Although there have been studies that have shown the importance of dietary essential fatty acids (EFAs) for healthy neurodevelopment (Crawford, 1993), until recently there had been no studies of infant feeding practices in relation to subsequent schizophrenia. It has been shown that the children of women pregnant during the Dutch famine (19441945) were significantly more likely to develop schizophrenia in later life (Susser & Lin, 1992). Although these women suffered multiple dietary deficiencies and not just PUFA, it is known that during early development infants require healthy amounts of AA and DHA to maintain normal brain development (Rogers, 1978; Rogan & Gladen 1993; Lucas et al., 1992). What the Dutch data do demonstrate is that dietary impairment in utero, presumably by affecting neurodevelopment of the fetus, can have substantial effects in adulthood. Two initial studies of breast feeding in schizophrenia, one by our group and one in Scotland (McCreadie, 1997), produced consistent results. Our study (Peet et al., 1999) used a case-control methodology and the Scottish study compared patients with controls from the general population. Both studies showed that patients who developed schizophrenia were less likely to have been breast-fed as infants. This is consistent with a protective effect of breast-feeding resulting from a better balance of PUFAs, particularly DHA and AA, which were historically lacking in formula feeds. It was suggested that a genetic predisposition to abnormal PUFA metabolism may be modulated by diet in infancy, leading to impaired neurodevelopment and subsequent schizophrenia. However, there are two recent negative studies (Sasaki et al., 2000; Leask et al., 2000) and the issue is unresolved.
In adults with established schizophrenia, two studies suggest that increased consumption of PUFA, and particularly of n-3 PUFAs, is beneficial to the short-term symptoms and longer-term outcome of schizophrenia. It is well recognized that the long-term outcome of schizophrenia is better in undeveloped nations than it is in the West. The reasons for this are unclear, but Christensen and Christensen (1988) made a detailed analysis of World Health Organization data on prevalence and outcome in schizophrenia around the world. They correlated these data with that relating to the national diet and found that a high intake of total fat and saturated fat from land animals and birds and a relatively low intake of PUFAs was significantly associated with an unfavourable outcome of schizophrenia.
Our group conducted a detailed analysis of dietary fatty acid intake in 20 patients hospitalized with chronic schizophrenia (Mellor et al., 1996). All of these patients were receiving optimal dosages of neuroleptic medication but still suffered from schizophrenic symptoms. The normal dietary intake of each patient was assessed over 7 d using weighed intake for set meals and food diaries to record snacks at other times. The dietary data were analyzed with the use of the FOODBASE program (Institute of Brain Chemistry and Human Nutrition, London); this program gives a full fatty acid analysis. Schizophrenic symptomatology was rated using the Positive and Negative Syndrome Scale (PANSS) (Kay et al., 1987) and tardive dyskinesia was rated using the Abnormal Involuntary Movement Scale (AIMS) (Kane et al., 1992). The relationship between dietary fatty acid intake and symptomatology was examined using Pearson's correlation coefficients, followed by multiple regression analysis. The strongest correlation (r = -0.55, p = 0.01) was between total n-3 fatty acids in the normal diet and severity of positive symptoms. Thus, the greater the dietary intake of n-3 PUFA, the less severe are the positive schizophrenic symptoms. Within the individual n-3 PUFA, EPA showed a significant negative correlation with both total PANSS score and severity of tardive dyskinsia. Multiple regression analysis confirmed that it was the n-3 fatty acids and particularly EPA that contributed most to the variance in schizophrenic symptoms and tardive dyskinesia. All relationships were negative, so that a greater dietary intake of total n-3 PUFA related to fewer schizophrenic symptoms.
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