Mind the gap: why many geneticists and psychological scientists have discrepant views about gene-environment interaction (G×E) research

Abstract

As our field seeks to elucidate the biopsychosocial etiologies of mental health disorders, many traditional psychological and social science researchers have added, or plan to add, genetic components to their programs of research. An understanding of the history, methods, and perspectives of the psychiatric genetics community is useful in this pursuit. In this article we provide a brief overview of psychiatric genetic methods and findings. This overview lays the groundwork for a more thorough review of gene-environment interaction (G×E) research and the candidate gene approach to G×E research that remains popular among many psychologists and social scientists. We describe the differences in perspective between psychiatric geneticists and psychological scientists that have contributed to a growing divide between the research cited and conducted by these two related disciplines. Finally, we outline a strategy for the future of research on gene-environment interactions that capitalizes on the relative strengths of each discipline. (PsycINFO Database Record (c) 2014 APA, all rights reserved).

Figure 1

Hypothetical Example in Which the Number of PTSD Symptoms Is Influenced by an Interaction Between Genotype and Severity of Trauma Exposure Note. Genotype is represented by a genetic variant with two alleles, A and G, yielding three genotypes: GG, GA, and AA. Note that this simplified example refers to a single genotype that interacts with an environmental variable. In reality there are likely many interactions—each with small effects. PTSD = posttraumatic stress disorder.

Figure 2

Histogram of cG×E Studies Published by Year for the First Decade of cG×E Research in Psychiatry Note. Gray and white portions of the bars depict replication attempts of Caspi et al., 2002, and Caspi et al., 2003, respectively, the two most commonly studied candidate gene–environment interactions (cG×Es). 5-HTTLPR = serotonin transporter linked polymorphic region; MAOA = monoamine oxidase A.

Figure 3

Phenotypic, Genotypic, and Environmental Variables Studied Most Often in cG×E Studies Note. cG×E = candidate gene–environment interaction; ADHD = attention-deficit/hyperactivity disorder; PTSD = posttraumatic stress disorder. From “Gene–Environment Interactions in Behavioral Genetics” by L. E. Duncan, 2014, in S. H. Rhee & A. Ronald (Eds.), Behavior Genetics of Psychopathology (p. 267), New York, NY: Springer. Copyright 2014 by Springer Science&Business Media New York. Adapted with permission.

Figure 4

Graphical Depiction of Sample Sizes and Percentages of Each Sample That Are Male and Female for All 103 Samples From the First Decade of cG×E Research in Psychiatry Note. Each column represents one study, and column width is proportional to study N. Samples (columns) are ordered according to decreasing female:male sex ratio for ease of interpretation. cG×E = candidate gene–environment interaction.

Figure 5

Graphical Depiction of Sample Sizes and Racial/Ethnic Composition (for All Studies That Reported It) in the First Decade of cG×E Research in Psychiatry Note. Each column represents one study, and column width is proportional to study N. Samples (columns) are ordered according to majority ethnicity for ease of interpretation. cG×E = candidate gene–environment interaction.