Social behaviour is heritable but heterogeneous. An international team of EAGLE and R2D2-MH consortia researchers, led by the Max Planck Institute for Psycholinguistics, Nijmegen, the Netherlands, conducted a large-scale genome-wide study of social behaviour in context, investigating two social domains at different ages and with multiple reporters. Identified patterns of genetic signals and genetic correlations, including links with mental health outcomes such as ADHD and autism, differed by context, offering new insight into neurodevelopment.
A mother reporting on her toddler learning to share, a teacher observing a schoolchild navigating friendships and peer relations, and a teenager describing their own social relations are all examples of social behaviour within a social context.
An international study published in Nature Human Behaviour demonstrated that the genetic architecture of social behaviour changes depending on what social behaviour is measured, at what age and who is reporting it.
Researchers led by the Max Planck Institute for Psycholinguistics, Nijmegen, the Netherlands, and embedded within the EAGLE and R2D2-MH consortia performed a genetic meta-analysis studying nearly 500,000 social behavioural observations from more than 73,000 individuals, often with multiple assessments across the ages of 2 – 29 years, helping them to examine developmental change.
The study focused on two broad domains of social behaviour. The first, low prosocial behaviour, captures behavioural differences in helping, sharing or comforting others. The second, peer and social difficulties, includes problems forming or maintaining relationships such as making friends.
Most large genome-wide studies combine information across individuals and measurements to obtain a single overall estimate. Here, the researchers adopted a meta-regression approach that explicitly models how genetic effects change across different social measures, reported by multiple informants at different ages, collectively termed social context.
The analysis identified six regions of the genome to be associated with social behaviour and all showed evidence that their associations differed according to behavioural domain, reporter and age. The strongest association signal was found within CADM2, a gene involved in organising connections between nerve cells, in particular for self-reported low prosocial behaviour during late childhood and early adolescence. Different genetic variations within CADM2 have been previously linked to autism and other traits.
Between 2 to 7% of variation in social behaviour was captured by common genetic variation (so-called single-nucleotide polymorphisms, SNPs). At this broader level, the researchers found that the genetic architecture of social behaviour can be described by four interrelated overarching genetic factors: Two genetic factors captured the two behavioural domains which were low prosocial behaviour and peer and social problems. The remaining two factors reflected differences between parent and teacher perspectives.
“Children move through many different social worlds requiring different types of behaviour – at home, at school – and their behaviour changes with age. Our findings show that genome-wide studies need to take these behavioural differences into account rather than averaging these effects into a single estimate”, says Beate St Pourcain, senior investigator of the study. First author Lucía de Hoyos adds “Human development is dynamic. Our analyses offer an opportunity to make genome-wide studies dynamic, too”. Thomas Bourgeron, the coordinator of the R2D2-MH consortium, reminds that “Genetic variants matter, but they are not destiny. With the right environment, support, and opportunities, people can adapt and flourish.”
Next, the researchers constructed polygenic scores, which summarise many small SNP effects, studying 16,305 people from independent validation cohorts of European and African ancestry and found that predictions improved when social context across studied cohorts was matched.
The researchers also examined genetic relationships between childhood social behaviour and traits measured later in life, including mental health-related outcomes such as autism and ADHD. The findings suggested that genetic correlations become detectable at different developmental stages, depending on the particular social context studied, offering new insight into neurodevelopment.
The authors emphasise that the findings cannot be used to predict how an individual child will behave. Instead, the study demonstrates that understanding the biology of human behaviour requires understanding the context in which behaviour develops. “Our findings can help to better understand the developmental trajectories of social behaviour and their links with later-life and mental-health outcomes” says St Pourcain. “We will follow up our research with a sex-specific meta-regression approach studying differences across males and females.”
R2D2-MH has been funded by Horizon Europe [grant agreement no. 101057385], by UK Research and Innovation (UKRI) under the UK government’s Horizon Europe funding guarantee [grant no.10039383] and by the Swiss State Secretariat for Education, Research and Innovation (SERI) under contract number 22.00277.
JOURNAL
Nature Human Behaviour