Dietary fatty acid and antioxidant intake in community-dwelling patients suffering from schizophrenia.

INTRODUCTION

Brain phospholipids are uniquely rich in polyunsaturated fatty acids (PUFAs). Most PUFAs such as alpha-linolenic acid 18:3(n-3), eicosapentaenoic acid 20:5(n-3), and docosahexaenoic acid 22:6(n-3) are essential and must be provided through the diet. PUFAs are also very sensitive to oxidative stress. Decreased essential fatty acid content has been observed in cell membranes of various tissue types of schizophrenia patients, including neural cell membranes. A number of mechanisms may account for these deficits, such as inadequate dietary supply or increased oxidation. It is known that patients with schizophrenia make poor dietary choices. However, whether their dietary fatty acid or antioxidant intake is insufficient and contributes to the observed deficiencies has not been assessed.

METHODS

After obtaining informed consent, a 24-h diet recall was administered to elicit nutritional information in 146 outpatients with schizophrenia. Intake of fatty acids and antioxidants including vitamins A, C, and E was compared to U.S. population standards according to the National Health and Nutrition Examination Survey Cycle III (NHANES III) results.

RESULTS

Saturated and polyunsaturated fatty acid (PUFA) intake was significantly higher in schizophrenia patients than in controls (p<or=0.05; p<or=0.005, respectively). No differences were found with regard to dietary intake of gamma-linolenic acid (18:3n-3), eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3). Similarly, antioxidant intake was not different between schizophrenia patients and controls.

CONCLUSION

The observed cell membrane deficits in PUFA and essential fatty acid content do not appear to derive from decreased dietary supply. Rather, intrinsic membrane phospholipid metabolism abnormalities may be causative. Overall increased fat intake in schizophrenia patients may contribute to the development of serious medical comorbidities, and further advance the risk for cumbersome metabolic side effects of antipsychotic treatment such as new-onset diabetes mellitus.