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Given the result of the recent US presidential election, minority groups worldwide are understandably worried about the future. Already social media platforms are awash with reports of emboldened bigots verbally, and in some disturbing cases, physically assaulting people of color, Muslims, and members of the LGBTQI+ community (though see update).
But where does this animosity come from? A popular adage is that racists are not born but rather they are made, and while this message is ultimately a hopeful one, it ignores a substantial portion of the story: that of biology. As I discuss in the Cambridge Handbook of the Psychology of Prejudice, there are multiple lines of evidence pointing to a genetic basis for prejudicial attitudes and behavior and if we hope to reduce net prejudice, understanding this is of critical importance.
The primary source of this evidence comes from the field of behavioral genetics. This endeavor relies on the natural experiment provided by contrasting identical and non-identical twin pairs. Where identical twins share all of their parents’ segregating genes (i.e. are 100% genetically identical), non-identical twins on average share only half of these genes. Based on this knowledge, one can assume that a trait shared more strongly by identical twins than non-identical twins is influenced by genes. If, however, identical and non-identical twin pairs are equally similar then presumably the environment the twins share has had an influence on the trait[1].
Combining this relatively simple premise with complex mathematical modeling yields researchers incredible power to dissect variation (i.e. differences between individuals) into that caused by genetic effects, the environment shared by twins (e.g. their household and religious and political up-bringing), and finally, variation caused by individual experiences, chance biological effects, and any error in measurement of the trait.
For instance, 30 years of research using the twin method has revealed that genes account for between 20 and 40% of the variation in political orientation (as I’ve covered previously). Similarly, twin studies have revealed substantial genetic effects on prejudicial attitudes.
One study from 1986 observed that identical twins were more similar in their attitudes towards white superiority, apartheid and mixed marriage than non-identical twins. Further modeling revealed that between 30 and 40% of variation in these attitudes was due to genes. Surprisingly, the shared environment of the twins, which includes shared aspects of the family household, accounted for less than 15% of variation in the same attitudes[2].
A more recent study including attitudes to equal rights for gays and women found that a third of the variation support for these ideas was due to genetic effects[3]. From ethnocentrism (18%)[4], negative attitudes to non-Europeans (32%)[5], generalized prejudice (38%) [6] and in-group favoritism (i.e. preferring one’s own religious, political or ethnic group: 46%)[7], twin data has consistently shown strong genetic effects influencing bigoted attitudes, generally with small influences of the home environment.
This seems counter-intuitive: how can genes influence acquired attitudes while shared environmental influences are small?
It’s important to understand that genes aren’t coding for specific attitudes: there is no gene for racism. What these results indicate is that genes are contributing to behavioral and psychological dispositions to regard out-group members, such as those that are ethnically or culturally different, negatively. Whether these genes are different for different types of out-groups, such as those of a different sexuality vs. those of a different religion, remains to be seen, though it seems likely that most prejudices stem from a similar mechanism, one that fosters fear and suspicion of out-group members. Despite these genetic influences, the specific attitudes (i.e. “immigrants get more than they deserve from the government”) are almost certainly derived from the environment, with genes influencing the degree to which they are endorsed. Consequently, in an environment densely populated with bigoted rhetoric (such as many experienced during the recent election campaign) individuals with a genetic predisposition to out-group hostility may find themselves more readily espousing prejudicial attitudes.
This is ultimately mixed news: unfortunately, it means that more heritable attitudes are more firmly entrenched[8] but by observing the changes in prejudice over time, it is clear that the specific types and strengths of prejudice within a society are open to change. Key to this is the understanding that heritability refers only to causes of variation, and says nothing about the average level of the trait itself. Take intelligence as an example: intelligence is highly heritable (~85%), yet since IQ testing began, psychologists have consistently observed generational increases in the average intelligence of the population, referred to as the Flynn Effect. The causes of these increases are largely unknown but could be attributed to better nutrition, more widely accessible education, or a lower burden of disease. Regardless of the cause, the heritability of intelligence has not changed for the most part, while the average IQ has continued to shift upwards.
The same is possible for prejudice. While genes may maintain some variation in how strongly prejudice is endorsed, overall prejudice within society can be reduced: a rising tide lifts all boats. Even across the few studies mentioned above, it is apparent that the focus of prejudice rapidly shifts from racism (i.e. issues of segregation) to those concerning gay rights within the space of 20 years.
However, it is incredibly important to consider these genetic effects when attempting to understand and intervene in prejudice. Multiple studies have shown that the family environment contributes relatively little to the maintenance of prejudicial attitudes over and above genes—likely racism tends to cluster within families because of shared genes. As a result, social interventions should be tailored, taking into account the fact that genetic variation may mitigate their effectiveness for certain individuals.
Humans have made great strides in overcoming the burden of prejudice but it is often a lack of understanding that keeps us from truly succeeding: We can no more assume that all individuals are equally prone to bigotry based on their environment than we can assume that one’s genes entirely determine their future. Rather, to resolve complex social issues requires a nuanced understanding of the interaction between biology and behavior, one that starts at the level of a single gene and extends to the entirety of modern culture. In the uncertain days to come it will be crucial to bear this in mind.
References
1. Neale, M.C. and L.C. Cardon, Methodology for genetic studies of twins and families. 1992, Kluwer, Boston: Kluwer Academic Publishers.
2. Martin, N.G., et al., Transmission of social attitudes. Proceedings of the National Academy of Sciences of the United States of America, 1986. 83(12): p. 4364-4368.
3. Alford, J., C. Funk, and J. Hibbing, Are Political Orientations Genetically Transmitted?, J. Alford, Editor. 2005. p. 153-167.
4. Orey, B.D. and H. Park, Nature, nurture, and ethnocentrism in the Minnesota Twin Study. Twin Research and Human Genetics, 2012. 15(01): p. 71-73.
5. Kandler, C., et al., The genetic and environmental roots of variance in negativity toward foreign nationals. Behavior Genetics, 2015. 45(2): p. 181-199.
6. Lewis, G.J., C. Kandler, and R. Riemann, Distinct heritable influences underpin in-group love and out-group derogation. Social Psychological and Personality Science, 2014. 5(4): p. 407-413.
7. Lewis, G.J. and T.C. Bates, Common heritable effects underpin concerns over norm maintenance and in‐group favoritism: Evidence from genetic analyses of right‐wing authoritarianism and traditionalism. Journal of Personality, 2014. 82(4): p. 297-309.
8. Bourgeois, M.J., Heritability of attitudes constrains dynamic social impact. Personality and Social Psychology Bulletin, 2002. 28(8): p. 1063-1072.
