Gene–environment correlations: a review of the evidence and implications for prevention of mental illness

Abstract

Family studies have demonstrated genetic influences on environmental exposure: the phenomenon of gene-environment correlation (rGE). A few molecular genetic studies have confirmed the results, but the identification of rGE in studies that measure genes and environments faces several challenges. Using examples from studies in psychology and psychiatry, we integrate the behavioral and molecular genetic literatures on rGE, describe challenges in identifying rGE and discuss the implications of molecular genetic findings of rGE for future research on gene-environment interplay and for attempts to prevent disease by reducing environmental risk exposure. Genes affect environments indirectly, via behavior and personality characteristics. Associations between individual genetic variants and behaviors are typically small in magnitude, and downstream effects on environmental risk are further attenuated by behavioral mediation. Genotype-environment associations are most likely to be detected when the environment is behaviorally modifiable and highly specified and a plausible mechanism links gene and behavior. rGEs play an important causal role in psychiatric illness. Although research efforts should concentrate on elucidating the genetic underpinnings of behavior rather than the environment itself, the identification of rGE may suggest targets for environmental intervention even in highly heritable disease. Prevention efforts must address the possibility of confounding between rGE and gene-environment interaction (G Â E).

Early childhood adversity and adolescent depression: the mediating role of continued stress

“…The current study complements these findings by demonstrating stress continuity prospectively over 15 years, using a wide range of non-traumatic early stressors and interviewer-based measures of chronic and episodic stress in adolescence. The current study design could not specify mechanisms of the continuity due to its circumscribed measurement periods, but it likely arises from reciprocal and cascading interactions between environmental factors, childhood symptoms and genetic factors that are the subject of increasing study (Jaffee & Price, 2007). Continued study of these processes incorporating more tightly spaced data collection times (see Cole et al 2006) and genetic data will prove valuable for better understanding the processes by which stressful circumstances are propagated across childhood and adolescence.…”

The genetic and environmental influences on childhood obesity: a systematic review of twin and adoption studies

“…Geneenvironment correlation can be because of a passive, active or reactive correlation. 64 In obesity, passive gene-environment correlation would be created, for example, if obese parents transfer not only their genes predisposing to obesity but also the role model to their children. Active gene-environment correlation would mean that those persons with genetic predisposition to obesity would actively seek an environment that increases obesity.…”

Evidence of a unique and common genetic etiology between the CAR and the remaining part of the diurnal cycle: A study of 14 year-old twins

“…Similar findings are also emerging in regards to peer victimization in adolescence (Ouellet-Morin et al, 2011a;Ouellet-Morin et al, 2011b;Vaillancourt et al, 2008), reflecting the sensitive nature of HPA axis activity to changing social environments. It remains unclear, however, to which extent these associations reflect acquired and/or inherited influences, as some experiences may partly arise as a function of the individuals' genetic makeup (Jaffee and Price, 2007). Delineating the etiology of cortisol circadian rhythm represents a key building block to ascertain its impact on health.…”