MedWire News: Maternal depression during pregnancy may additionally increase the risk for schizophrenia in offspring with a family history of psychosis, research suggests.

There was not an increased risk in offspring without a family history of psychosis, however.

“This finding is an example of a gene–environment or gene–gene interaction in the development of schizophrenia,” say Pirjo Mäki (University of Oulu, Finland) and colleagues.

Family psychosis would be considered a genetic factor and maternal depression an environmental risk factor, they explain. Alternatively, it could be that the increased risk for schizophrenia in individuals born to depressed mothers may be a psychosis gene–depression gene interaction.

At mid-gestation, the mothers of 12,058 children born in Northern Finland in 1966 were asked if they felt depressed. The children were then followed-up for over 30 years for subsequent schizophrenia and other psychoses. The familial risk for psychosis was also determined using the Finnish Hospital Discharge Register.

Children born to mothers who were depressed during pregnancy and had a parent with psychosis were 9.4 times more likely to develop schizophrenia than children born to mothers without depression and no parental history of psychosis.

This increased risk was greater than that for children born to mothers with antenatal depression but no parental history of psychosis and for those born to mothers without antenatal depression but a parental history of psychosis, at odds ratios of 1.0 and 2.6, respectively.

The combination of having a father with psychosis and an antenatally depressed mother resulted in the highest risk for schizophrenia, with an odds ratio of 14.2.

The researchers note in the American Journal of Psychiatry that they did not have information on the fathers’ depression history and this major limitation makes it difficult to determine whether the interaction is a gene–environment or a gene–gene one.

They conclude: “Maternal depressed mood during pregnancy per se is unlikely to increase the risk for schizophrenia in the offspring but it may affect subjects with increased risk for psychosis.”

In a related editorial, John Gilmore, from University of North Carolina in Chapel Hill, USA, pointed out that following on from these findings of a gene–gene or gene–environment interaction, research now needs to focus on the developmental trajectories that these interactions contribute to.

“Only by focusing our research on understanding human development trajectories can we develop interventions that recognize and modify, either with pharmacologic or cognitive/behavioral approaches, abnormal developmental trajectories that lead to schizophrenia,” he said.

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