The term ‘schizophrenia’ refers to a group of disorders that seem to occur worldwide, with clinical pictures being strikingly similar across cultures. Evolutionary explanations of these disorders are warranted for at least two reasons: the first concerns their prevalence in all known ethnicities; the second relates to the need to explain the paradox as to why the conditions are maintained despite the greatly decreased fecundity of the affected individuals. Accordingly, a plethora of heterogeneous hypotheses – unparalleled among other psychiatric disorders – have been put forth, some of which deal with genetic considerations, others with environmental risk factors, and a few consider the adaptive advantages associated with the genes that predispose to schizophrenia. None of the evolutionary scenarios has the potential to account for the diversity of the symptomatology or to cover all of the biological and non-biological aspects of schizophrenia or schizophrenia spectrum disorders. This chapter aims at discussing the most relevant evolutionary hypotheses of schizophrenia, arguing that a symptom-based approach to psychotic disorders from an evolutionary perspective may improve upon the existing models of schizophrenia.

Discovering why natural selection has left humans vulnerable to mental disorders will make psychiatry more sensible and effective, but defining the appropriate objects and kinds of explanation remains challenging. Asking how a disorder increases fitness is a mistake; disorders are not adaptations and they do not have evolutionary explanations. The correct objects of explanation are the traits that make all members of a species vulnerable to a disorder. Task 1 is to describe the evolutionary origins and functions of the traits involved. Task 2 is to describe the proximate processes that result in the disorder. Task 3 is to discover why natural selection left the traits vulnerable to malfunction. Five main kinds of explanation need to be considered: stochasticity, path dependence, mismatch, trade-offs that benefit the individual and traits that benefit gene transmission at a cost to the individual. Depression, addiction, eating disorders, autism and schizophrenia are used to illustrate the opportunities and challenges of framing and testing hypotheses about vulnerability. Multiple explanations are often needed for a single disorder, frustrating the wish for simplicity. However, recognising the fundamental differences between organic and designed systems offers opportunities for resolving – or at least understanding – some enduring controversies in psychiatry.

We discuss evolutionary perspectives on two neurodevelopmental disorders: attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). Both have a genetic background, and we explore why these genes may have survived the process of natural selection. We draw on the concept of evolutionary mismatch, in which a trait that may have conferred advantages in the past can become disadvantageous when the environment changes. We also describe the non-genetic influences on these conditions. We point out that children with neurodevelopmental conditions are more likely to suffer maltreatment, so it is important to consider both the genes and the environment in which children have grown up. In hunter-gatherer societies, ADHD may have favoured risk-taking, which may explain why it has survived. The contemporary model of schooling, in which children are expected to sit still for many hours a day, does not favour this. Understanding ADHD in terms of an evolutionary mismatch therefore raises ethical issues regarding both medication and the school environment. ASDs are far more heterogeneous and are characterised by high heritability and low reproductive success. At the severe end of the spectrum, ASD is highly disadvantageous and often co-occurs with intellectual disability. On the other hand, high-functioning ASD may have been adaptive in our evolutionary past in terms of the potential for the development of specialist skills and can still be so today in the right environment.

In Western culture, both the lay public and mental health professionals tend to believe that mothers evolved to love all of their children instinctually and unconditionally. In contrast, any mother who feels ambivalence or hostility towards her child is typically seen as unnatural, and a mother who maltreats her child is seen as behaving pathologically. This chapter draws on evolutionary research to challenge this widespread view of motherhood. In particular, it describes how raising children has required mothers to negotiate a series of complex, precarious and layered trade-offs, and it argues that maternal negativity and child maltreatment can arise from this. The goal of this chapter is to foster a more evolutionarily valid, nuanced and compassionate understanding of motherhood. Such an understanding has the potential to contribute to clinical work with faltering mothers as well as to programmes focused on preventing maternal maltreatment of children.

The currently dominant model of health and disease in psychiatry and medicine is Engel’s biopsychosocial (BPS) model, proposed in the 1970s to advance reductionistic biomedicine by integrating psychological and social factors. Although the BPS model represented progress, its scientific and philosophical foundations remain questionable and it cannot be considered complete or sufficient. In this chapter, we provide a historical and conceptual analysis of the BPS model before showing that the integration of evolutionary theory can provide a suitable next step from the BPS model, much as the BPS model was a step forward from the biomedical approach. Evolutionary theory justifies and enhances the BPS model’s recognition of multiple levels of causation and expands it by recognising both ultimate and proximate causation. It allows a clearer distinction of biological function from dysfunction and encourages a phylogenetic perspective on biology, which can guide research in new directions. In connecting the model of health with the most fundamental theory of biology, this approach provides the philosophical and scientific coherence that the BPS model sorely lacked.

Humans and alcohol share a deep evolutionary history: our capacity to convert alcohol into useable sugars is a trait we share with the African great apes (gorillas and chimpanzees) and is unique to this taxonomic family among the primates. Although the archaeological record only allows us to date the production of alcohol back about 9,000 years (by which time it is already on an industrial scale), a cottage industry of alcohol production must date back a great deal further. With the exception of where its consumption has been prohibited on religious grounds, alcohol use occurs in every culture and society. Notwithstanding its hedonic properties, its real functional benefit is primarily social, playing an important role in rituals and group bonding. I review studies that demonstrate its functional consequences in terms of social bonding, mediated by alcohol’s ability to trigger the brain’s endorphin system. The endorphin system is the central basis for social bonding in primates. The health and other benefits that arise from social bonding are considerable.