67 In addition, Ozer et al found that psychosis and rickets were inherited independently in their study of a multigenerational family overloaded with both disorders.68 Disordered folate metabolism has been suggested as a risk factor for later schizophrenia via effects on neurodevelopment, but again this has been little researched.69 The role of nutrition in Inhibitors,research,lifescience,medical early life on later development of psychosis is clearly an area that warrants further investigation, but is likely to be limited by the difficulties inherent in accurate measurement of nutritional status, and the role of confounding factors.

Childhood environment A number of environmental risk factors Inhibitors,research,lifescience,medical have been proposed to act during the intermediate period between the prenatal period and life immediately prior to illness onset; these include child-rearing experiences, head injury and possibly child abuse. The impact of these factors on an understanding of the etiology of schizophrenia has perhaps not been as great as the insights provided by the recognition of earlier and later life risks. In addition, it must be recognized that the environment during childhood is likely to be interacting with the social, behavioral, and cognitive antecedents of psychosis known to predate illness in vulnerable children.7 The impact of the child-rearing environment has been highlighted Inhibitors,research,lifescience,medical by results from an Israeli study,70

which examined the role of child rearing by comparing the effects of kibbutz versus family upbringing. The investigators concluded that kibbutz-rearing of high-risk children may increase their risk of developing a psychiatric disorder, though Inhibitors,research,lifescience,medical not Sotrastaurin supplier necessarily schizophrenia. Risk of later schizophrenia has also variously been found to be associated with atypical Inhibitors,research,lifescience,medical mother-infant interaction,71 early parental loss,72 and poor mothering.73 In the Dunedin

longitudinal birth cohort study, mothers of offspring later diagnosed with schizophreniform disorder were significantly more likely to have atypical mother-child interactions compared to controls (OR 2.65; CI 1.2-5.6).71 This was not true for mothers of offspring with other psychiatric disorders such as mania, anxiety or depression. In those adoptees already at high familial risk of schizophrenia, the quality of adoptive childhood rearing experiences has also been found to be heptaminol important.74 In a national Finnish sample, offspring of mothers with schizophrenia given up for adoption had, as expected, significantly higher proportions of both psychoses and other severe mental illness compared with a matched control sample of adoptees. Interestingly though, in this sample, the difference between high and low genetic propensity was only found among those with a disturbed adoptive family environment suggesting a gene-environment interaction.