Children with a genetic predisposition to schizophrenia appear to be more sensitive to environmental influences--including parental communication patterns--than children who do not have a genetic predisposition.

Moreover, that heightened sensitivity makes the genetically predisposed child more "reactive" to both protective and predisposing environmental influences, according to findings from the Finnish Adoptive Family Study of Schizophrenia reported by Karl-Erik Wahlberg, Ph.D., of the University of Oulu, Finland, and colleagues.

The study appears in this month's American Journal of Psychiatry.

Lyman Wynne, M.D., of the department of psychiatry at the University of Rochester and one of the coauthors of the report, told Psychiatric News that the study especially supports the concept of "genetic control of sensitivity to the environment."

That is, individuals with a genetic predisposition are more prone to influences from the environment, regardless of whether those influences are healthy or unhealthy, he said.

The investigators compared 58 adoptees who had biological mothers with schizophrenia (and who were thus presumed to have a higher genetic risk for psychosis) with 96 adoptees at ordinary genetic risk.

Using a measure of "communication deviance" to assess communication patterns between children and adoptive parents, the investigators found that greater communication deviance among adoptive parents was not associated with greater thought disorder among the comparison adopted children, who had no increased genetic risk.

So communication deviance alone cannot be linked to thought disturbance, Wynne explained.

However, there was a strong interactive effect between genetic predisposition and communication deviance at both extremes, he noted.

For instance, evidence of thought disorder was significantly more common among adoptees at high genetic risk who were reared by parents with high communication deviance levels than among low-risk comparison adoptees reared by parents with equally high levels of communication deviance.

Meanwhile, adoptees at high genetic risk who were reared by parents with low communication deviance levels were actually less likely to have thought disorder than were low-risk adoptees reared by parents with low communication deviance levels.

What this suggests, Wynne said, is that the high-risk children are more sensitive to extremes in the environment, whether those factors are healthy or dysfunctional.

Moreover, the "extremes" do not have to be very extreme, Wynne said: the levels of communication deviance, whether low or high, were actually within the range of the patterns found among normal families.

He emphasized that in no way can parents be blamed for communication patterns that may be associated with thought disorder among high-risk children.

Rather, he said, the findings support the idea that the child who is genetically at risk for schizophrenia is more "reactive"--more easily influenced--by a host of environmental factors, including those that are well within the range of normal.

Wynne and colleagues cite a model of gene-environment interaction first put forward by Kenneth Kendler, M.D., and L.J. Eaves in the American Journal of Psychiatry (1986) to explain what they hypothesize is happening between children with a genetic predisposition and their parents.

"In this model," Wynne and colleagues write, "genes control the degree to which the individual is sensitive to predisposing, risk-increasing aspects of the environment or to the protective, risk-reducing aspects of the environment. Kendler and Eaves proposed that 'insensitive' (relatively invulnerable) genotypes would have relatively flat slopes in the change in liability to illness from protective to predisposing environments. In contrast, 'sensitive' (relatively vulnerable) genotypes would show a steeper slope, with a greater increase in liability in the predisposing environment and a greater decrease in liability in the protective environment."

(Psychiatric News, April 4, 1997)