Schizophrenia
From The Nutritional Health Bible by Linda Lazarides (1997). This free database is provided for interest only. Linda's later writings refer to more up-to-date research.
Some causative factors- Abnormal essential fatty acid metabolism
- Coenzyme Q10 deficiency
- Deficiencies of vitamins C, B3 and/or B6 and zinc
- Food allergy
- Gluten intolerance
- Heavy metal poisoning
- Histamine imbalances
- Prenatal (before birth) starvation
Imagawa M: Low erythrocyte coenzyme Q10 levels in schizophrenic patients. Jap J Psych Neurol 43(2):143-145, 1989. Biochemical markers of vitamin B1, B2 and B6 deficiency were measured in 172 successive admissions to a hospital psychiatric unit. 53% of the patients were deficient in at least one vitamin and 12% in more than one. Schizophrenics tended to be deficient in vitamin B1, and mood disorder patients to be deficient in B2 and B6. Carney MW et al: Thiamine, riboflavin and pyridoxine deficiency in psychiatric in-patients. Br J Psychiatry 141:271-2, 1982.
The vitamin B1 status of 42 physically healthy non-alcoholic psychiatric patients was measured by assessing transketolase activity. 16 of the patients showed evidence of vitamin B1 deficiency, despite, in some cases, having received vitamin B1-containing supplements for up to six weeks before testing. Schwartz RA et al: Transketolase activity in psychiatric patients. J Clin Psychiatry 40(10):427-9, 1979.
Comparisons between mentally ill subjects with and without mercury amalgam (silver) tooth fillings revealed significant differences in reports of mental health. Subjects who had amalgam fillings removed reported a subsequent reduction or disappearance of mental symptoms. Siblerud RL: The relationship between mercury from dental amalgam and mental health. Am J Psychother 43(4):575-87, 1989.
Current evidence indicates that a disturbance in the balance of trace elements in the human body can lead to various psychiatric syndromes. The role of trace elements is important in treatment and prevention. Srinivasan DP: Trace elements in psychiatric illness. Br J Hosp Med 32(2):77-9, 1984.
Zinc deficiency during pregnancy may give rise to schizophrenia in genetically susceptible offspring. Andrews RC: Unification of findings in schizophrenia by reference to the effects of gestational zinc deficiency. Med Hypotheses 31(2):141-53, 1990.
Four lines of evidence in the literature support prenatal nutritional deficiencies as a plausible risk factor for the development of schizophrenia. For instance prenatal malnutrition affects maternal functions which are critical to the nervous system of the developing foetus. Brown AS et al: Neurobiological plausibility of prenatal nutritional deprivation as a risk factor for schizophrenia. J Nerv Ment Dis 184(2):71-85.
Essential fatty acids and the prostaglandins derived from them are important regulators of nerve cell function. There is evidence that the production of prostaglandin E1 is impaired in schizophrenia. Clinical trials with E1 and its precursors GLA and DGLA have shown modest therapeutic benefits. Horrobin DF: The relationship between schizophrenia and essential fatty acid and eicosanoid metabolism. Prostaglandins Leukot Essent Fatty Acids 46(1):71-7, 1992.
The risk of schizophrenia was compared in individuals exposed or not exposed to the Dutch Hunger Winter of 1944-45 in Holland. It was found that those conceived at the height of the famine were twice as likely to develop schizophrenia. Susser E et al: Schizophrenia after prenatal famine. Further evidence. Arch Gen Psychiatry 53(1):25-31, 1996.
Promising nutritional researchVitamin C seems to have an increased turnover in schizophrenia patients and supplementation appears to help them. Kanofsky JD: Vitamin C and schizophrenia. Nutrition Report 8(9):65-72, 1990
Folic acid treatment for sub-acute degeneration of the spinal cord due to folate deficiency was associated with an improvement in the patient's mental condition, diagnosed as schizophrenia. Donnelly S et al: Subacute combined degeneration of the spinal cord due to folate deficiency in association with a psychotic illness. Ir Med J 83(2):73-4, 1990.
33% of 123 patients with acute clinical depression or schizophrenia were found to be folate deficient. After treatment with methylfolate or placebo for 6 months in addition to their standard psychiatric drugs, those given methylfolate had experienced a significantly improved clinical and social recovery. Procter A: Enhancement of recovery from psychiatric illness by methylfolate. Br J Psychiatry 159:271-2, 1991.
Trials treating schizophrenia with essential fatty acids or prostaglandins have shown modestly promising results, particularly those where essential fatty acid were combined with nutritional supplements. Vaddadi KS: Use of gamma-linolenic acid in the treatment of schizophrenia and tardive dyskinesia. Prostaglandins Leukot Essent Fatty Acids 46(1):67-70, 1992.
In a controlled study of red cell membrane fatty acids in schizophrenia patients, both omega-3 and omega-6 fatty acids were at low levels, particularly arachidonic acid and docosahexaenoic acid. While dietary fatty acid intake was not abnormal, a higher intake of omega-3 fatty acids was associated with less severe symptoms. A significant improvement in symptoms was obtained with supplementation of 10 g per day of fish oil supplements. Laugharne JD et al: Fatty acids and schizophrenia. Lipids 31 Suppl:S163-5, 1996.