymatic substance which is metabolically bound to copper is high.
Inheriting a condition that predisposes one to accumulate copper, even if it’s an abnormal enzyme metabolism, is not the same as inheriting hallucinations. This type of research by Wolf T.L., Kotun J., Meador-Woodruff J.H., uses knowledge of symptoms from another disease to make analogies and inferences which can be used as hypothesis in studying treatments for schizophrenia.
Chelation is a method by which targeted excess minerals are eliminated from the body by substances known to bind them. Although regularly performed in cases of excess of specific minerals, chelation, as a distinct treatment method, is not recognized by the American Medical Association. Some chelation proponents claim mental diseases are some of the conditions that may benefit from this therapy.
Firstly, some cases of Parkinson’s and Alzheimer’s were found to be linked with metal toxicity, and secondly, there is much research literature that reveals brain diseases are in great part caused or aggravated by oxidation and arterial damage caused by plaque, which is one of the conditions targeted by chelation therapy. (Calcium is a component of plaque). Chelation, which is usually performed with a substance called EDTA and with chelating minerals is a medical treatment that has to be done under strict supervision. However, there is a type of chelation people can do at home. Anti-oxidant vitamins, essential fatty acids, and many Phytochemicals in fruits and vegetables have chelating action.
Most scientists see the genes that allow for excess copper ‘abnormal,’ genes that are missing in action or ‘bad’ genes (do not express an enzyme, for instance, or express it too much). In the light of what is known about genes, evolution and the environmental factors and their relationship with genes, this view is naïve. Some genes are ‘damaged’ indeed, however, extremely rare. Most of the type genes are just different, due to some adaptation to environment.
There is evidence that some ‘abnormal’ genes respond to nutrient supplementation. An abnormal copper/iron balance gene may simply be a form of adaptation to a different environment. Minerals, like anything else in the body, are needed in relatively fixed ratios and a gene that conserves copper may be beneficial in a medium that has too much iron or Zinc.
Low levels of folic acid, as well as excessive levels have been related to schizophrenia. Most commonly however, people seem to be deficient in this B vitamin.
A subgroup of schizophrenia (about 25% of hospitalized mental patients in a 1967 study) was found to have a folic acid deficiency. Lack of folic acid has long been linked with psychosis, Depression, confusion, disorientation, and dementia, as well as other neurological conditions and symptoms, as pointed out by Melvyn R.Werbach, M.D. in his book Nutritional Influences of Illness (Third Line Press, 1987).
However, the excess of folic acid was found to cause psychotic reactions as well.
About 3 mg daily of folic acid for two weeks raised the folate level in the red blood cells to the point of leading to abnormal behavior. In another study 1 g of folic acid showed symptoms after five months. The subjects of these clinical cases where schizophrenic patients who were on psychotic medications.
While folic acid is one of the most common nutritional deficiency, and is being justifiably popularized as effective against the heart-killer high-blood homocysteine , the need for moderation (as with everything) must be emphasized here. The 1967 study mentioned by Werbach found that, the subgroup of schizophrenia ‘histapenic’ patients (with low histamine and high copper) improved the mental symptoms and corrected the histapenic condition when treated with folic acid, vitamin B12, Zinc, niacin and vitamin C (Zinc counteracts copper and is also needed in brain neurotransmitter synthesis). On the other hand, folic acid worsened the situation in “pyroluric” patients (deficient in B6 and Zinc).
It is tragic that there are so few of such promising studies that differentiate between patients’ needs. One cannot help but speculate that putting all patients in the same basket facilitates drug studies and drug marketing, as new drugs are being continuously created to mitigate the adverse effects of drugs.
Scientists from the Department of Neuropsychiatry at the Seoul National University Hospital, Korea found that a specific type of schizophrenic patients display low levels of an enzyme that uses folates (such as folic acid, a B vitamin) to reduce homocysteine level in the blood. The researchers found a specific gene characteristic to a certain schizophrenic subgroup (a genotype), that is related to that enzyme’s detrimental behavior.
High homocysteine blood levels and low folate has long been linked with schizophrenia, as well as with Heart disease. The Korean scientists conclude “These findings suggest that folate supplement may be beneficial to some schizophrenic patients with homocysteinemia due to the genetic defect of methylenetetrahydrofolate reductase.”
One of the folate environmental factor occurs in uterus. There is evidence that babies born to mothers who lack folates in their diet have a higher risk of developing schizophrenia later in life. Even with prenatal folic acid supplementation, some individuals may have a higher need of this vitamin.
Folic acid, often found deficient, especially in the elderly, has long been associated with cognitive and mood disturbances, including dementia. Studies on brains of Alzheimer’s have determined a common folic acid deficiency.
Swedish researchers from the Institute of Clinical Neuroscience at Goteborg University found new hope for prevention and treatment of schizophrenia writing that: “The findings point to a new area of schizophrenia research: the role of nutrients and antioxidants.” Their conclusion is based on the fact that “Schizophrenic patients generally appear to have a disturbed single-carbon metabolism.” Single-carbon metabolism can be modified by natural means, these researchers note. According to a clinical study analyzed by these researchers, a majority of schizophrenia patients were found to have elevated levels of methionine (an amino-acid), while a smaller group was found to have high homocysteine levels. Homecysteine can be lowered by taking folic acid supplements.
While folic acid is a well-known factor in lowering homocysteine levels, researchers in Milan, Italy in trying to prevent deadly circulatory diseases considered to be due to homocysteine levels found that in some patients vitamin B12 was also useful to this end in some patients who had a genetic tendency towards high homocysteine levels.
Adding to the argument made earlier regarding the relation between nutrient intake and ‘genetic’ diseases, these researchers found that “ Subjects carrying the MTHFR 677TT genotype have higher folate and vitamin B12 requirements irrespective of the A2756G polymorphism of the MS gene.”
Vitamin B12 happens to be found deficient in numerous mental conditions
Another group of schizophrenia is characterized by deficiency in pyridoxine (vitamin B6) and Zinc. It is well know that these two nutrients are co-factors in the neurotransmitter synthesis. Zinc is in fact needed in more than two hundred enzymatic processes in the body, and, according to well known nutritionist Edwin Haas, it is one of the minerals most difficult to absorb, especially by elderly individuals and those whose digestive system is less than perfect.
Megadozes of Zinc and pyridoxine are dangerous and should never be attempted.
So much for ‘abnormal’ homocysteine reducing enzyme and schizophrenia: researchers at the Massachusetts General Hospital in Boston found that homocysteine level correlated with glucose metabolism in a group of schizophrenic patients. Specifically, the high homocysteine levels were linked with impaired fasting glucose (IFG). The same group was found to have a higher degree of insulin resistance, and higher Blood pressure.
This condition, which is on the increase in the developed world, is mostly nutritional. Excess sugar and fats (especially the wrong fats such as hydrogenated, saturated, and Omega-6) have been linked with what has been called the ‘metabolic syndrome,’ insulin resistance, blood glucose swings, and ultimately Heart disease and diabetes. Statistically, schizophrenia is linked with a higher risk of cardiovascular disease, the latter being linked with the metabolic syndrome and high homocysteine.
Lifestyle, finally, is now recognized as a major factor in the ‘metabolic syndrome’ and it results as a factor in schizophrenia as well. Glucose control, and avoidance of insulin swings prevent brain damage by arteriosclerosis and oxygen deprivation. Considering that glucose metabolism affects the brain hormones dopamine and serotonin in a direct manner, it is a great puzzle that glucose control is not a primary aspect of schizophrenia treatment.
Interestingly, people with a deficiency of the lipid precursor of the Omega 3 fatty acids (alpha-linolenic acid) perceive sugar less sweet than those with normal levels of this essential fat.
Some food allergies, such as those to wheat and milk, are known to cause full blown psychosis in some people. According to Udo Erasmus, symptoms brought about by allergy to wheat often cannot be distinguished from symptoms of schizophrenia Some forward-thinking clinicians have withdrew this allergens from their mental patients, with considerable improvement in symptoms. Gluten, a protein in wheat, rye, corn and other grains is a known allergen.
When schizophrenic patients were put on a gluten-free diet, their symptoms improved overall. It is now recognized that a much higher percentage of people as previously believed have allergies to grains, especially those of Northern Europe extraction. Strong allergic reactions can take place from an extremely small amount of the offending item. Moreover, the patient who has an allergy to gluten will crave gluten. Another protein in wheat was found to attach to the same receptors in the brain as opium. Allergies are an expression of the working of the immune system and allergens are likely to affect mental function, since the brain neurotransmitters/hormones are affected by prostaglandins and the prostaglandins are affected by the immune system; they are in fact a part of that system.
Caffeine should not be used by people with schizophrenia, according to Melvyn R. Werbach M.D., author of Nutritional Influences on Illness, as it can trigger hormonal imbalance. The methyl-xanthine increases norepinephrine release and synthesis in the central nervous system (CNS). Caffeine was also found to increase brain serotonin (low, normal levels of serotonin are calming while high levels increase aggressiveness). Serious serotonin imbalance, however, is linked with many mental disorders, from clinical Depression to murderous psychopathology.
Caffeine affects dopamine balance as well, raising it at first and then lowering it. Dopamine imbalance is linked with several brain diseases, too much of it with Parkinson’s and various neurological disorders, too little of it has been implicated in hallucinations and schizophrenia.
Caffeine may also cause depletion of water soluble vitamins such as B and C, as well as certain minerals, all of which are needed for normal brain metabolism. These vitamins are antioxidants, and many medical scientist now believe that oxidative stress, a basically a form of inflammation in the brain destroys neurons and might be the cause of a majority of brain diseases, including senility, Alzheimer’s and schizophrenia.
While high Cholesterol is associated with arterial plaque, low Cholesterol levels have been also associated with schizophrenia. Cholesterol lowering drugs are among the most prescribed drugs in the United States, however, many health writers denounced them as very detrimental to health, as they have been linked with strokes, kidney disease, and in general a high rate of morbidity of any kind. Studies that correlated Cholesterol lowering drugs with schizophrenia have found no association.
According to Italian researchers U. Ambanelli and P. Manganelli degradation of tryptophan metabolism is linked, among other diseases, with schizophrenia and Depression. While the researchers are not sure if the degradation of this amino acid is a cause or an effect of the diseases with which it is linked, they note that “The degradation of tryptophan is particularly influenced by steroid hormones and vitamins’ want.”
Sugar and stress are known to activate natural body steroid hormones. It has been recognized that some cases of psychosis are triggered or aggravated by the stress factor. Stress also lowers the immune system, which, mentioned earlier, is linked with neurotransmitter metabolism as well.
Commercial steroid hormones found in inhalants and in prescription drugs may also alter neurotransmitter metabolism, by altering the immune system as well as hormonal balance.
Many prescription drugs which affect the immune system, trigger Depression or psychotic symptoms in some people. The Asthma medication Singulair for example, according to Asthma patients and parents whose children have taken the drug, has psychotic effects which are identical with those of schizophrenia (on-line chat). The NSAIDs (non steroidal anti-inflammatory drugs) widely used for pain of any kind, has been linked with Depression. As mental disorders are on the increase, long term, honest studies are needed to determine the long term effect of such drugs on brain integrity.
A new fascinating and encouraging scientific development suggests that at least some cases of mental diseases may be caused by parasites, or more precisely, by the parasite Toxoplasma Gondii. Firstly, scientists have observed that, when infected with the parasite Toxoplasma Gondii, the mice lose their sense of preservation relative to cats. In other words, the mice become engaged in reckless, suicidal behavior. Further, one of the drugs that alleviate schizophrenia has turned out to be effective against this particular parasite.
Mega quantities of vitamin C are on record as being greatly beneficial to most schizophrenia patients in several studies. In fact several studies show that schizophrenia patients, as a group, have a higher need of vitamin C than the population at large. When ingesting the same quantities and reaching the same blood quantity of the vitamin with the non-schizophrenia group, the mentally ill individuals still excrete less of the vitamin. Vitamin C being a powerful antibiotic, may also help against the T.G. parasite, when present.
The Chinese Traditional Medicine treats mental diseases as a Liver Disease. Indeed, most enzymes which affect the metabolic path that leads to neurotransmitters are metabolized in the liver. The liver is also the organ that eliminates the toxic load in the body, and determines the quality of the immune system. One of the Chinese herbs used in mental diseases, schizandra (schizandra chinensis) is an herb that was found to have a liver-supporting action in Western studies as well.
Toxicologist expert Cynthia Watson describes schizandra as an adaptogen that boosts brain function and help detoxify the body from carbon tetrachloride. According to her the herbs is also effective in hepatitis. (Liver Protection in Life Extension and Memory Boosters, Health Quest Publications, 1993) . Other herbs that the Chinese have used in mental problems are often the same as the ones used in the digestive system. The digestive system is, of course, where the nutrients, including Zinc and B vitamins are absorbed, and it is closely related to the immune system as well.
The role of the present environment is also not getting enough attention. Stress is known to modify hormone levels. Studies on stress reveal that the body is able to compensate for bouts of stress, however, long term chronic stress is likely to create disease by disabling the body defenses – through using up our resources. Holistic health practitioners emphasize the need for an increase in micronutrients during times of stress.
In example of how social environment affects us is offered by research on serotonin levels ( a hormone that is in part a measure of our assertiveness and aggressiveness) on population groups. This research revealed that this neurotransmitter/hormone is increased in people of low social status. Our body knows that it needs to make us more aggressive and more assertive when we are unemployed and hungry. (low serotonin levels may explain why people in secure government jobs are so relaxed and socially active on the phone, behind their little glass cubicles).
There are many ways in which mental disease can occur, as many as the number of paths that may lead to brain disruption of metabolic equilibrium. While there is no financial incentive for the medical establishment to pursue studies on nutrition, food remains the major factor in brain health, and orthomolecular psychiatry appears a valid choice.
Picker JD, Coyle JT. Do maternal folate and homocysteine levels play a role in neurodevelopmental processes that increase risk for schizophrenia? Harv Rev Psychiatry. 2005 Jul-Aug;13(4):197-205. firstname.lastname@example.org
Muntjewerff JW, van der Put N, Eskes T, Ellenbroek B, Steegers E, Blom H, Zitman F. GGz Nijmegen Homocysteine metabolism and B-vitamins in schizophrenic patients: low plasma folate as a possible independent risk factor for schizophrenia. Psychiatry Res. 2003 Nov 1;121(1):1-9
Regland B., Schizophrenia and single-carbon metabolism. Prog Neuropsychopharmacol Biol Psychiatry. 2005, Sep;29(7):1124-32
Schizophr Res. 2006 Jul 12; [Epub ahead of print] Links
Plasma copper, iron, ceruloplasmin and ferroxidase activity in schizophrenia.Wolf TL, Kotun J, Meador-Woodruff JH.
Department of Psychiatry, University of Michigan Medical School, Ann Arbor, MI, United States.
Mularski RA, Grazer RE, Santoni L, Strother JS, Bizovi KE.
Treatment advice on the internet leads to a life-threatening adverse reaction: hypotension associated with Niacin overdose. Clin Toxicol (Phila). 2006;44(1):81-
Henderson DC, Copeland PM, Nguyen DD, Borba CP, Cather C, Eden Evins A, Freudenreich O, Baer L, Goff DC., Homocysteine levels and glucose metabolism in non-obese, non-diabetic chronic schizophrenia. Acta Psychiatr Scand. 2006 Feb;113(2):121-5.
Botez T et al. Neuropsychological disorders responsive to folic acid therapy: A report of 39 cases. Excerpta Medica Internat. Congress Series 427:202, 1977 in Melvyn R. Werbach, M.D., Nutritional Influences on Illness, Third Line Press, Keats Publishing, New Canaan, CT, 1987.
Peet M, Stokes C. Omega-3 fatty acids in the treatment of psychiatric, Drugs. 2005;65(8):1051-9. Links
Bourre JM. J, Roles of unsaturated fatty acids (especially omega-3 fatty acids) in the brain at various ages and during ageing, Nutr Health Aging. 2004;8(3):163-74. Links
Young GS, Conquer JA, Thomas R., Effect of randomized supplementation with high dose olive, flax or fish oil on serum phospholipid fatty acid levels in adults with Attention Deficit hyperactivity disorder, Reprod Nutr Dev. 2005 Sep-Oct;45(5):549-58
Young G, Conquer J., Omega-3 fatty acids and neuropsychiatric disorders. Reprod Nutr Dev. 2005 Jan-Feb;45(1):1-28.
Peet M.,The metabolic syndrome, omega-3 fatty acids and inflammatory processes in relation to schizophrenia. Prostaglandins Leukot Essent Fatty Acids. 2006 Aug 24
McNamara RK, Ostrander M, Abplanalp W, Richtand NM, Benoit SC, Clegg DJ. , Modulation of phosphoinositide-protein kinase C signal transduction by omega-3 fatty acids: Implications for the pathophysiology and treatment of recurrent neuropsychiatric illness. Prostaglandins Leukot Essent Fatty Acids. 2006 Aug 25;
du Bois TM, Deng C, Bell W, Huang XF., Fatty acids differentially affect serotonin receptor and transporter binding in the rat brain. Neuroscience Institute for Schizophrenia and Allied Disorders, Neurobiology Research Centre for Metabolic and Psychiatric Disorders, Department of Biomedical Science, University of Wollongong, Wollongong, NSW, Australia. email@example.com
Rummel C, Hamann J, Kissling W, Leucht S, New generation antipsychotics for first episode schizophrenia, Cochrane Library
This article written by, Elena Marcuscomment be the first to comment