Recently, a membrane phospholipid hypothesis of schizophrenia has been proposed1 that not only provides an underlying explanation for those aspects of schizophrenia traditionally explained by the dopamine hypothesis, but also can account for many other clinical features. These include the inverse relationship between schizophrenia and some inflammatory disorders; the high resistance to pain shown by some patients; the dramatic remission of symptoms that may occur with pyrexia; the increased risk associated with exposure to viral infections or maternal malnutrition during fetal development; and the difference in severity and prognosis in different countries.2 Recent biochemical, cerebral magnetic resonance spectroscopy, and molecular genetics findings suggest that schizophrenia is associated with a cell membrane deficiency of arachidonic acid and docosahexaenoic acid (DHA), arising from excess activity of 1 of the phospholipase A2 (PLA2) group of enzymes.3-7 Thus, there is mounting evidence for the membrane phospholipid hypothesis; however, an important issue for clinicians is whether it has any useful implications for treatment.
Puri BK, Richardson AJ. Sustained Remission of Positive and Negative Symptoms of Schizophrenia Following Treatment With Eicosapentaenoic Acid. Arch Gen Psychiatry. 1998;55(2):188–189. doi:
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