Reduced membrane EFA in schizophrenia Abnormal membrane GPL EFA metabolism has been suggested to contribute to the aetiopathophysiology of schizophrenia. A recent review of 15 published studies confirmed a depletion of bioactive lipids in cell membranes of patients with schizophrenia (Fenton et al., 2000). The most consistent findings were reductions in AA and its precursors, and these were independent of drug treatment (Yao et al., 1996). Reductions in AA and its precursors have also been found in post mortem brains of patients with schizophrenia, relative to normal control brains [Yao et al., 2000]. Yao and van Kammen (1996) suggested that defective uptake of AA into membrane GPL was a possible aetiopathological mechanism in schizophrenia, whereas Peet et al. (1996), who reported an additional increase of EFA peroxidation products, suggested there was increased breakdown of membrane GPL.