Schizophrenia: A critical view on genetic effects

Abstract

The main justification for molecular genetics studies of enduring psychosis (schizophrenia) are high heritability estimates obtained from classical twin studies. The classical twin method rests upon the equal environment assumption (EEA), which holds that reared-together identical and fraternal twin pairs grow up experiencing equally similar environmental exposures. However, a review of prior twin studies shows that identical twins are more similar than fraternal twins on childhood exposures that are central to the etiology of psychosis. Such exposures include bullying, sexual abuse, physical maltreatment, emotional neglect and abuse, and general trauma. An additional assumption presented by twin researchers, that the differential intraclass correlation for child social adversities can be explained by evocative gene–environment covariation, is not consistent with the available evidence. Moreover, due to an array of methodological problems and questionable assumptions, adoption studies provide misleading indications in support of genetic effects. As a result, direct studies of DNA variations in schizophrenia must stand on their own ground. Possible minor findings from such molecular genetics studies, when combined with the available evidence of environmental effects, support a stress-based sociopsychobiological model of schizophrenia etiology.