Abstract

Individual differences in our capacity to read other people's emotions and to remember faces we have seen before are highly variable in the general population. Some people are super-recognizers; others have difficulty remembering their own family members. Such abilities are also highly heritable, implying our genetic makeup exerts an important influence. But what genes are involved in social perception? Where do they act when our brains process social signals? What happens if the social perception system malfunctions? How does it affect our social behaviour? These are questions I aim to answer in this lecture.

The neuropeptides (brain hormones) oxytocin and vasopressin are evolutionarily conserved regulators of social behaviour. Evidence is building that they are especially important for interpersonal bonding throughout mammalian species, from rodents through primates to humans. Oxytocin probably has a greater influence on the social perceptions and behaviour of females than males (influenced by female sex hormones such as oestrogen), and the impact of vasopressin may be rather greater upon male social perceptions and behaviour (influenced by male sex hormones or androgens). Recent research has suggested that, in people with autism, social motivation might be decreased because they do not find social interactions as rewarding as neurotypical individuals. The value we place on social reward appears to be influenced by oxytocin. Giving extra oxytocin to people with autism (for example, by nasal spray) improves the accuracy of their social perceptions (and potentially, the concomitant reward from a social encounter), at least temporarily.

If oxytocin in the brain impacts upon individual differences in sensitivity to social cues, the efficiency with which the hormone's receptor in the brain is activated might be important. We studied whether genetic variants of the oxytocin receptor affect face recognition memory in families where there was an autistic child. We discovered that possession of a single relatively common oxytocin receptor variant, of a type that could influence gene activity, accounted for up to 10% of their performance. Remarkably, our finding was replicated in both UK and in Finnish populations. About 35% of family members were homozygous for the risk genotype, meaning they possessed two copies of the gene variant that was associated with relatively less good facial memory than the population average. Our findings imply oxytocin and its receptor in the brain play a significant role in accounting for individual differences in our ability to remember the faces of unfamiliar people. On the whole, that influence is relatively subtle. Nevertheless, one in three of us possesses only the genetic version of the oxytocin receptor that is relatively inefficient. If we are in that large minority, it is unlikely we will ever be able to match the remarkable face memory skills of a Bill Clinton.