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One of my interests is affective empathy, the involuntary desire not only to understand another person’s emotional state but also to make it one’s own—in short, to feel the pain and joy of other people. This mental trait has a heritability of 68% and is normally distributed along a bell curve within any one population (Chakrabarti and Baron-Cohen, 2013). Does it also vary statistically among human populations? This is possible. Different cultures give varying importance to affective empathy, and humans have adapted much more to their cultural environments than to their natural environments. This is why human genetic evolution accelerated over 100-fold about 10,000 years ago when humans began to abandon hunting and gathering for farming, which in turn led to increasingly diverse forms of social organization (Hawks et al., 2007).
I have argued previously that Europeans to the north and west of the Hajnal Line (an imaginary line running from Trieste to Saint-Petersburg) have adapted to a cultural environment of weaker kinship and, conversely, greater individualism. In such an environment, the reciprocal obligations of kinship are insufficient to ensure compliance with social rules. This isn’t a new situation. Weak kinship is inherent to the Western European Marriage Pattern, which goes back to at least the 12th century, if not earlier.
This cultural environment has selected for a package of mental adaptations:
- capacity to internalize punishment for disobedience of social rules (guilt proneness)
- capacity to simulate and then transfer to oneself the emotional states of people who may be affected by rule-breaking (affective empathy)
- desire to seek out and expel rule-breakers from the moral community (ideological intolerance).
The above mental package has enabled Northwest Europeans to free themselves from the limitations of kinship and organize their societies along other lines, notably the market economy, the modern State, and political ideology. They have thus managed to meet the threefold challenge of creating larger societies, ensuring greater compliance with social rules, and making possible a higher level of personal autonomy.
So much for the theory. What direct evidence do we have that affective empathy is stronger on average in Northwest Europeans? We know that a higher capacity for affective empathy is associated with a larger amygdala, which seems to control our response to facial expressions of fear and other signs of emotional distress (Marsh et al., 2014). Two studies, one American and one English, have found that “conservatives” tend to have a larger right amygdala (Kanai et al., 2011; Schreiber et al., 2013). In both cases, my hunch is that “conservatives” are disproportionately drawn from populations that have, on average, a higher capacity for affective empathy.
But testing this kind of hunch would require a large-scale comparative study, which in turn would require cutting up a lot of cadavers or doing a lot of MRIs. It would be nicer to have a genetic marker that shows up on a simple test. It would also be cheaper.
We may now have that marker: a deletion variant of the ADRA2bgene. Carriers remember emotionally arousing images more vividly and for a longer time, and they also show more activation of the amygdala when viewing such images (Todd and Anderson, 2009;Todd et al., 2015). This is not to say that the ADRA2b deletion variant is the sole reason or even the major reason why some people have increased capacity for affective empathy. As with intelligence, an increase in capacity seems to have come about through changes of small effect at many genes.
Nor can we say that “emotional memory” is equivalent to affective empathy. Instead, it seems to be one component, albeit a critical one: the capacity to imagine an emotional state based on visual information (a picture of a person’s face, a puppy dog, etc.) and then keep it as part of one’s current emotional experience. Emotional memory may be upstream to affective empathy, being perhaps closer to cognitive empathy—the ability to imagine how another person feels without involuntarily making that feeling one’s own.
Does its incidence differ among human populations?
This variant was first studied in the United States. Small et al. (2001) found a higher incidence in Caucasians (31%) than in African Americans (12%). Belfer et al. (2005) likewise found a higher incidence in Caucasians (37%) than in African Americans (21%).
In a press release, the authors of the latest study noted that this variant is not equally common in all humans:
The ADRA2b deletion variant appears in varying degrees across different ethnicities. Although roughly 50 per cent of the Caucasian population studied by these researchers in Canada carry the genetic variation, it has been found to be prevalent in other ethnicities. For example, one study found that just 10 per cent of Rwandans carried the ADRA2b gene variant. (UBC News, 2015)
Curiously, its incidence seems higher among “Canadian Caucasians” (50%) than among “American Caucasians” (31-37%). This may reflect differences in participant recruitment or in ethnic mix between the two countries. Indeed, the “Caucasian” category may prove to be problematic because it includes people from both sides of the Hajnal Line. If the average incidence is 31% to 50%, there may be populations that score much higher.
I have found only three studies on specific European ethnicities. The first study found an incidence of 50% in Swiss participants (de Quervain, 2007). The second one found an incidence of 56% in Dutch participants (Cousijn et al., 2010). The third one had two groups of participants: Israeli Holocaust survivors and a control group of European-born Israelis who had emigrated with their parents to the British Mandate of Palestine. The incidence was 48% in the Holocaust survivors and 63% in the controls (Fridman et al., 2012).
From East Asia, a study on Chinese participants reported an incidence of 68% (Zhang et al., 2005). This is surprising because Chinese seem less likely to distinguish between cognitive empathy and affective empathy (Siu and Shek,2005). Japanese participants had an incidence of 56% in one study (Suzuki et al., 2003) and 71% in another (Ishii et al., 2015). Among the Shors, a Turkic people of Siberia, the incidence was 73%. Curiously, the incidence was higher in men (79%) than in women (69%). It may be that male non-carriers had a higher death rate, since the incidence increased with age (Mulerova et al., 2015).
The picture is still incomplete but the incidence of the ADRA2bdeletion variant seems to range from a low of 10% in some sub-Saharan African groups to a high of 50-65% in some European groups and 55-75% in some East Asian groups. Given the high values for East Asians, I suspect this variant is not a marker for affective empathy per se but rather for empathy in general (cognitive and affective).
It may be significant that a high incidence was found among the Shors, who were largely hunter-gatherers until recent times. This suggests that empathy reached high levels in Eurasia long before the advent of complex societies, or even farming. The example of the Shors also suggests that non-carriers of the deletion variant suffer from higher mortality—a somewhat surprising finding, given the evidence that carriers have a higher risk of heart disease.
More research is needed on how this variant interacts with variants at other genes. For instance, it has been found that people with at least one copy of the short allele of 5-HTTLPR tend to be too sensitive to negative emotional information. This effect seems to be attenuated by the deletion variant of ADRA2b, which either keeps one from dwelling too much on a bad emotional experience or helps one anticipate and prevent repeat experiences (Naudts et al., 2012). Nonetheless, too much affective empathy may lead to an overload where one ends up helping others to the detriment of oneself and one’s family and kin.
Belfer, I., B. Buzas, H. Hipp, G. Phillips, J. Taubman, I. Lorincz, C. Evans, R.H. Lipsky, M.-A. Enoch, M.B. Max, and D. Goldman. (2005). Haplotype-based analysis of alpha 2A, 2B, and 2C adrenergic receptor genes captures information on common functional loci at each gene. Journal of Human Genetics, 50, 12-20.
Chakrabarti, B. and S. Baron-Cohen. (2013). Understanding the genetics of empathy and the autistic spectrum, in S. Baron-Cohen, H. Tager-Flusberg, M. Lombardo. (eds). Understanding Other Minds: Perspectives from Developmental Social Neuroscience. Oxford: Oxford University Press.
Cousijn, H., M. Rijpkema, S. Qin, H.J.F. van Marle, B. Franke, E.J. Herman, G. van Wingen, and G. Fernández. (2010). Acute stress modulates genotype effects on amygdala processing in humans.Proceedings of the National Academy of Sciences U.S.A., 107, 9867-9872.
de Quervain, D.J. F., I.-T. Kolassa, V. Ertl, L.P. Onyut, F. Neuner, T. Elbert, and A. Papassotiropoulos. (2007). A deletion variant of the alpha2b-adrenoceptor is related to emotional memory in Europeans and Africans. Nature Neuroscience, 10, 1137-1139.
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Todd, R.M., M.R. Ehlers, D. J. Muller, A. Robertson, D.J. Palombo, N. Freeman, B. Levine, and A.K. Anderson (2015). Neurogenetic Variations in norepinephrine availability enhance perceptual vividness. The Journal of Neuroscience, 35, 6506-6516.
UBC News. (2015). How your brain reacts to emotional information is influenced by your genes, May 6
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