The effects of life experiences and polygenic risk for depression on the development of positive and negative cognitive biases across adolescence: The CogBIAS hypothesis.

The Cognitive Bias (CogBIAS) hypothesis proposes that cognitive biases develop as a function of environmental influences (which determine the valence of biases) and the genetic susceptibility to those influences (which determines the potency of biases). The current study employed a longitudinal, polygenic-by-environment approach to examine the CogBIAS hypothesis. To this end, measures of life experiences and polygenic scores for depression were used to assess the development of memory and interpretation biases in a three-wave sample of adolescents (12-16 years) (N = 337). Using mixed effects modeling, three patterns were revealed. First, positive life experiences (PLEs) were found to diminish negative and enhance positive forms of memory and social interpretation biases. Second, and against expectation, negative life experiences and depression polygenic scores were not associated with any cognitive outcomes, upon adjusting for psychopathology. Finally, and most importantly, the interaction between high polygenic risk and greater PLEs was associated with a stronger positive interpretation bias for social situations. These results provide the first line of polygenic evidence in support of the CogBIAS hypothesis, but also extend this hypothesis by highlighting positive genetic and nuanced environmental influences on the development of cognitive biases across adolescence.

Gene-environment interaction and psychiatric disorders: Review and future directions.

Empirical studies suggest that psychiatric disorders result from a complex interplay between genetic and environmental factors. Most evidence for such gene-environment interaction (GxE) is based on single candidate gene studies conducted from a Diathesis-Stress perspective. Recognizing the short-comings of candidate gene studies, GxE research has begun to focus on genome-wide and polygenic approaches as well as drawing on different theoretical concepts underlying GxE, such as Differential Susceptibility. After reviewing evidence from candidate GxE studies and presenting alternative theoretical frameworks underpinning GxE research, more recent approaches and findings from whole genome approaches are presented. Finally, we suggest how future GxE studies may unpick the complex interplay between genes and environments in psychiatric disorders.