Numerous findings over the last decade have led to wide acceptance that, for most traits, the effects of individual genes are too small to stand out against the combined influence of all other genes and environmental factors (e.g., Hill et al 2008; Visscher 2008). Thus, our p-value of 0.02 on a sample of 2000 individuals should be treated cautiously. The expectation in genetics is that only repeated efforts to replicate associations will verify initial findings like these. Thus, perhaps the most valuable contribution of this study is not to declare that “a gene was found” for anything, but rather, to provide the first evidence for a possible gene-environment interaction for political ideology.
Many large-scale analyses of political behaviors ignore the potential for genetic effects. Of those that do not, few offer a model which builds a hypothesis based on social and cultural influences that interact with a specific neurotransmitter that is regulated by a specific genetic marker (for an exception see Hatemi 2008
). It is our hope that more scholars will begin to explore the potential interaction of biology and environment, thus leading to the development of consortiums for social and political traits that will allow for the replication or combination of findings across samples.
Given these cautions, we reiterate the main results of our investigation. Using a family-based genetic association study, we find that political ideology in early adulthood is significantly associated with an interaction between a gene previously linked to novelty-seeking behavior (DRD4-7R), and an environmental influence, the number of adolescent friendships. We do not claim that this evidence proves a causal relationship between DRD4 and political ideology. However, the association is consistent with a causal theory that we develop about the way genes and environments combine to affect political ideology.
It is important to note that the 7R allele by itself does not make a person liberal and neither does simply having a greater number of friends as a teenager. Additionally, the 7R allele does not cause an individual to have more friends (see the Appendix
), and twin studies have shown that the number of friends one names is not significantly heritable (Fowler, Dawes, Christakis 2009
). Rather, it is the crucial interaction of two factors—the genetic predisposition of having a greater number of 7R alleles and the environmental condition of having many friends in adolescence—that is associated with being more liberal.
Geneticists are sometimes skeptical of associations where an interaction effect exists and a main effect does not. The reason for this skepticism is a concern with the potential to produce false positive results. If we were testing 100 genes and 100 environmental factors, there would be 10,000 possible interactions, and many of these would yield significant results. However, in our case, the Add Health data contains only five genes, greatly reducing the number of possible interactions one could test. This does not necessarily reduce the possibility of false positive for a given test, but does offer protection from unreported multiple testing. Political scientists also typically guard against false positives by requiring ex-ante theorizing. In our case, we were only interested in DRD4 for political ideology because of its association with novelty-seeking behavior, and we developed an explicit theory that suggests the interaction between DRD4 and friendships—and not the main effects—would be significant. Since our test was not able to contradict the theory, the way forward is to seek replication in different populations and age groups.
While our finding is statistically significant, the strength of the association is quite small. However, even in a biometric trait such as height, less than 15% of the variation has been attributed to specific genes. Genetic effects take place in complex interaction with other genes and environments, and it is likely the combination of hundreds if not thousands of genes interacting with each other and with external stimuli that influence political attitudes and behavior.
There are several factors that would be instrumental for future replication studies. There is no measure in the Add Health data that has been validated against typical measures of novelty-seeking; the questions that are conceptually related in the survey are inappropriate for comparison to other studies which include the behavioral trait in the analysis. If we did have such a measure, we could test the extent to which it accounts for the associations we observe here. Additionally, both number of friends nominated and ideology were single self-report measures. While we have good reason to believe that self-reported ideology is an accurate representation of a person’s true ideological beliefs (Lau and Redlawsk 1997
), we are using a standard, but very simple, measure that may not fully capture the breadth and depth of a person’s ideological beliefs. Finally, past work suggests that political sophistication plays an important role in the manifestation of ideology (Converse 1964
; Sniderman et al. 1993
), but we cannot address the role that political sophistication might play in our results because there were no reliable measures in Add Health. All of these limitations suggest that we should develop datasets that include genes, psychological questions to create valid constructs, and political data.
In light of these and other findings, political scientists can no longer afford to view ideology as a strictly social construct, perfectly malleable and completely subject to historically-changing circumstances. As Jost et al. (2003)
suggest, there appears to be both a stable definitional core and changing peripheral associations involved in a conservative political ideology. Our work builds upon this growing literature in psychology and genetics by offering a genetic basis for the link between motivated social cognition and ideology.
Finally, the results here suggest that, contrary to Mannheim’s assertion and the body of work that followed him, the social and institutional environment cannot entirely explain a person’s political attitudes and beliefs. We must take into account the role of genes and gene-environment interactions in the formation and maintenance of political beliefs. Our findings do not undermine the rich body of literature that has developed regarding the environmental influences that shape political behavior. Rather, we hope to complement prior work and seek to show how incorporating a role for specific genes into our models of political behavior can enrich our understanding of the origin and nature of these behaviors. Political scientists have a wealth of material from which to form hypotheses about potential gene-environment interactions that influence deeply held political ideas and values.