Acknowledgments 1. Culture Is Essential 2. Culture Exists 3. Culture Evolves 4. Culture Is an Adaptation 5. Culture Is Maladaptive 6. Culture and Genes Coevolve 7. Nothing about Culture Makes Sense except in the Light of Evolution.

"Unsere Literatur ist voll von Klagen über den chaotischen Zustand der Systematik der Psychosen, und jeder Psychiater weiß, daß man sich auf Grund der alten Diagnosen gar nicht genügend verständigen kann. (...) So können sich mit den alten Begriffen nicht einmal die Koryphäen der Wissenschaft verständigen, und viele Patienten tragen genau so viele Diagnosen mit sich herum, als sie Anstalten besucht haben. (...) Irrtümer hindern die Wissenschaft am meisten am Fortschreiten; sie zu beseitigen hat mehr praktischen Wert, als eine neue (...) Erkenntnis zu gewinnen. Und hier ist ein ganzes Chaos von Namen beseitigt worden, hinter denen man fälschlicherweise brauchbare Krankheitsbegriffe suchte, und ein Wald von Grenzpfählen, von denen keiner an einer natürlichen Grenze stand. (...) Mit dem Namen der Dementia praecox oder der Schizophrenie bezeichnen wir eine Psychosengruppe, die bald chronisch, bald in Schüben verläuft, in jedem Stadium Halt machen oder zurückgehen kann, aber wohl keine volle Restitutio ad integrum erlaubt. Sie wird charakterisiert durch eine spezifisch geartete, sonst nirgends vorkommende Alteration des Denkens und Fühlens und der Beziehungen zur Außenwelt.". (shrink)

Schizophrenia may not have reduced reproductive success in ancestral times as much as it does today, so explaining how genes for it evolved is more understandable given this prehistoric perspective. Ethological analysis of schizophrenia – understanding how basic emotional behaviors, such as dominance striving, are affected by the condition – might prove useful for comprehending and treating its social emotional symptoms.

Evolutionary theories of schizophrenia must account for the maintenance of putative alleles in past and present populations despite reduced fitness among the affected. Such models must also account for extant intersex and population-level variability in the expression of schizophrenia. We argue that genetic balanced-polymorphism hypotheses remain the most robust in terms of modeling and testing these processes in populations.

Sociopaths are “outstanding” members of society in two senses: politically, they draw our attention because of the inordinate amount of crime they commit, and psychologically, they hold our fascination because most ofus cannot fathom the cold, detached way they repeatedly harm and manipulate others. Proximate explanations from behavior genetics, child development, personality theory, learning theory, and social psychology describe a complex interaction of genetic and physiological risk factors with demographic and micro environmental variables that predispose a portion of the population (...) to chronic antisocial behavior. More recent, evolutionary and game theoretic models have tried to present an ultimate explanation of sociopathy as the expression of a frequency-dependent life strategy which is selected, in dynamic equilibrium, in response to certain varying environmental circumstances. This paper tries to integrate the proximate, developmental models with the ultimate, evolutionary ones, suggesting that two developmentally different etiologies of sociopathy emerge from two different evolutionary mechanisms. Social strategies for minimizing the incidence of sociopathic behavior in modern society should consider the two different etiologies and the factors that contribute to them. (shrink)

If alleles that predispose to schizophrenia have reduced Darwinian fitness, their persistence in modern times is puzzling. Burns identifies the evolutionary genetics of schizophrenia as a central issue, but his treatment of it is not clear. Recent advances in evolutionary genetics can help explain the persistence of alleles that predispose to debilitating disorders such as schizophrenia, and can buttress Burns' core argument.

Authors frequently refer to gene-based selection in biological evolution, the reaction of the immune system to antigens, and operant learning as exemplifying selection processes in the same sense of this term. However, as obvious as this claim may seem on the surface, setting out an account of “selection” that is general enough to incorporate all three of these processes without becoming so general as to be vacuous is far from easy. In this target article, we set out such a general (...) account of selection to see how well it accommodates these very different sorts of selection. The three fundamental elements of this account are replication, variation, and environmental interaction. For selection to occur, these three processes must be related in a very specific way. In particular, replication must alternate with environmental interaction so that any changes that occur in replication are passed on differentially because of environmental interaction. One of the main differences among the three sorts of selection that we investigate concerns the role of organisms. In traditional biological evolution, organisms play a central role with respect to environmental interaction. Although environmental interaction can occur at other levels of the organizational hierarchy, organisms are the primary focus of environmental interaction. In the functioning of the immune system, organisms function as containers. The interactions that result in selection of antibodies during a lifetime are between entities (antibodies and antigens) contained within the organism. Resulting changes in the immune system of one organism are not passed on to later organisms. Nor are changes in operant behavior resulting from behavioral selection passed on to later organisms. But operant behavior is not contained in the organism because most of the interactions that lead to differential replication include parts of the world outside the organism. Changes in the organism's nervous system are the effects of those interactions. The role of genes also varies in these three systems. Biological evolution is gene-based (i.e., genes are the primary replicators). Genes play very different roles in operant behavior and the immune system. However, in all three systems, iteration is central. All three selection processes are also incredibly wasteful and inefficient. They can generate complexity and novelty primarily because they are so wasteful and inefficient. Key Words: evolution; immunology; interaction; operant behavior; operant learning; replication; selection; variation. (shrink)

Multidisciplinary studies indicate that auditory hallucinations may arise from speech perception neurocircuitry without disrupted theory of mind capacities. Computer simulations of excessive pruning in speech perception neural networks provide a model for these hallucinations and demonstrate that connectivity reductions just below a “psychotogenic threshold” enhance information processing. These data suggest a process whereby vulnerability to schizophrenia is maintained in the human population despite reproductive disadvantages of this illness.

While schizophrenia may be genetically determined up to a point, neither it nor its nearest relatives offer any sort of reproductive advantage to its sufferers. Instead, from an evolutionary point of view, schizophrenia is benign – it neither promotes nor inhibits survival to reproduction. Because it is benign, its rate of occurrence should remain fairly constant over time.

Genes dance. They dance with culture. Theydance with environment. Genes act on the world through the brain, mind and behavior. Historically, psychologists, therapists,educators and most lay people have understoodgenes in the context of Gregor Mendel'sexperiments, which were only partiallyexplained to us. While many studies show thatbrain structures and behaviors have quiterobust influences from inheritance, mostbehavior is not influenced in the classic waywe were taught in our introduction to genetics– which has been revolutionized by molecularstudies and understandings that most of theimportant (...) genes of everyday life arequantitative, or polygenic.Popular culture and naïve theory has a verysimplistic view of genes. They are bad,impolite and vaguely anti-democratic if notsinister. A very simple truth exists, however.Were it not for the genes of our grandparents,no one would be reading this article.This article introduces the reader to an ideathat emerges from evolutionary psychology andbehavior genetics, which may turn our thinkinginside out. For the most part, genes are giftsof nature to solve problems, and to hedge a beton the future. Most true genetic diseases,regulated by the classic processes that Mendelobserved, are extremely rare – typically belowone in several hundred. Most of the behaviorsthat cause us grief or joy in our homes,schools and communities and with some form ofgenetic contribution happen far more often –3%, 5%, 10% or more of the time in thepopulation. If such behaviors were ``defects''harming our reproductive success, Mother Naturewould have quickly made short work of thosegenes in a handful of generations. The factthat many of the genes related to thesebehaviors and subtle changes in the brain seemto have been recent changes (pejorativelycalled by some ``mutations'') in the past fewthousand years implies that these changes are insome sense Nature's Gifts.Gifts are to be treasured, saved and perhapspassed on. Sometimes a gift may be burdensome. This paper is about reframing and explainingadvances in science in the past 10 years or so,parallel to the brain imaging studies. Themolecular studies, explored in the context ofevolutionary psychology and behavioral geneticsprovide a new model for human development,enhancing our understanding of more traditionalviews of human phylogeny and ontogeny. Thesame molecular studies, when framed in thecontext of twin, adoption and longitudinalstudies, provide new insights for parenting,schools, community and therapy. (shrink)

This paper elaborates the hypothesis that the unique demography and sociology of Ashkenazim in medieval Europe selected for intelligence. Ashkenazi literacy, economic specialization, and closure to inward gene flow led to a social environment in which there was high fitness payoff to intelligence, specifically verbal and mathematical intelligence but not spatial ability. As with any regime of strong directional selection on a quantitative trait, genetic variants that were otherwise fitness reducing rose in frequency. In particular we propose that the well-known (...) clusters of Ashkenazi genetic diseases, the sphingolipid cluster and the DNA repair cluster in particular, increase intelligence in heterozygotes. Other Ashkenazi disorders are known to increase intelligence. Although these disorders have been attributed to a bottleneck in Ashkenazi history and consequent genetic drift, there is no evidence of any bottleneck. Gene frequencies at a large number of autosomal loci show that if there was a bottleneck then subsequent gene flow from Europeans must have been very large, obliterating the effects of any bottleneck. The clustering of the disorders in only a few pathways and the presence at elevated frequency of more than one deleterious allele at many of them could not have been produced by drift. Instead these are signatures of strong and recent natural selection. (shrink)

Schizophrenia is a worldwide, prevalent disorder with a multifactorial but highly genetic aetiology. A constant prevalence rate in the face of reduced fecundity has caused some to argue that an evolutionary advantage exists in unaffected relatives. Here, I critique this adaptationist approach, and review – and find wanting – Crow's “speciation” hypothesis. In keeping with available biological and psychological evidence, I propose an alternative theory of the origins of this disorder. Schizophrenia is a disorder of the social brain, and it (...) exists as a costly trade-off in the evolution of complex social cognition. Paleoanthropological and comparative primate research suggests that hominids evolved complex cortical interconnectivity (in particular, frontotemporal and frontoparietal circuits) to regulate social cognition and the intellectual demands of group living. I suggest that the ontogenetic mechanism underlying this cerebral adaptation was sequential hypermorphosis and that it rendered the hominid brain vulnerable to genetic and environmental insults. I argue that changes in genes regulating the timing of neurodevelopment occurred prior to the migration of Homo sapiens out of Africa 100,000–150,000 years ago, giving rise to the schizotypal spectrum. While some individuals within this spectrum may have exhibited unusual creativity and iconoclasm, this phenotype was not necessarily adaptive in reproductive terms. However, because the disorder shared a common genetic basis with the evolving circuitry of the social brain, it persisted. Thus schizophrenia emerged as a costly trade-off in the evolution of complex social cognition. Key Words: cortical connectivity; evolution; heterochrony; metarepresentation; primates; psychiatry; schizophrenia; social brain; social cognition. (shrink)

Social behaviour is but an expression of instinctive mechanisms whereby the aggressive instinct is of particular importance, having given rise to most of the complexity of social behaviour through processes of phylogenetic and cultural ritualisation. The role of the aggressive instinct is to dynamically maintain the ranking order in a group, and much of social interaction is concerned with this, including monetary exchange. What is certain, is that with the elimination of aggression, … the tackling of a task or problem, (...) the self-respect [in] everything that a man does from morning till evening, from the morning shave to the sublimest artistic or scientific creation, would lose all impetus; everything associated with ambition, ranking order, and countless other equally indispensable behaviour patterns would probably also disappear from human life. — Konrad Lorenz (1963/2002, p. 269) (Published Online April 5 2006). (shrink)

Based on recent insight into the thalamocortical system and its role in perception and conscious experience, a unified pathophysiological framework for hallucinations in neurological and psychiatric conditions is proposed, which integrates previously unrelated neurobiological and psychological findings. Gamma-frequency rhythms of discharge activity from thalamic and cortical neurons are facilitated by cholinergic arousal and resonate in networks of thalamocortical circuits, thereby transiently forming assemblies of coherent gamma oscillations under constraints of afferent sensory input and prefrontal attentional mechanisms. If perception is based (...) on synchronisation of intrinsic gamma activity in the thalamocortical system, then sensory input to specific thalamic nuclei may merely play a constraining role. Hallucinations can be regarded as underconstrained perceptions that arise when the impact of sensory input on activation of thalamocortical circuits and synchronisation of thalamocortical gamma activity is reduced. In conditions that are accompanied by hallucinations, factors such as cortical hyperexcitability, cortical attentional mechanisms, hyperarousal, increased noise in specific thalamic nuclei, and random sensory input to specific thalamic nuclei may, to a varying degree, contribute to underconstrained activation of thalamocortical circuits. The reticular thalamic nucleus plays an important role in suppressing random activity of relay cells in specific thalamic nuclei, and its dysfunction may be implicated in the biological vulnerability to hallucinations in schizophrenia. Combined with general activation during cholinergic arousal, this leads to excessive disinhibition in specific thalamic nuclei, which may allow cortical attentional mechanisms to recruit thalamic relay cells into resonant assemblies of gamma oscillations, regardless of their actual sensory input, thereby producing an underconstrained perceptual experience. Key Words: Charles Bonnet syndrome; gamma oscillations; hallucinations; late paraphrenia; Lewy body dementia; perception; schizophrenia; thalamocortical system. (shrink)

1 Adaptationism is a research strategy that seeks to identify adaptations and the specific selective forces that drove their evolution in past environments. Since the mid-1970s, paleontologist Stephen J. Gould and geneticist Richard Lewontin have been critical of adaptationism, especially as applied toward understanding human behavior and cognition. Perhaps the most prominent criticism they made was that adaptationist explanations were analogous to Rudyard Kipling's Just So Stories. Since storytelling is an inherent part of science, the criticism refers to the acceptance (...) of stories without sufficient empirical evidence. In particular, Gould, Lewontin, and their colleagues argue that adaptationists often use inappropriate evidentiary standards for identifying adaptations and their functions, and that they often fail to consider alternative hypotheses to adaptation. Playing prominently in both of these criticisms are the concepts of constraint, spandrel, and exaptation. In this article we discuss the standards of evidence that could be used to identify adaptations and when and how they may be appropriately used. Moreover, building an empirical case that certain features of a trait are best explained by exaptation, spandrel, or constraint requires demonstrating that the trait's features cannot be better accounted for by adaptationist hypotheses. Thus, we argue that the testing of alternatives requires the consideration, testing, and systematic rejection of adaptationist hypotheses. Where possible, we illustrate our points with examples taken from human behavior and cognition. Key Words: adaptation; ADHD; brain allometry; constraint; epistemology; evolutionary psychology; exaptation; female orgasm ; optimization; special design; waist-hip ratio. Footnotes1 The authors contributed equally to this paper. Order of authorship was determined alphabetically. Correspondence may be addressed to any of the authors. (shrink)

The ability to be creative is often considered a unique characteristic of conscious beings and many efforts have been directed at demonstrating a relationship between creativity and the personality construct of psychoticism. The present study sought to investigate this link explicitly by focusing on discrete facets of creative cognition, namely the originality/novelty dimension and the practicality/usefulness dimension. Based on Eysenck’s conceptualisation of psychoticism as being characterised by an overinclusive cognitive style, it was expected that higher levels of psychoticism would accompany (...) a greater degree of conceptual expansion and elevated levels of originality in creative imagery, but would be unrelated to the practicality/usefulness of an idea. These hypotheses were confirmed in 80 healthy participants who were contrasted based on their EPQ psychoticism scale scores. Our findings suggest that the link between psychoticism and creativity is based on associative thinking and broader but weak top-down activation patterns rather than on goal-related thinking. (shrink)

The nature/nurture debate is not dead. Dichotomous views of development still underlie many fundamental debates in the biological and social sciences. Developmental systems theory offers a new conceptual framework with which to resolve such debates. DST views ontogeny as contingent cycles of interaction among a varied set of developmental resources, no one of which controls the process. These factors include DNA, cellular and organismic structure, and social and ecological interactions. DST has excited interest from a wide range of researchers, from (...) molecular biologists to anthropologists, because of its ability to integrate evolutionary theory and other disciplines without falling into traditional oppositions. The book provides historical background to DST, recent theoretical findings on the mechanisms of heredity, applications of the DST framework to behavioral development, implications of DST for the philosophy of biology, and critical reactions to DST. (shrink)

Lately, it seems that not a day passes without the media proclaiming yet another sensational breakthrough in the search for the physical origins of mental illness. But beyond all the fanfare and media hype, is there a single shred of hard, empirical evidence to substantiate the existence of "a gene for alcoholism," or "the brain chemistry behind schizophrenia"? More to the point, in fact, is it scientifically sound to limit the search for the roots of mental illness to processes occurring (...) within the body, while dismissing socioeconomic, familial, and experiential influences as, at best, mere "triggering mechanisms"? And, if not, what harm is being done by psychiatry's current obsession with these somatic chimeras? This groundbreaking book offers answers to those questions and more. While Dr. Ross and Professor Pam clearly assert from the outset that biological psychiatry "is dominated by a reductionist ideology which distorts and misrepresents much of its research," this is by no means a raw polemic voiced by an overzealous opposition. Instead, it is a reasoned discourse based on a clear-sighted and methodical examination of the professional literature. Contributors to this volume include distinguished researchers and clinicians from the fields of psychiatry, psychology, sociology, and psychopharmacology. Their common purpose in coming together was to alert the mental health community to the ideological blind spots and conceptual errors in the basic logic and methodology of biological psychiatry, to demonstrate the need for a more scientifically based psychiatric practice, and to suggest alternative approaches to understanding and treating mental illness. Readers will find their arguments stimulating, provocative, and highly persuasive. Among the cutting-edge issues they explore are: the historical origins of biological psychiatry; genetics and mental illness; the current state of psychiatric training; psychopharmacology and drug therapy; the public health, legal, and ethical implications of biological psychiatry; and the funding, power, and politics of research. This book is essential reading for all mental health professionals. It also has many important things to say to health care administrators, political analysts, and public policy-makers. Of related interest... INSANITY The Idea and Its Consequences Thomas Szasz In this provocative book, Dr. Thomas Szasz, one of the most celebrated and controversial psychiatric thinkers of our time, presents a carefully crafted, systematic analysis of the precise character and practical consequences of the idea of mental illness. His findings and opinions have captured the attention of organized psychiatry and given everyone concerned with the human condition a better understanding of this almost universally misunderstood "disease." 1990 (0-471-52534-0) 432 pp. CRUEL COMPASSION Psychiatric Control of Society's Unwanted Thomas Szasz Cruel Compassion is the capstone of Thomas Szasz's critique of psychiatric practices. Reexamining psychiatric interventions from a cultural-historical and political-economic perspective, Szasz demonstrates that the main problem that faces mental health policymakers today is adult dependency. He gives us a sobering look at some of our most cherished notions about our humane treatment of society's unwanted and about ourselves as a compassionate and democratic people. 1994 (0-471-01012-X) 260 pp. (shrink)

The next time you get sick, consider this before picking up the aspirin: your body may be doing exactly what it's supposed to. In this ground-breaking book, two pioneers of the science of Darwinian medicine argue that illness as well as the factors that predispose us toward it are subject to the same laws of natural selection that otherwise make our bodies such miracles of design. Among the concerns they raise: When may a fever be beneficial? Why do pregnant women (...) get morning sickness? How do certain viruses "manipulate" their hosts into infecting others? What evolutionary factors may be responsible for depression and panic disorder? Deftly summarizing research on disorders ranging from allergies to Alzheimer's, and form cancer to Huntington's chorea, Why We Get Sick, answers these questions and more. The result is a book that will revolutionize our attitudes toward illness and will intrigue and instruct lay person and medical practitioners alike. (shrink)

Causality offers the first comprehensive coverage of causal analysis in many sciences, including recent advances using graphical methods. Pearl presents a unified account of the probabilistic, manipulative, counterfactual and structural approaches to causation, and devises simple mathematical tools for analyzing the relationships between causal connections, statistical associations, actions and observations. The book will open the way for including causal analysis in the standard curriculum of statistics, artificial intelligence, business, epidemiology, social science and economics.

The 'Evolution of Cooperation' addresses a simple yet age-old question; If living things evolve through competition, how can cooperation ever emerge? Despite the abundant evidence of cooperation all around us, there existed no purely naturalistic answer to this question until 1979, when Robert Axelrod famously ran a computer tournament featuring a standard game-theory exercise called The Prisoner's Dilemma. To everyone's surprise, the program that won the tournament, named Tit for Tat, was not only the simplest but the most "cooperative" entrant. (...) This unexpected victory proved that cooperation - one might even say altruism - is mathematically possible and therefore needs no hidden hand or divine agent to create and sustain it. A great roadblock to the understanding of all sorts of behavior was at last removed. The updated edition includes an extensive new chapter on cooperation in cancer cells and among terrorist organizations. (shrink)

Second, this collection of cognitive programs evolved in the Pleistocene to solve the adaptive problems regularly faced by our hunter-gatherer ancestors-...

A model is presented to account for the natural selection of what is termed reciprocally altruistic behavior. The model shows how selection can operate -against the cheater (non-reciprocator) in the system. Three instances of altruistic behavior are discussed, the evolution of which the model can explain: (1) behavior involved in cleaning symbioses; (2) warning cries in birds: and (3) human reciprocal altruism. Regarding human reciprocal altruism, it is shown that the details of the psychological system that regulates this altruism can (...) be explained by the model. Specifically, friendship,d islike, moralistic aggression, gratitude, sympathy, trust, suspicion, trustworthiness, aspects of guilt, and some forms of dishonesty and hypocrisy can be explained as important adaptations to regulate the altruistic system. Each individual human is seen as possessing altruistic and cheating tendencies, the expression of which is sensitive to developmental variables that were selected to set the tendencies at a balance appropriate to the local social and ecological environment. (shrink)

Both scientific evidence and folklore have suggested that madness is associated with creativity, especially in the arts. Recently, more rigorous studies have confirmed to some extent these previous observations. The current view is that it is not severe and acute insanity that is related to heightened creativity, but the personality roots and soft manifestations of both schizophrenic and bipolar psychoses. The affective and cognitive peculiarities associated with schizotypic and hypomanic personalities may be preferentially related to different kinds of creative endeavours, (...) such as the sciences and arts, respectively. The connection between personality traits and creativity is produced because they share some biological-cognitive-personality features, such as cognitive disinhibition. Additionally, it has been shown that the genetic liability for both bipolar and schizophrenic psychoses is related to creativity. A prevailing hypothesis is that creativity may be one type of 'compensatory advantage' for those carrying the genes for psychosis. (shrink)