Genetic Contributions to Intergroup Responses: A Cautionary Perspective

Abstract

We live in an era where genomic informa-tion can be collected with the ease of a saliva sample and the cost of genotyping is plummeting (Hirschhorn and Daly, 2005; Quinque et al., 2006 ). Intergroup research-ers interested in incorporating biologi-cal approaches into their methodological toolbox are thus faced with the question of whether molecular genetics can provide novel insight into their understanding of people’s responses to members of other groups. In the current commentary, we stitch together human and animal neuro-science with insight from molecular biology to posit mechanisms through which genetic variation and life experience may give rise to responses during intergroup situations. We then discuss avenues for empirical inves-tigation and urge for responsible research practices that take into consideration the negative societal consequences that can result from overinterpreting genetic data.Intergroup phenomena, such as dis-crimination and ethnic violence, emerge at the interindividual level, and as a result, cannot be fully explained by intrapsychic processes. However, in order to understand the effects of intergroup influences on the individual, it is useful to examine the pro-cesses unfolding in the person’s mind and brain. For this reason, researchers have increasingly combined experimental social psychology and neuroimaging techniques to dissect the neural basis of affective and cognitive mechanisms that contribute to intergroup responses. This approach has revealed many interconnected, but disso-ciable, brain regions involved in perceiving, evaluating, and regulating behaviors toward other people, including the amygdala, fusi-form gyrus, anterior cingulate cortex, and various parts of the prefrontal cortex. For comprehensive reviews of the existing neu-roscience research pertaining to intergroup relations we direct readers to Amodio and Ratner (2011) , Cunningham and Van Bavel (2009), Ito and Bartholow (2009), and Kubota et al. (2012).To understand how these neuroimag-ing findings might relate to genetics, it is important to recognize that communica-tion between neurons is facilitated by neu-rochemicals, such as neurotransmitters (e.g., serotonin, dopamine), neurotrophic factors (e.g., BDNF), and hormones (e.g., cortisol, testosterone, and oxytocin). The enzymes that synthesize these molecules, the receptors to which they bind, and the reuptake mechanisms and enzymes that determine their availability are all pro-teins that are coded for by genes (Way and Gurbaxani, 2008). Thus, the cellular and molecular levels of analysis, although not currently considered by most intergroup researchers, have the potential to provide unique insight into how genetic variation might influence intergroup responses.Genes are biologically meaningful seg-ments of DNA ( Snyder and Gerstein, 2003 ). Each gene consists of a sequence of nucleo-tides. Frequent variations in the ordering, number, type, and repetition of nucleotides are called polymorphisms. A single gene can have many different types of polymor -phisms (den Dunnen and Antonarakis, 2001; Gibson and Muse, 2002). In order for polymorphisms to influence cellular functioning, their genetic code has to be transcribed into RNA and this RNA needs to be translated into amino acids. The type of amino acids that are produced and their configuration determine the form of the resultant proteins (e.g., enzymes, receptors; Crick, 1958).Gene expression occurs when bio-chemical processes within a cell stimulate transcription factors that bind to particu-lar DNA motifs (i.e., specified nucleotide sequences) in the promoter region of a gene. Extracellular events can control genomic responses through receptor-mediated chan-nels (Cole, 2009). Relevant to the present concerns, social stressors, such as interact-ing with unknown outgroup members, have been shown to elevate levels of the hormone cortisol (Page-Gould et al., 2008; Amodio, 2009). Other research indicates that cor-tisol binds to corticosteroid receptors and then the bound receptors translocate to the nucleus and act as transcription factors. One effect is that they bind to sites in the promoter of the serotonin transporter gene to trigger the synthesis of proteins that con-trol the reuptake of extracellular serotonin. The availability of serotonin has impor-tant effects on an individual’s emotional responses and also indirectly contributes to serotonin regulation by influencing hypo-thalamic–pituitary–adrenal (HPA) path-ways that release cortisol ( Glatz et al., 2003; Heisler et al., 2007; Way and Gurbaxani, 2008). Thus, at the level of gene expression there is a bidirectional relationship between the genetic code and the environment.The expression of a gene can also be influenced by epigenetic factors, such as DNA methylation and histone modification (Goldberg et al., 2007). DNA methylation occurs when a methyl group attaches to the promoter region and blocks DNA transcrip-tion. Environmental factors (e.g., stress) can increase DNA methylation, and thus have long-term effects on gene expression. Research in rodents has shown that DNA methylation can persist through the repro-ductive process, and as a result, can influence