OBJECTIVE: Early somatic developmental anomalies may be one expression of a genetic influence toward psychosis. The purpose of this study was to investigate whether higher rates of early developmental anomalies are associated with heightened genetic risk for psychosis. METHOD: Rates of congenital malformations and minor structural developmental anomalies were prospectively investigated in 84 high-risk offspring of women with histories of psychosis of nonorganic origin (schizophrenic, schizoaffective, affective, and other psychoses) and in 100 offspring of demographically similar control women with no history of psychosis. Data were collected by means of multiple physical examinations through the first 3-4 years of the offspring's lives. RESULTS: The rates of total congenital malformations were high, but the great majority of these malformations in both the index group and the control group represented minor physical aberrations. Rates of congenital malformations in the offspring of the index women (or any specific diagnostic subgroup of these women) were not different from those in the offspring of the control women. CONCLUSIONS: The inferred genetic risk for psychosis does not appear to be associated with greater rates of early somatic developmental anomalies, suggesting that early developmental anomalies do not represent an expression of genetic influence toward psychosis.
OBJECTIVE: Early somatic developmental anomalies may be one expression of a genetic influence toward psychosis. The purpose of this study was to investigate whether higher rates of early developmental anomalies are associated with heightened genetic risk for psychosis. METHOD: Rates of congenital malformations and minor structural developmental anomalies were prospectively investigated in 84 high-risk offspring of women with histories of psychosis of nonorganic origin (schizophrenic, schizoaffective, affective, and other psychoses) and in 100 offspring of demographically similar control women with no history of psychosis. Data were collected by means of multiple physical examinations through the first 3-4 years of the offspring's lives. RESULTS: The rates of total congenital malformations were high, but the great majority of these malformations in both the index group and the control group represented minor physical aberrations. Rates of congenital malformations in the offspring of the index women (or any specific diagnostic subgroup of these women) were not different from those in the offspring of the control women. CONCLUSIONS: The inferred genetic risk for psychosis does not appear to be associated with greater rates of early somatic developmental anomalies, suggesting that early developmental anomalies do not represent an expression of genetic influence toward psychosis.