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In the last decade, no other branch of clinical pharmacology has been subject to as much criticism of failed innovation and unsatisfactory effectiveness as psychopharmacology. Evolutionary psychiatry can offer original insights on the problems that complicate pharmacological research. Considering that invalid phenotyping is a major obstacle to drug development, an evolutionary perspective suggests targeting clinical phenotypes related to evolved behavior systems because they are more likely to map onto the underlying biology than constructs based on predetermined diagnostic criteria. Because of their emphasis on symptom remission, pharmacological studies of psychiatric populations rarely include functional capacities as the primary outcome measure and neglect the impact of social context on the effects of psychiatric drugs. Evolutionary psychiatry explains why it is appropriate to replace symptoms with functional capacities as the primary target of psychiatric therapies and why social context should be a major focus of studies assessing the effectiveness of drugs currently used and new drugs under development. When the focus of research shifts to those questions that go beyond the "disease-based" concept of drug action, evolutionary psychiatry clearly emerges as a reference framework to assess drug effectiveness and to optimize clinicians' decisions about prescribing, deprescribing, and non-prescribing.

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Evolutionary biology provides a unifying theory for testing hypotheses about the relationship between hormones and person perception. Person perception usually receives attention from the perspective of sexual selection. However, because person perception is one trait in a suite regulated by hormones, univariate approaches are insufficient. In this Perspectives article, quantitative genetics is presented as an important but underutilized framework for testing evolutionary hypotheses within this literature. We note tacit assumptions within the current literature on psychiatric genetics, which imperil the interpretation of findings thus far. As regulators of a diverse manifold of traits, hormones mediate tradeoffs among an array of functions. Hormonal pleiotropy also provides the basis of correlational selection, a process whereby selection on one trait in a hormone-mediated suite generates selection on the others. This architecture provides the basis for conflicts between sexual and natural selection within hormone-mediated suites. Due to its role in person perception, psychiatric disorders, and reproductive physiology, the sex hormone estrogen is highlighted as an exemplar here. The implications of this framework for the evolution of person perception are discussed. Empirical quantification of selection on traits within hormone-mediated suites remains an important gap in this literature with great potential to illuminate the fundamental nature of psychiatric disorders.

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Unlike other medical specialties, psychiatry has not been involved in the theoretical shift that replaced the syndromal approach with the clinico-pathological method, which consists in explaining clinical manifestations by reference to morbid anatomical and physiological changes. Past and present discussions on the applicability of the clinico-pathological method in psychiatry are based on a pre-Darwinian concept of biology as the study of proximate causation. Distinguishing between mediating mechanisms and evolved functions, an evolutionary perspective offers an original contribution to the debate by overcoming the opposite views of dualism (i.e., the clinico-pathological method is not applicable to disorders of the mind) and neuroessentialism (i.e., the definitive way of explaining psychiatric disorders is by reference to the brain and its activity). An evolutionary perspective offers original insights on the utility of the clinico-pathological method to solve critical questions of psychiatric research and clinical practice, including the distinction between mental health and illness, a better understanding of the etiology and pathophysiology, the classification and differential diagnosis of psychiatric disorders, and the development of more efficacious psychiatric treatments.

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Addiction poses significant social, health, and criminal issues. Its moderate heritability and early-life impact, affecting reproductive success, poses an evolutionary paradox: why are humans predisposed to addictive behaviours? This paper reviews biological and psychological mechanisms of substance and behavioural addictions, exploring evolutionary explanations for the origin and function of relevant systems. Ancestrally, addiction-related systems promoted fitness through reward-seeking, and possibly self-medication. Today, psychoactive substances disrupt these systems, leading individuals to neglect essential life goals for immediate satisfaction. Behavioural addictions (e.g. video games, social media) often emulate ancestrally beneficial behaviours, making them appealing yet often irrelevant to contemporary success. Evolutionary insights have implications for how addiction is criminalised and stigmatised, propose novel avenues for interventions, anticipate new sources of addiction from emerging technologies such as AI. The emerging potential of glucagon-like peptide 1 (GLP-1) agonists targeting obesity suggest the satiation system may be a natural counter to overactivation of the reward system.

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This paper celebrates the life and legacy of psychiatrist and Jungian author Anthony Stevens, who passed away at age 90 on July 13, 2023. It outlines Stevens's origins as a research fellow in Greece, where his work on infant attachment led to a lifelong dedication to establishing the biological and evolutionary foundation of psychiatry. It details his instrumental role in the debate about the theory of archetypes and describes the current state of the literature including the responses and reactions to Stevens's biological innatist position. The paper concludes with a career retrospective in which Stevens's major works are introduced and briefly described.

Cet article célèbre la vie et l'héritage du psychiatre et auteur jungien Anthony Stevens, décédé à l'âge de 90 ans le 13 juillet 2023. L'article décrit les origines de Stevens en tant que chercheur en Grèce, où ses travaux sur l'attachement du nourrisson l'ont conduit à se consacrer toute sa vie à établir le fondement biologique de la psychiatrie, dans une perspective évolutionniste. L'article détaille son rôle important dans le débat sur la théorie des archétypes et décrit l'état actuel de la littérature, y compris les réponses et réactions à la position biologique innéiste de Stevens. L'article se termine par une rétrospective de sa carrière, dans laquelle les œuvres majeures de Stevens sont présentées et brièvement décrites.

Este artículo celebra la vida y el legado del psiquiatra y autor Junguiano Anthony Stevens, quien falleció a los 90 años el 13 de julio de 2023. Describe los orígenes de Stevens como investigador en Grecia, donde su trabajo sobre el apego infantil lo llevó a una dedicación de por vida para establecer los fundamentos biológicos y evolutivos de la psiquiatría. Detalla su papel instrumental en el debate sobre la teoría de los arquetipos y describe el estado actual del arte, incluyendo las respuestas y reacciones a la posición biológica innatista de Stevens. El artículo concluye con una retrospectiva de su carrera en la que se presentan y describen brevemente las principales obras de Stevens.

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Perspectives on autism and psychiatric conditions are affected by a mix of scientific and social influences. Evolutionary psychiatry (EP) and the neurodiversity movement are emerging paradigms that reflect these distinct influences, with the former grounded in scientific theory and the latter driven by political and social principles. Despite their separate foundations, there is a significant overlap between EP and neurodiversity that has not been explored. Specifically, both paradigms reframe disorders as natural cognitive differences rather than disease; expand the concept of "normal" beyond that implied in modern psychiatry; focus on relative strengths; recognize that modern environments disadvantage certain individuals to cause functional impairment; emphasize cognitive variation being socially accommodated and integrated rather than treated or cured; and can help reduce stigmatization. However, in other ways, they are distinct and sometimes in conflict. EP emphasizes scientific explanation, defines "dysfunction" in objective terms, and differentiates heterogenous cases based on underlying causes (e.g. autism due to de novo genetic mutations). The neurodiversity movement emphasizes social action, removes barriers to inclusion, promotes inclusive language, and allows unrestricted identification as neurodivergent. By comparing and contrasting these two approaches, we find that EP can, to some extent, support the goals of neurodiversity. In particular, EP perspectives could be convincing to groups more responsive to scientific evidence and help achieve a middle ground between neurodiversity advocates and critics of the movement.

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This editorial outlines the formation of a new special interest group (SIG) in evolution and psychiatry. The formative beginnings of the evolutionary psychiatry field and founding of the group in Ireland are presented, identifying central figures of the field and their contributions. Furthermore, key milestones and accomplishments are discussed with current and future directions. Additionally, foundational texts and seminal papers are included to guide the reader in their journey to discover more about evolution and psychiatry. We hope this will be of relevance to those interested in how SIGs form and also to clinicians with an interest in evolutionary psychiatry.

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This article presents a novel theoretical perspective on the role of cognitive biases within the autism and schizophrenia spectrum by integrating the evolutionary and computational approaches. Against the background of neurodiversity, cognitive biases are presented as primary adaptive strategies, while the compensation of their shortcomings is a potential cognitive advantage. The article delineates how certain subtypes of autism represent a unique cognitive strategy to manage cognitive biases at the expense of rapid and frugal heuristics. In contrast, certain subtypes of schizophrenia emerge as distinctive cognitive strategies devised to navigate social interactions, albeit with a propensity for overdetecting intentional behaviors. In conclusion, the paper emphasizes that while extreme manifestations might appear non-functional, they are merely endpoints of a broader, primarily functional spectrum of cognitive strategies. The central argument hinges on the premise that cognitive biases in both autism and schizophrenia spectrums serve as compensatory mechanisms tailored for specific ecological niches.

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Evolutionary biology provides a crucial foundation for medicine and behavioral science that has been missing from psychiatry. Its absence helps to explain slow progress; its advent promises major advances. Instead of offering a new kind of treatment, evolutionary psychiatry provides a scientific foundation useful for all kinds of treatment. It expands the search for causes from mechanistic explanations for disease in some individuals to evolutionary explanations for traits that make all members of a species vulnerable to disease. For instance, capacities for symptoms such as pain, cough, anxiety and low mood are universal because they are useful in certain situations. Failing to recognize the utility of anxiety and low mood is at the root of many problems in psychiatry. Determining if an emotion is normal and if it is useful requires understanding an individual's life situation. Conducting a review of social systems, parallel to the review of systems in the rest of medicine, can help achieve that understanding. Coping with substance abuse is advanced by acknowledging how substances available in modern environments hijack chemically mediated learning mechanisms. Understanding why eating spirals out of control in modern environments is aided by recognizing the motivations for caloric restriction and how it arouses famine protection mechanisms that induce binge eating. Finally, explaining the persistence of alleles that cause serious mental disorders requires evolutionary explanations of why some systems are intrinsically vulnerable to failure. The thrill of finding functions for apparent diseases is evolutionary psychiatry's greatest strength and weakness. Recognizing bad feelings as evolved adaptations corrects psychiatry's pervasive mistake of viewing all symptoms as if they were disease manifestations. However, viewing diseases such as panic disorder, melancholia and schizophrenia as if they are adaptations is an equally serious mistake in evolutionary psychiatry. Progress will come from framing and testing specific hypotheses about why natural selection left us vulnerable to mental disorders. The efforts of many people over many years will be needed before we will know if evolutionary biology can provide a new paradigm for understanding and treating mental disorders.

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Personality disorders (PDs) are currently considered dysfunctions. However, personality differences are older than humanity and are ubiquitous in nature, from insects to higher primates. This suggests that a number of evolutionary mechanisms-other than dysfunctions-may be able to maintain stable behavioral variation in the gene pool. First of all, apparently maladaptive traits may actually improve fitness by enabling better survival or successful mating or reproduction, as exemplified by neuroticism, psychopathy, and narcissism. Furthermore, some PDs may harm important biological goals while facilitating others, or may be globally beneficial or detrimental depending on environmental circumstances or body condition. Alternatively, certain traits may form part of life history strategies: Coordinated suites of morphological, physiological and behavioral characters that optimize fitness through alternative routes and respond to selection as a whole. Still others may be vestigial adaptations that are no longer beneficial in present times. Finally, variation may be adaptative in and by itself, as it reduces competition for finite resources. These and other evolutionary mechanisms are reviewed and illustrated through human and non-human examples. Evolutionary theory is the best-substantiated explanatory framework across the life sciences, and may shed light on the question of why harmful personalities exist at all.

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The field of psychopathology is in a transformative phase, and is witnessing a renewed surge of interest in theoretical models of mental disorders. While many interesting proposals are competing for attention in the literature, they tend to focus narrowly on the proximate level of analysis and lack a broader understanding of biological function. In this paper, we present an integrative framework for mental disorders built on concepts from life history theory, and describe a taxonomy of mental disorders based on its principles, the fast-slow-defense model (FSD). The FSD integrates psychopathology with normative individual differences in personality and behavior, and allows researchers to draw principled distinctions between broad clusters of disorders, as well as identify functional subtypes within current diagnostic categories. Simulation work demonstrates that the model can explain the large-scale structure of comorbidity, including the apparent emergence of a general "p factor" of psychopathology. A life history approach also provides novel integrative insights into the role of environmental risk/protective factors and the developmental trajectories of various disorders.

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Schizophrenia has been an evolutionary paradox: it has high heritability, but it is associated with decreased reproductive success. The causal genetic variants underlying schizophrenia are thought to be under weak negative selection. To unravel this paradox, many evolutionary explanations have been suggested for schizophrenia. We critically discuss the constellation of evolutionary hypotheses for schizophrenia, highlighting the lack of empirical support for most existing evolutionary hypotheses-with the exception of the relatively well supported evolutionary mismatch hypothesis. It posits that evolutionarily novel features of contemporary environments, such as chronic stress, low-grade systemic inflammation, and gut dysbiosis, increase susceptibility to schizophrenia. Environmental factors such as microbial infections (e.g., Toxoplasma gondii) can better predict the onset of schizophrenia than polygenic risk scores. However, researchers have not been able to explain why only a small minority of infected people develop schizophrenia. The new etiological synthesis of schizophrenia indicates that an interaction between host genotype, microbe infection, and chronic stress causes schizophrenia, with neuroinflammation and gut dysbiosis mediating this etiological pathway. Instead of just alleviating symptoms with drugs, the parasite x genotype x stress model emphasizes that schizophrenia treatment should focus on detecting and treating possible underlying microbial infection(s), neuroinflammation, gut dysbiosis, and chronic stress.

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This paper proposes an integrative perspective on evolutionary, cultural and computational approaches to psychiatry. These three approaches attempt to frame mental disorders as multiscale entities and offer modes of explanations and modeling strategies that can inform clinical practice. Although each of these perspectives involves systemic thinking, each is limited in its ability to address the complex developmental trajectories and larger social systemic interactions that lead to mental disorders. Inspired by computational modeling in theoretical biology, this paper aims to integrate the modes of explanation offered by evolutionary, cultural and computational psychiatry in a multilevel systemic perspective. We apply the resulting Evolutionary, Cultural and Computational (ECC) model to Major Depressive Disorder (MDD) to illustrate how this integrative approach can guide research and practice in psychiatry.

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Traditional evolutionary theory invoked natural and sexual selection to explain species- and sex-typical traits. However, some heritable inter-individual variability in behaviour and psychology - personality - is probably adaptive. Here we extend this insight to common psychopathological traits. Reviewing key findings from three background areas of importance - theoretical models, non-human personality and evolved human social dynamics - we propose that a combination of social niche specialisation, negative frequency-dependency, balancing selection and adaptive developmental plasticity should explain adaptation for individual differences in psychology - 'specialised minds' - explaining some variance in personality and psychopathology trait dimensions, which share various characteristics. We suggest that anthropological research of behavioural differences should be extended past broad demographic factors (age and sex) to include individual specialisations. As a first step towards grounding psychopathology in ancestral social structure, we propose a minimum plausible prevalence, given likely ancestral group sizes, for negatively frequency-dependent phenotypes to be maintained as specialised tails of adaptive distributions - below the calculated prevalence, specialisation is highly unlikely. For instance, chronic highly debilitating forms of autism or schizophrenia are too rare for such explanations, whereas attention-deficit-hyperactivity disorder and broad autism phenotypes are common enough to have existed in most hunter-gatherer bands, making adaptive explanations more plausible.

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Bipolar disorder is a mental health disorder characterized by extreme shifts in mood, high suicide rate, sleep problems, and dysfunction of psychological traits like self-esteem (feeling inferior when depressed and superior when manic). Bipolar disorder is rare among populations that have not adopted contemporary Western lifestyles, which supports the hypothesis that bipolar disorder results from a mismatch between Homo sapiens's evolutionary and current environments. Recent studies have connected bipolar disorder with low-grade inflammation, the malfunctioning of the internal clock, and the resulting sleep disturbances. Stress is often a triggering factor for mania and sleep problems, but stress also causes low-grade inflammation. Since inflammation desynchronizes the internal clock, chronic stress and inflammation are the primary biological mechanisms behind bipolar disorder. Chronic stress and inflammation are driven by contemporary Western lifestyles, including stressful social environments, unhealthy dietary patterns, limited physical activity, and obesity. The treatment of bipolar disorder should focus on reducing stress, stress sensitivity, and inflammation by lifestyle changes rather than just temporarily alleviating symptoms with psychopharmacological interventions.

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OBJECTIVE: Excessive activation of defence modules leads to some dysfunctional outcomes, which can be broadly classified to defence activation disorders. Defence activation disorders have high mortality, low fertility, high prevalence and high heritability. In this study, agent-based simulation model is formulated for solving this evolutionary paradox. METHODS: The emotional system is considered as a superordinate cognitive module for grasping the average resource amount and the average diminishing returns of resources, based on the Marginal Value Theorem. Under the assumption, the evolutionary ecological model was proposed and analysed. RESULTS: Individuals utilising suboptimal strategies can be stably maintained in agent-based evolutionary simulation environments. Individuals were adapted to have different d-values according to the local niche. The simulation runs stably within the calibrated range of the variables for a long time. Agents establish locally optimal strategies based on their given d-values, and the relative proportion of subpopulation maintained stably in the heterogeneous habitat with the resource gradient. CONCLUSION: This study verifies the evolutionary mechanism of defence activation disorders in computer-simulated environments by using agent-based modelling with the Marginal Value Theorem. Balancing selection appears to be a plausible evolutionary mechanism that makes the suboptimal levels of defence activation the evolutionarily stable strategies.

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Eating disorders are evolutionarily novel conditions. They lead to some of the highest mortality rates of all psychiatric disorders. Several evolutionary hypotheses have been proposed for eating disorders, but only the intrasexual competition hypothesis is extensively supported by evidence. We present the mismatch hypothesis as a necessary extension to the current theoretical framework of eating disorders. This hypothesis explains the evolutionarily novel adaptive metaproblem that has arisen when mating motives conflict with the large-scale and easy availability of hyper-rewarding but obesogenic foods. This situation is exacerbated particularly in those contemporary environments that are characterized by sedentary lifestyles, ever-present junk foods, caloric surplus and the ubiquity of social comparisons that take place via social media. Our psychoneuroimmunological model connects ultimate-level causation with proximate mechanisms by showing how the adaptive metaproblem between mating motives and food rewards leads to chronic stress and, further, to disordered eating. Chronic stress causes neuroinflammation, which increases susceptibility to OCD-like behaviors that typically co-occur with eating disorders. Chronic stress upregulates the serotonergic system and causes dysphoric mood in anorexia nervosa patients. Dieting, however, reduces serotonin levels and dysphoric mood, leading to a vicious serotonergic-homeostatic stress/starvation cycle whereby cortisol and neuroinflammation increase through stringent dieting. Our psychoneuroimmunological model indicates that between-individual and within-individual variation in eating disorders partially arises from (co)variation in gut microbiota and stress responsivity, which influence neuroinflammation and the serotonergic system. We review the advances that have been made in recent years in understanding how to best treat eating disorders, outlining directions for future clinical research. Current evidence indicates that eating disorder treatments should aim to reduce the chronic stress, neuroinflammation, stress responsivity and gut dysbiosis that fuel the disorders. Connecting ultimate causes with proximate mechanisms and treating biopsychosocial causes rather than manifest symptoms is expected to bring more effective and sophisticated long-term interventions for the millions of people who suffer from eating disorders.

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Psychiatric disorder as dysfunctional behavioural syndrome is a paradoxical phenomenon that is difficult to explain evolutionarily because moderate prevalence rate, high heritability and relatively low fitness are shown. Several evolutionary genetic models have been proposed to address this paradox. In this paper, I explain each model by dividing it into selective neutrality, mutation-selection balance, and balancing selection hypothesis, and discuss the advantages and disadvantages of them. In addition, the feasibility of niche specialization and frequency dependent selection as the plausible explanation about the central paradox is briefly discussed.

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Like the body of Hominin, mind is the result of natural selection. Therefore, an evolutionary approach in the biological aspects is essential for an intrinsic understanding of mental disorders. However, the evolutionary medical approach to mental disordershas not been well researched because evolutionary psychiatry is not widely accepted, and the conceptual paradigm has not been unified. Nevertheless, some evolutionary hypotheses about some mental disorders have been proposed, including the following: 1) thesimple disease argument that mental disorder is a mere disease, 2) the genomic lag hypothesis that current genes are incompatible with evolutionary environmental changes, 3) the developmental mismatch hypothesis that brain development cannot reflect entire-information of surrounding environment, 4) the trade-off hypothesis that costs are offset by other adaptive benefits, 5) the by-product hypothesis that mental disorders are inevitable outcome of evolutionary design, 6) the cliff-edge model that the encephalizationin the Hominin caused mental disorders, 7) the inclusive fitness hypothesis that costs of individual are compensated by benefits of kinship, 8) the antagonistic polymorphism hypothesis that differential costs and benefits according to sex or age cause ofpolymorphic psychological traits 9) the heterozygote advantage hypothesis that the heterozygous genotypes have higher relative fitness, so they can persist even though homozygous genotypes cause mental disorders, and 10) a genomic imprinting hypothesis that conflicts between maternal genes and paternal genes cause mental disorders. I will summarize and compare the evolutionary hypotheses of mental disorders and present the lim itations of each hypothesis.

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