Although psychopathy is widely conceptualised as a mental disorder, some researchers question the maladaptive nature of psychopathy, and argue that it might be advantageous from an evolutionary point of view. According to this view, psychopathy can be seen as an evolutionary adaptative strategy that relies on deception and manipulation to gain short-term reproductive benefits. Psychopathy is also identified as a fast life strategy in response to early life stress and an adaptation to harsh environments. This paper investigates the evidence that psychopathic traits are adaptive, while also addressing the limitations of current evolutionary models of psychopathy based on frequency-dependent selection and life history theory. We review recent studies on the fitness correlates of psychopathy and find that psychopathic traits present potential adaptive trade-offs between fertility and mortality, and offspring quantity and quality. On a proximate level, individual differences in stress reactivity and environmental risk factors in early development predispose to psychopathy through gene–environment interactions. We propose that environmental, developmental, social and cultural factors can mediate the relationship between psychopathic traits and fitness and therefore should be considered to make accurate predictions on the adaptive potential of psychopathy. We end by outlining gaps in the literature and making recommendations for future evolutionary research on psychopathy.

While converging evidence suggests that both environmental and genetic factors underlie variations in diurnal cortisol, the extent to which these sources of influence vary according to socioeconomic status (SES) has seldom been investigated, particularly in adolescence. To investigate whether a distinct genetic and environmental contribution to youth’s diurnal cortisol secretion emerges according to family SES and whether the timing of these experiences matters. Participants were 592 twin pairs, who mostly came from middle-income and intact families and for whom SES was measured in childhood and adolescence. Diurnal cortisol was assessed at age 14 at awakening, 30 min later, in the afternoon and evening over four nonconsecutive days. SES–cortisol phenotypic associations were specific to the adolescence period. Specifically, higher awakening cortisol levels were detected in wealthier backgrounds, whereas higher cortisol awakening response (CAR) and diurnal changes were present at both ends of the SES continuum. Moreover, smaller genetic contributions emerged for awakening cortisol in youth from poorer compared to wealthier backgrounds. The results suggest that the relative contribution of inherited factors to awakening cortisol secretion may be enhanced or suppressed depending on the socio-family context, which may help to decipher the mechanisms underlying later adjustment.

Schizophrenia and other types of psychosis incur suffering, high health care costs and loss of human potential, due to the combination of early onset and poor response to treatment. Our ability to prevent or cure psychosis depends on knowledge of causal mechanisms. Molecular genetic studies show that thousands of common and rare variants contribute to the genetic risk for psychosis. Epidemiological studies have identified many environmental factors associated with increased risk of psychosis. However, no single genetic or environmental factor is sufficient to cause psychosis on its own. The risk of developing psychosis increases with the accumulation of many genetic risk variants and exposures to multiple adverse environmental factors. Additionally, the impact of environmental exposures likely depends on genetic factors, through gene–environment interactions. Only a few specific gene–environment combinations that lead to increased risk of psychosis have been identified to date. An example of replicable gene–environment interaction is a common polymorphism in the AKT1 gene that makes its carriers sensitive to developing psychosis with regular cannabis use. A synthesis of results from twin studies, molecular genetics, and epidemiological research outlines the many genetic and environmental factors contributing to psychosis. The interplay between these factors needs to be considered to draw a complete picture of etiology. To reach a more complete explanation of psychosis that can inform preventive strategies, future research should focus on longitudinal assessments of multiple environmental exposures within large, genotyped cohorts beginning early in life.

Analysis of DNA methylation data in epigenome-wide association studies provides many bioinformatics and statistical challenges. Not least of these, are the non-independence of individual DNA methylation marks from each other, from genotype and from technical sources of variation. In this review we discuss DNA methylation data from the Infinium450K array and processing methodologies to reduce technical variation. We describe recent approaches to harness the concordance of neighbouring DNA methylation values to improve power in association studies. We also describe how the non-independence of genotype and DNA methylation has been used to infer causality (in the case of Mendelian randomization approaches); suggest the mediating effect of DNA methylation in linking intergenic single nucleotide polymorphisms, identified in genome-wide association studies, to phenotype; and to uncover the widespread influence of gene and environment interactions on methylation levels.

There is an ever-increasing body of literature examining gene–environment interactions in psychiatry, reflecting a widespread belief that such studies will aid identification of novel risk factors for disease, increase understanding about underlying pathological mechanisms, and aid identification of high-risk groups for targeted interventions. In this article we discuss to what extent studies of gene–environment interactions are likely to lead to any such benefits in the future.