Behavioural public policy is increasingly interested in scaling-up experimental insights to deliver systemic changes. Recent evidence shows some forms of individual behaviour change, such as nudging, are limited in scale. We argue that we can scale-up individual behaviour change by accounting for nuanced social complexities in which human responses to behavioural public policies are situated. We introduce the idea of the ‘social brain’, as a construct to help practitioners and policymakers facilitate a greater social transmission of welfare-improving behaviours. The social brain is a collection of individual human brains, who are connected to other human brains through ‘social cues’, and who are affected by the material and immaterial properties of the physical environment in which they are situated (‘social complex’). Ignoring these cues and the social complex runs the risk of fostering localised behavioural changes, through individual actors, which are neither scalable nor lasting. We identify pathways to facilitate changes in the social brain: either through path dependencies or critical mass shifts in individual behaviours, moderated by the brain's property of social cohesion and multiplicity of situational and dispositional factors. In this way, behavioural changes stimulated in one part of the social brain can reach other parts and evolve dynamically. We recommend designing public policies that engage different parts of the social brain.

According to the social brain hypothesis, the human brain includes a network designed for the processing of social information. This network includes several brain regions that elaborate social cues, interactions and contexts, i.e. prefrontal paracingulate and parietal cortices, amygdala, temporal lobes and the posterior superior temporal sulcus. While current literature suggests the importance of this network from both a psychological and evolutionary perspective, little is known about its neurobiological bases. Specifically, only a paucity of studies explored the neural underpinnings of constructs that are ascribed to the social brain network functioning, i.e. objective social isolation and perceived loneliness. As such, this review aimed to overview neuroimaging studies that investigated social isolation in healthy subjects. Social isolation correlated with both structural and functional alterations within the social brain network and in other regions that seem to support mentalising and social processes (i.e. hippocampus, insula, ventral striatum and cerebellum). However, results are mixed possibly due to the heterogeneity of methods and study design. Future neuroimaging studies with longitudinal designs are needed to measure the effect of social isolation in experimental v. control groups and to explore its relationship with perceived loneliness, ultimately helping to clarify the neural correlates of the social brain.

Schizophrenia is a worldwide, prevalent disorder with a multifactorial but highly genetic aetiology. A constant prevalence rate in the face of reduced fecundity has caused some to argue that an evolutionary advantage exists in unaffected relatives. Here, I critique this adaptationist approach, and review – and find wanting – Crow's “speciation” hypothesis. In keeping with available biological and psychological evidence, I propose an alternative theory of the origins of this disorder. Schizophrenia is a disorder of the social brain, and it exists as a costly trade-off in the evolution of complex social cognition. Paleoanthropological and comparative primate research suggests that hominids evolved complex cortical interconnectivity (in particular, frontotemporal and frontoparietal circuits) to regulate social cognition and the intellectual demands of group living. I suggest that the ontogenetic mechanism underlying this cerebral adaptation was sequential hypermorphosis and that it rendered the hominid brain vulnerable to genetic and environmental insults. I argue that changes in genes regulating the timing of neurodevelopment occurred prior to the migration of Homo sapiens out of Africa 100,000–150,000 years ago, giving rise to the schizotypal spectrum. While some individuals within this spectrum may have exhibited unusual creativity and iconoclasm, this phenotype was not necessarily adaptive in reproductive terms. However, because the disorder shared a common genetic basis with the evolving circuitry of the social brain, it persisted. Thus schizophrenia emerged as a costly trade-off in the evolution of complex social cognition.