Towards a Unified Account of Aberrant Salience in Psychosis: Proximate and Evolutionary Mechanisms

Abstract

The “Aberrant Salience Hypothesis” (ASH) is arguably the pre-eminent proximate, theoretical model of psychosis in the current literature. As well as its consilience with phenomenological accounts, since its initial proposal, subsequent neuroscientific work has updated its empirical basis by demonstrating a functionally distinct large-scale brain network known as the “salience network” (SN), and crucially, demonstrated SN dysregulation in psychosis. Here, we elaborate upon this hypothesis through the application of evolutionary thinking, structured upon Tinbergen’s 4 questions. After delineating how the mechanism proposed by the ASH has been bolstered by subsequent neuroscientific advances, the ontogeny of psychosis is then considered. A critical aetiological role is attributed to toxic stress resulting from complex interactions between factors including urban living, migrant-status, male-sex, low socioeconomic status, subjective social status, and adverse childhood experiences. Our model, the modified ASH (“MASH”), seeks to provide a crucial bridge to the consideration of the evolutionary roots of psychosis. Environmental mismatch is implicated as the key evolutionary process. The model helps resolve the apparent puzzle of the persistence of psychosis, despite its detrimental effect on fitness. The adaptive significance of what shall be termed the “Salience Evaluation System” in humans is discussed, with particular reference to the uniquely complex human social environment. This provides an explanation for a further puzzle: that psychosis appears to be a human, species-specific phenomenon. Finally, we offer a number of testable predictions for future research.