The evolutionary psychologist Geoffrey Miller has argued that various features of human psychology have been sculpted, at least in part, by the evolutionary process of sexual selection via mate choice. This paper specifically examines the central claim of Miller’s account, namely that certain cognitive traits have evolved to function as good genes fitness indicators. First, I expound on and clarify key foundational concepts comprising the focal hypothesis, especially condition-dependence, mutation target size, and mutation-selection balance. Second, I proceed to highlight some (...) subtle distinctions with respect to the concepts of exaptation and adaptation, as well as Fisherian runaway selection and good genes sexual selection, all of which in turn bear importantly on the overall framework of cognitive traits as fitness indicators. Third and finally, I close out the paper by examining various conceptual and methodological criteria which are integral to identifying sexually selected adaptations, then briefly examine some empirical work that has aimed to test the hypothesis that traits such as humor and creativity function as sexually attractive fitness indicators. (shrink)

Siblings compete for parental care and feeding, while parents must allocate scarce resources to those offspring most likely to survive and reproduce. This could cause offspring to evolve traits that advertise health, and thereby attract parental resources. For example, experimental evidence suggests that bright orange filaments covering the heads of North American coot chicks may have evolved for this fitness-advertising purpose. Could any human mental disorders be the equivalent of dull filaments in coot chicks—low-fitness extremes of mental abilities that evolved (...) as fitness indicators? One possibility is autism. Suppose that the ability of very young children to charm their parents evolved as a parentally selected fitness indicator. Young children would vary greatly in their ability to charm parents, that variation would correlate with underlying fitness, and autism could be the low-fitness extreme of this variation. This view explains many seemingly disparate facts about autism and leads to some surprising and testable predictions. (shrink)

Autistic-spectrum conditions and psychotic-spectrum conditions (mainly schizophrenia, bipolar disorder, and major depression) represent two major suites of disorders of human cognition, affect, and behavior that involve altered development and function of the social brain. We describe evidence that a large set of phenotypic traits exhibit diametrically opposite phenotypes in autistic-spectrum versus psychotic-spectrum conditions, with a focus on schizophrenia. This suite of traits is inter-correlated, in that autism involves a general pattern of constrained overgrowth, whereas schizophrenia involves undergrowth. These disorders also (...) exhibit diametric patterns for traits related to social brain development, including aspects of gaze, agency, social cognition, local versus global processing, language, and behavior. Social cognition is thus underdeveloped in autistic-spectrum conditions and hyper-developed on the psychotic spectrum.;>We propose and evaluate a novel hypothesis that may help to explain these diametric phenotypes: that the development of these two sets of conditions is mediated in part by alterations of genomic imprinting. Evidence regarding the genetic, physiological, neurological, and psychological underpinnings of psychotic-spectrum conditions supports the hypothesis that the etiologies of these conditions involve biases towards increased relative effects from imprinted genes with maternal expression, which engender a general pattern of undergrowth. By contrast, autistic-spectrum conditions appear to involve increased relative bias towards effects of paternally expressed genes, which mediate overgrowth. This hypothesis provides a simple yet comprehensive theory, grounded in evolutionary biology and genetics, for understanding the causes and phenotypes of autistic-spectrum and psychotic-spectrum conditions. (shrink)

Essentialism is one of the most pervasive problems in mental health research. Many psychiatrists still hold the view that their nosologies will enable them, sooner or later, to carve nature at its joints and to identify and chart the essence of mental disorders. Moreover, according to recent research in social psychology, some laypeople tend to think along similar essentialist lines. The main aim of this article is to highlight a number of processes that possibly explain the persistent presence and popularity (...) of essentialist conceptions of mental disorders. One such process is the general tendency of laypeople to essentialize conceptual structures, including biological, social, and psychiatric categories. Another process involves the allure of biological psychiatry. Advocating a categorical and biological approach, this strand of psychiatry probably reinforced the already existing lay essentialism about mental disorders. As such, the question regarding why we essentialize mental disorders is a salient example of how cultural trends zero in on natural tendencies, and vice versa, and how both can boost each other. (shrink)

The idea has recently taken root that evolutionary theory and social constructivism are less antagonistic than most theorists thought, and we have even seen attempts at integrating constructivist and evolutionary approaches to human thought and behaviour. We argue in this article that although the projected integration is possible, indeed valuable, the existing attempts have tended to be vague or overly simplistic about the claims of social constructivist. We proceed by examining how to give more precision and substance to the research (...) programme of evolutionary social constructivism, a task we accomplish by focusing on the specific selection pressures that may have shaped the psychological and cultural mechanisms that give rise to social constructions. The benefit of such an integration for social constructivism is to have a solid foundation in the natural sciences. For evolutionists, evolutionary social constructivism offers a wider assortment of methods with which to study the interplay between culture and human nature. (shrink)

In evolutionary medicine, researchers characterize some outcomes as evolutionary mismatch. Mismatch problems arise as the result of organisms living in environments to which they are poorly adapted, typically as the result of some rapid environmental change. Depression, anxiety, obesity, myopia, insomnia, breast cancer, dental problems, and numerous other negative health outcomes have all been characterized as mismatch problems. The exact nature of evolutionary mismatch itself is unclear, however. This leads to a lack of clarity about the sorts of problems that (...) evolutionary mismatch can actually explain. Resolving this challenge is important not only for the evolutionary health literature, but also because the notion of evolutionary mismatch involves central concepts in evolutionary biology: fitness, evolution in changing environments, and so forth. In this paper, I examine two characterizations of mismatch currently in the literature. I propose that we conceptualize mismatch as a relation between an optimal environment and an actual environment. Given an organism and its particular physiology, the optimal environment is the environment in which the organism’s fitness is maximized: in other words, the optimal environment is that in which the organism’s fitness is as high as it can possibly be. The actual environment is the environment in which the organism actually finds itself. To the extent that there is a discordance between the organism’s actual and optimal environments, there is an evolutionary mismatch. In the paper, I show that this account of mismatch gives us the right result when other accounts fail, and provides useful targets for investigation. (shrink)

A recent literature review of commentaries and ‘state of the art’ articles from researchers in psychiatric genetics (PMG) offers a consensus about progress in the science of genetics, disappointments in the discovery of new and effective treatments, and a general optimism about the future of the field. I argue that optimism for the field of psychiatric molecular genetics (PMG) is overwrought, and consider progress in the field in reference to a sample estimate of US National Institute of Mental Health funding (...) for this paradigm for the years 2008 and 2009. I conclude that the amounts of financial investment in PMG is questionable from an ethical perspective, given other research and clinical needs in the USA. (shrink)

Crespi & Badcock (C&B) convincingly argue that autism and schizophrenia are diametric malfunctions of the social brain, but their core imprinting hypothesis is less persuasive. Much of the evidence they cite is unrelated to their hypothesis, is selective, or is overstated; their hypothesis lacks a clearly explained mechanism; and it is unclear how their explanation fits in with known aspects of the disorders.

Attention-deficit/hyperactivity disorder is a neurodevelopmental disorder with a childhood prevalence of 5%. In about two-thirds of the cases, ADHD symptoms persist into adulthood and often cause significant functional impairment. Based on the results of family and twin studies, the estimated heritability of ADHD approximates 80%, suggests a significant genetic component in the etiological background of the disorder; however, the potential genetic effects on disease risk, symptom severity, and persistence are unclear. This article provides a brief review of the genome-wide and (...) candidate gene association studies with a focus on the clinical aspects, summarizing findings of ADHD disease risk, ADHD core symptoms as dimensional traits, and other traits frequently associated with ADHD, which may contribute to the susceptibility to other comorbid psychiatric disorders. Furthermore, neuropsychological impairment and measures from neuroimaging and electrophysiological paradigms, emerging as potential biomarkers, also provide a prominent target for molecular genetic studies, since they lie in the pathway from genes to behavior; therefore, they can contribute to the understanding of the underlying neurobiological mechanisms and the interindividual heterogeneity of clinical symptoms. Beyond the aforementioned aspects, throughout the review, we also give a brief summary of the genetic results, including polygenic risk scores that can potentially predict individual response to different treatment options and may offer a possibility for personalized treatment for the therapy of ADHD in the future. (shrink)

Evolutionary psychiatrists invariably consider schizophrenia to be a paradox: how come natural selection has not yet eliminated the infamous ‘genes for schizophrenia’ if the disorder simply crushes the reproductive success of its carriers, if it has been around for thousands of years already, and if it has a uniform prevalence throughout the world? Usually, the answer is that the schizophrenic genotype is subject to some kind of balancing selection: the benefits it confers would then outbalance the obvious damage it does. (...) In this paper, however, I will show that the assumptions underlying such evolutionary accounts of schizophrenia are at least implausible, and sometimes even erroneous. First of all, I will examine some factual assumptions, in particular about schizophrenia’s impact on reproductive success, its genetics, its history, and its epidemiology. Secondly, I will take a critical look at a major philosophical assumption in evolutionary psychiatric explanations of schizophrenia. Indeed, evolutionary psychiatrists take it for granted that schizophrenia is a natural kind, i.e. a bounded and objectively real entity with discrete biological causes. My refutation of this natural kind view suggests that schizophrenia is in fact a reified umbrella concept, covering a heterogeneous group of disorders. Therefore, schizophrenia, as we now know it, simply doesn’t have an evolutionary history. (shrink)

Crespi & Badcock (C&B) present an appealing and parsimonious synthesis arguing that schizophrenia and autism are differentially regulated by maternal versus paternal genomic imprinting, respectively. We argue that animal models related to schizophrenia and autism provide a useful platform to explore the mechanisms outlined by C&B. We also note that schizophrenia and autism share certain risk factors such as advanced paternal age. Apart from genomic imprinting, copy number variants related to advanced paternal age may also contribute to the differential trajectory (...) of brain development associated with autism and schizophrenia. (shrink)

The commentaries on our target article, reflect the multidisciplinary yet highly fragmented state of current studies of human social cognition. Progress in our understanding of the human social brain must come from studies that integrate across diverse analytic levels, using conceptual frameworks grounded in evolutionary biology.

In this paper, I explain why evolutionary psychiatry is not where the next revolution in psychiatry will come from. I will proceed as follows. Firstly, I will review some of the problems commonly attributed to current nosologies, more specifically to the DSM. One of these problems is the lack of a clear and consensual definition of mental disorder; I will then examine specific attempts to spell out such a definition that use the evolutionary framework. One definition that deserves particular attention, (...) is one put forward by Jerome Wakefield. Despite my sympathy for his position, I must indicate a few reasons why I think his attempt might not be able to resolve the problems related to current nosologies. I suggest that it might be wiser for an evolutionary psychiatrist to adopt the more integrative framework of “treatable conditions”. As it is thought that an evolutionary approach can contribute to transforming the way we look at mental disorders, I will provide the reader with a brief sketch of the basic tenets of evolutionary psychology. The picture of the architecture of the human mind that emerges from evolutionary psychology is thought by some to be the crucial backdrop to identifying specific mental disorders and distinguishing them from normal conditions. I will also provide two examples of how evolutionary thinking is supposed to change our thinking about some disorders. Using the case of depression, I will then show what kind of problems evolutionary explanations of particular psychopathologies encounter. In conclusion, I will evaluate where evolutionary thinking leaves us in regard to what I identify as the main problems of our current nosologies. I’ll then argue that the prospects of evolutionary psychiatry are not good. (shrink)