The conditions animals experience during the early developmental stages of their lives can have critical ongoing effects on their future health, welfare, and proper development. In this paper we draw on evolutionary theory to improve our understanding of the processes of developmental programming, particularly Predictive Adaptive Responses (PAR) that serve to match offspring phenotype with predicted future environmental conditions. When these predictions fail, a mismatch occurs between offspring phenotype and the environment, which can have long-lasting health and welfare effects. Examples (...) include metabolic diseases resulting from maternal nutrition and behavioral changes from maternal stress. An understanding of these processes and their evolutionary origins will help in identifying and providing appropriate developmental conditions to optimize offspring welfare. This serves as an example of the benefits of using evolutionary thinking within veterinary science and we suggest that in the same way that evolutionary medicine has helped our understanding of human health, the implementation of evolutionary veterinary science (EvoVetSci) could be a useful way forward for research in animal health and welfare. (shrink)

Mismatch is a prominent concept in evolutionary medicine and a number of philosophers have published analyses of this concept. The word ‘mismatch’ has been used in a diversity of ways across a range of sciences, leading these authors to regard it as a vague concept in need of philosophical clarification. Here, in contrast, we concentrate on the use of mismatch in modelling and experimentation in evolutionary medicine. This reveals a rigorous theory of mismatch within which the term ‘mismatch’ is indeed (...) used in several ways, not because it is ill-defined but because different forms of mismatch are.distinguished within the theory. Contemporary evolutionary medicine has unified the idea of ‘evolutionary mismatch’, derived from the older idea of ‘adaptive lag’ in evolution, with ideas about mismatch in development and physiology derived from the Developmental Origins of Health and Disease (DOHaD) paradigm. A number of publications in evolutionary medicine have tried to make this theoretical framework explicit. We build on these to present the theory in as simple and general a form as possible. We introduce terminology, largely drawn from the existing literature, to distinguish the different forms of mismatch. This integrative theory of mismatch captures how organisms track environments across space and time on multiple scales in order to maintain an adaptive match to the environment, and how failures of adaptive tracking lead to disease. Mismatch is a productive organising concept within this theory which helps researchers articulate how physiology, development and evolution interact with one another and with environmental change to explain health outcomes. (shrink)

In recent years, quite a few evolutionary psychologists have come to embrace a heuristic interpretation of the discipline. They claim that, no matter how methodologically incomplete, adaptive thinking works fine as a good heuristic that effectively reduces the hypothesis space by generating novel and promising hypotheses that can eventually be empirically tested. The purpose of this article is to elucidate the use of heuristics in evolutionary psychology, thereby clarifying the role adaptive thinking has to play. To that end, two typical (...) heuristic interpretations—Machery’s "bootstrap strategy" and Goldfinch’s heuristically streamlined evolutionary psychology—are examined, focusing on the relationship between adaptive thinking and heuristics. The article draws two primary conclusions. The first is that the reliability of the heuristic hypothesis generation procedure should count no less than the conclusiveness of the final testing procedure in establishing scientific facts; nature does not always get the last word. Philosophy also counts. The second is that adaptive thinking constitutes a core heuristic in evolutionary psychology that provides the discipline with its raison d'être, but this is only possible when adaptive thinking is substantiated with sufficient historical underpinnings. (shrink)

This article gives a short presentation of reflexive imperativism, the intentionalist theory of valence I developed with Max Khan Hayward. The theory says that mental states have valence in virtue of having reflexive imperative content. More precisely, mental states have positive valence (i.e., feel good) in virtue of issuing the command "More of me!", and they have negative valence (i.e., feel bad) in virtue of issuing the command "Less of me!" The article summarises the main arguments in favour of reflexive (...) imperativism and against other intentionalist treatments of valence. (shrink)

The future harbours the potential for myriad threats to the fitness of organisms, and many species prepare accordingly based on indicators of hazards. Here, we distinguish between defensive responses on the basis of sensed cues and those based on autocues generated by mental simulations of the future in humans. Whereas sensed threat cues usually induce specific responses with reference to particular features of the environment or generalized responses to protect against diffuse threats, autocues generated by mental simulations of the future (...) enable strategic preparation for hazards that may not require an immediate response. The overlap of these mechanisms makes defence effective and versatile, yet can manifest as contemporary anxiety disorders in humans. (shrink)

Defenders of evolutionary medicine claim that medical professionals and public health officials would do well to consider the role of evolutionary biology with respect to the teaching, research, and judgments pertaining to medical theory and practice. An integral part of their argument is that the human body should be understood as a bundle of evolutionary compromises. Such an appreciation, which includes a proper understanding of biological function and physiological homeostasis, would provide a crucial perspective regarding the understanding and securing of (...) human health needs currently lacking in the medical arena. (shrink)

Chomskyian claims of a genetically hard-wired and cognitively autonomous “universal grammar” are being promoted by generative linguistics as facts about language to the present day. The related doctrine of an evolutionary discontinuity in language emergence, however, is based on misconceptions about the notions of homology and preadaptation. The obvious lack of equivalence between symbolic communicative capacities in existing nonhuman primates and human language does not preclude common roots. Normal and disordered language development is strongly influenced by the genome, but there (...) is no evidence for the existence of specific genes underlying “universal grammar.” In the mature brain, stages of language processing can be distinguished and “first-pass” syntactic analyses appear to precede semantic decoding. However, this partial seriality – as well as behavioral and clinical dissociations between lexical and functional categories – can be best described, not in terms of serially activated and discrete modules, but in terms of classes of cell assemblies that differ in their distributional properties. Whereas cell assemblies involved in semantic interpretation (“content word” assemblies) are widely distributed and are generally less vulnerable to focal lesion, those involved in structural decoding (functor assemblies) are primarily distributed within the left perisylvian cortices and are selectively vulnerable to left perisylvian lesion. These distributional differences are explained in terms of the perceptuomotor components involved in the acquisition of relevant representations. The emerging “motivated” or “toposemantic” brain regional specificity can only be accommodated with “soft” and maturational versions of modularity. The failure to reproduce double dissociations in current connectionist models is due to overly simple neuroscientific assumptions, notably that of overall equipotentiality. Linguistic models should not be expected to be “implemented” in the brain, but need to be constrained by neuroscientific evidence on how biological brains function. (shrink)

Because Müiller fails to distinguish between two senses of the term “autonomy,” there is a danger that his results will be misinterpreted by both linguists and neuroscientists. Although he may very well have been successful in refuting one sense of autonomy, he may actually have helped to provide an explanation for the correctness of autonomy in its other sense.

The belief that syntax is an innate, autonomous, species-specific module is highly questionable. Syntax demonstrates the mosaic nature of evolutionary change, in that it made use of (and led to the enhancement of) numerous preexisting neurocognitive features. It is best understood as an emergent characteristic of the explosion of semantic complexity that occurred during hominid evolution.

Both autonomy and local specificity are compatible with observed interconnectivity at the cell level when considering two different levels: cell assemblies and brain systems. Early syntactic structuring processes in particular are likely to representan autonomous module in the language/brain system.

The conclusion that language is not really innate or modular is based on several fallacies. I show that the target article confuses communicative skills with linguistic abilities, and that its discussion of brain/language relations is replete with factual errors. I also criticize its attempt to contrast biological and linguistic principles. Finally, I argue that no case is made for the “alternative” approach proposed here.

Why does the practice of the siesta vary across human cultures? One explanation is that it is a form of energy conservation in environments with high temperatures and/or agricultural labor. Disease palliation and prevention represents another area where the siesta might be beneficial. A preliminary study used the Human Relations Area Files (HRAF) to examine the characteristics associated with siesta occurrence. Siestas were not statistically associated with high temperatures or agricultural labor (p>.05). They were, however, statistically associated with the occurrence (...) of malaria (p<.05) and marginally associated with parasitic and chronic infectious disease. Preliminary results suggest that siestas could be adaptive in environments with chronic infectious disease. (shrink)

This paper proposes that human expression of pain in the presence or absence of caregivers, and the detection of pain by observers, arises from evolved propensities. The function of pain is to demand attention and prioritise escape, recovery, and healing; where others can help achieve these goals, effective communication of pain is required. Evidence is reviewed of a distinct and specific facial expression of pain from infancy to old age, consistent across stimuli, and recognizable as pain by observers. Voluntary control (...) over amplitude is incomplete, and observers can better detect pain that the individual attempts to suppress rather than amplify or simulate. In many clinical and experimental settings, the facial expression of pain is incorporated with verbal and nonverbal vocal activity, posture, and movement in an overall category of pain behaviour. This is assumed by clinicians to be under operant control of social contingencies such as sympathy, caregiving, and practical help; thus, strong facial expression is presumed to constitute an attempt to manipulate these contingencies by amplification of the normal expression. Operant formulations support skepticism about the presence or extent of pain, judgments of malingering, and sometimes the withholding of caregiving and help. To the extent that pain expression is influenced by environmental contingencies, however, could equally plausibly constitute the release of suppression according to evolved contingent propensities that guide behaviour. Pain has been largely neglected in the evolutionary literature and the literature on expression of emotion, but an evolutionary account can generate improved assessment of pain and reactions to it. (shrink)

We suggest that human culture exhibits key Darwinian evolutionary properties, and argue that the structure of a science of cultural evolution should share fundamental features with the structure of the science of biological evolution. This latter claim is tested by outlining the methods and approaches employed by the principal subdisciplines of evolutionary biology and assessing whether there is an existing or potential corresponding approach to the study of cultural evolution. Existing approaches within anthropology and archaeology demonstrate a good match with (...) the macroevolutionary methods of systematics, paleobiology, and biogeography, whereas mathematical models derived from population genetics have been successfully developed to study cultural microevolution. Much potential exists for experimental simulations and field studies of cultural microevolution, where there are opportunities to borrow further methods and hypotheses from biology. Potential also exists for the cultural equivalent of molecular genetics in “social cognitive neuroscience,” although many fundamental issues have yet to be resolved. It is argued that studying culture within a unifying evolutionary framework has the potential to integrate a number of separate disciplines within the social sciences. (shrink)

The DSM-III, DSM-IV, DSM-IV-TR and ICD-10 have judiciously minimized discussion of etiologies to distance clinical psychiatry from Freudian psychoanalysis. With this goal mostly achieved, discussion of etiological factors should be reintroduced into the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. A research agenda for the DSM-V advocated the "development of a pathophysiologically based classification system". The author critically reviews the neuroevolutionary literature on stress-induced and fear circuitry disorders and related amygdala-driven, species-atypical fear behaviors of clinical severity in adult (...) humans. Over 30 empirically testable/falsifiable predictions are presented. It is noted that in DSM-IV-TR and ICD-10, the classification of stress and fear circuitry disorders is neither mode-of-acquisition-based nor brain-evolution-based. For example, snake phobia and dog phobia are clustered together. Similarly, research on blood-injection-injury-type-specific phobia clusters two fears different in their innateness: 1) an arguably ontogenetic memory-trace-overconsolidation-based fear and 2) a hardwired fear of the sight of one's blood or a sharp object penetrating one's skin. Genetic architecture-charting of fear-circuitry-related traits has been challenging. Various, non-phenotype-based architectures can serve as targets for research. In this article, the author will propose one such alternative genetic architecture. This article was inspired by the following: A) Nesse's "Smoke-Detector Principle", B) the increasing suspicion that the "smooth" rather than "lumpy" distribution of complex psychiatric phenotypes may in some cases be accounted for by oligogenic transmission, and C) insights from the initial sequence of the chimpanzee genome and comparison with the human genome by the Chimpanzee Sequencing and Analysis Consortium published in late 2005. Neuroevolutionary insights relevant to fear circuitry symptoms that primarily emerge overconsolidationally are presented. Also introduced is a human-evolution-based principle for clustering innate fear traits. The "Neuroevolutionary Time-depth Principle" of innate fears proposed in this article may be useful in the development of a neuroevolution-based taxonomic re-clustering of stress-triggered and fear-circuitry disorders in DSM-V. Four broad clusters of evolved fear circuits are proposed based on their time-depths: 1) Mesozoic circuits hardwired by wild-type alleles driven to fixation by Mesozoic selective sweeps; 2) Cenozoic circuits relevant to many specific phobias; 3) mid Paleolithic and upper Paleolithic circuits ; 4) Neolithic circuits. More importantly, the author presents evolutionary perspectives on warzone-related PTSD, Combat-Stress Reaction, Combat-related Stress, Operational-Stress, and other deployment-stress-induced symptoms. The Neuroevolutionary Time-depth Principle presented in this article may help explain the dissimilar stress-resilience levels following different types of acute threat to survival of oneself or one's progency. PTSD rates following exposure to lethal inter-group violence are usually 5-10 times higher than rates following large-scale natural disasters such as forest fires, floods, hurricanes, volcanic eruptions, and earthquakes. The author predicts that both intentionally-caused large-scale bioevent-disasters, as well as natural bioevents such as SARS and avian flu pandemics will be an exception and are likely to be followed by PTSD rates approaching those that follow warzone exposure. During bioevents, Amygdala-driven and locus-coeruleus-driven epidemic pseudosomatic symptoms may be an order of magnitude more common than infection-caused cytokine-driven symptoms. Implications for the red cross and FEMA are discussed. It is also argued that hospital phobia as well as dog phobia, bird phobia and bat phobia require re-taxonomization in DSM-V in a new "overconsolidational disorders" category anchored around PTSD. The overconsolidational spectrum category may be conceptualized as straddling the fear circuitry spectrum disorders and the affective spectrum disorders categories, and may be a category for which Pitman's secondary prevention propranolol regimen may be specifically indicated as a "morning after pill" intervention. Predictions are presented regarding obsessive-compulsive disorder and "culture-bound" acute anxiety symptoms. Also discussed are insights relevant to pseudoneurological symptoms and to the forthcoming Dissociative-Conversive disorders category in DSM-V, including what the author terms fright-triggered acute pseudo-localized symptoms. Speculations based on studies of the human abnormal-spindle-like, microcephaly-associated gene, the microcephaly primary autosomal recessive gene, and the forkhead box p2 gene are made and incorporated into what is termed "The pre-FOXP2 Hypothesis of Blood-Injection-Injury Phobia." Finally, the author argues for a non-reductionistic fusion of "distal neurobiology" with clinical "proximal neurobiology," utilizing neurological heuristics. It is noted that the value of re-clustering fear traits based on behavioral ethology, human-phylogenomics-derived endophenotypes and on ontogenomics can be confirmed or disconfirmed using epidemiological or twin studies and psychiatric genomics. (shrink)

The concept of Darwinian Happiness was coined to help people take advantage of knowledge on how evolution has shaped the brain; as processes within this organ are the main contributors to well-being. Fortuitously, the concept has implications that may prove beneficial for society: Compassionate behavior offers more in terms of Darwinian Happiness than malicious behavior; and the probability of obtaining sustainable development may be improved by pointing out that consumption beyond sustenance is not important for well-being. It is difficult to (...) motivate people to act against their own best interests. Darwinian Happiness offers a concept that, to some extent, combines the interests of the individual with the interests of society. (shrink)

After describing the disorder of psychopathy, I examine the theories and the evidence concerning the psychopaths’ deficient moral capacities. I first examine whether or not psychopaths can pass tests of moral knowledge. Most of the evidence suggests that they can. If there is a lack of moral understanding, then it has to be due to an incapacity that affects not their declarative knowledge of moral norms, but their deeper understanding of them. I then examine two suggestions: it is their deficient (...) practical reason or their stunted emotions that are at fault. The evidence supports both explanations. I conclude with an overview of the debate concerning whether they are morally or legally responsible for their actions. (shrink)

The goal of forming a science of intentional behavior requires a more richly detailed account of symbolic systems than is assumed by the authors. Cultural systems are not simply the equivalent in the ideational domain of culture of the purported Baldwin Effect in the genetic domain. © 2014 Cambridge University Press.

One can disagree with Müller that it is neurobiologically questionable to suppose that human language is innate, specialized, and species-specific, yet agree that the precise brain mechanisms controlling language in any individual will be influenced by epigenesis and genetic variability, and that the interplay between inherited and acquired aspects of linguistic capacity deserves to be investigated.

Segregated neural circuits that effect particular domain-specific behaviors can be differentiated from neuroanatomical structures implicated in many different aspects of behavior. The basal ganglionic components of circuits regulating nonlinguistic motor behavior, speech, and syntax all function in a similar manner. Hence, it is unlikely that special properties and evolutionary mechanisms are associated with the neural bases of human language.

Neurobiological models of language need a level of analysis that can account for the typical range of language phenomena. Because linguistically motivated models have been successful in explaining numerous language properties, it is premature to dismiss them as biologically irrelevant. Models attempting to unify neurobiology and linguistics need to be sensitive to both sources of evidence.

Evidence is presented from a polyglot savant to suggest that double dissociations between linguistic and nonverbal abilities are more important than Müller's target article implies. It is also argued that the special nature of syntax makes its assimilation to other aspects of language or to nonhuman communication systems radically implausible.

Müller misconstrues autonomy to mean strict locality of brain function, something quite different from the functional autonomy that linguists claim. Similarly, he misperceives the interaction of learned and innate components hypothesized in current generative models. Evidence from sign languages, Creole languages, and neurological studies of rare forms of aphasia also argues against his conclusions.

The study of signed languages has inspired scientific' speculation regarding foundations of human language. Relationships between the acquisition of sign language in apes and man are discounted on logical grounds. Evidence from the differential hreakdown of sign language and manual pantomime places limits on the degree of overlap between language and nonlanguage motor systems. Evidence from functional magnetic resonance imaging reveals neural areas of convergence and divergence underlying signed and spoken languages.

The concepts of the innateness, universality, species-specificity, and autonomy of the human language capacity have had an extreme impact on the psycholinguistic debate for over thirty years. These concepts are evaluated from several neurobiological perspectives, with an emphasis on the emergence of language and its decay due to brain lesion and progressive brain disease.Evidence of perceptuomotor homologies and preadaptations for human language in nonhuman primates suggests a gradual emergence of language during hominid evolution. Regarding ontogeny, the innate component of language (...) capacity is likely to be polygenic and shared with other developmental domains. Dissociations between verbal and nonverbal development are probably rooted in the perceptuomotor specializations of neural substrates rather than the autonomy of a grammar module. Aphasiologicaldata often assumed to suggest modular linguistic subsystems can be accounted for in terms of a neurofunctional model incorporating perceptuomotor-based regional specializationsand distributivity of representations. Thus, dissociations between grammatical functors and content words are due to different conditions of acquisition and resulting differences in neural representation. Human brains are characterized by multifactorial interindividual variability, and strict universality of functional organization is biologically unrealistic.A theoretical alternative is proposed according to which (1) linguistic specialization of brain areas is due to epigenetic and probabilistic maturational events, not to genetic ”hard-wiring,” and (2) linguistic knowledge is neurally represented in distributed cell assemblies whose topography reflects the perceptuomotor modalities involved in the acquisition and use of a given item of knowledge. (shrink)

Most attempts to craft a definition of disease seem to have tackled two tasks simultaneously: 1) trying to create a series of inclusion and exclusion criteria that correspond to medical usage of the word disease and 2) using this definition to understand the essence of what disease is. The first task has been somewhat accomplished, but cannot reach closure because the concept of “disease” is based on a prototype, not a logical category. The second task cannot be accomplished by deduction, (...) but only by understanding how the body works and what each component is for, in evolutionary detail. An evolutionary view of the origins of the body and its vulnerabilities that result in disease provides an objective foundation for recognizing pathology. Our social definition of disease will remain contentious, however, because values vary, and because the label “disease” changes judgments about the moral status of people with various conditions, and their rights to medical and social resources. (shrink)

Given that natural selection is so powerful at optimizing complex adaptations, why does it seem unable to eliminate genes (susceptibility alleles) that predispose to common, harmful, heritable mental disorders, such as schizophrenia or bipolar disorder? We assess three leading explanations for this apparent paradox from evolutionary genetic theory: (1) ancestral neutrality (susceptibility alleles were not harmful among ancestors), (2) balancing selection (susceptibility alleles sometimes increased fitness), and (3) polygenic mutation-selection balance (mental disorders reflect the inevitable mutational load on the thousands (...) of genes underlying human behavior). The first two explanations are commonly assumed in psychiatric genetics and Darwinian psychiatry, while mutation-selection has often been discounted. All three models can explain persistent genetic variance in some traits under some conditions, but the first two have serious problems in explaining human mental disorders. Ancestral neutrality fails to explain low mental disorder frequencies and requires implausibly small selection coefficients against mental disorders given the data on the reproductive costs and impairment of mental disorders. Balancing selection (including spatio-temporal variation in selection, heterozygote advantage, antagonistic pleiotropy, and frequency-dependent selection) tends to favor environmentally contingent adaptations (which would show no heritability) or high-frequency alleles (which psychiatric genetics would have already found). Only polygenic mutation-selection balance seems consistent with the data on mental disorder prevalence rates, fitness costs, the likely rarity of susceptibility alleles, and the increased risks of mental disorders with brain trauma, inbreeding, and paternal age. This evolutionary genetic framework for mental disorders has wide-ranging implications for psychology, psychiatry, behavior genetics, molecular genetics, and evolutionary approaches to studying human behavior. (Published Online November 9 2006) Key Words: adaptation; behavior genetics; Darwinian psychiatry; evolution; evolutionary genetics; evolutionary psychology; mental disorders; mutation-selection balance; psychiatric genetics; quantitative trait loci (QTL). (shrink)

Life history theory’s principle of allocation suggests that because immature organisms cannot expend reproductive effort, the major trade-off facing juveniles will be the one between survival, on one hand, and growth and development, on the other. As a consequence, infants and children might be expected to possess psychobiological mechanisms for optimizing this trade-off. The main argument of this paper is that the attachment process serves this function and that individual differences in attachment organization (secure, insecure, and possibly others) may represent (...) facultative adaptations to conditions of risk and uncertainty that were probably recurrent in the environment of human evolutionary adaptedness. (shrink)

I enlarge on the theme that the brain mechanisms required for languageand other aspects of the human mind evolved through selective changes in the regulatory genes governing growth. Extension of the period of postnatal growth increases the role of the environment in structuring the brain, and spatiotemporal programming (heterochrony) ofgrowth might explain hierarchical representation, hemispheric specialization, and perhaps sex differences.

The various behavioral disciplines model human behavior in distinct and incompatible ways. Yet, recent theoretical and empirical developments have created the conditions for rendering coherent the areas of overlap of the various behavioral disciplines. The analytical tools deployed in this task incorporate core principles from several behavioral disciplines. The proposed framework recognizes evolutionary theory, covering both genetic and cultural evolution, as the integrating principle of behavioral science. Moreover, if decision theory and game theory are broadened to encompass other-regarding preferences, they (...) become capable of modeling all aspects of decision making, including those normally considered “psychological,” “sociological,” or “anthropological.” The mind as a decision-making organ then becomes the organizing principle of psychology. (Published Online April 27 2007) Key Words: behavioral game theory; behavioral science; evolutionary theory; experimental psychology; gene-culture coevolution; rational actor model; socialization. (shrink)

Two decades ago, the eminent evolutionary biologist George C. Williams and his physician coauthor, Randolph Nesse, formulated the evolutionary medicine research program. Williams and Nesse explicitly made adaptationism a core component of the new program, which has served to undermine the program ever since, distorting its practitioners’ perceptions of evidentiary burdens and in extreme cases has served to warp practitioner’s understandings of the relationship between evolutionary benefits/detriments and medical ones. I show that the Williams and Nesse program more particularly embraces (...) the panselectionist variety of adaptationism (the empirical assumption that non-adaptive evolutionary processes are causally unimportant compared to natural selection), and argue that this has harmed the field. Panselectionism serves to conceal the enormous evidentiary hurdles that evolutionary medicine hypotheses face, making them appear stronger than they are. I use two examples of evolutionary medicine texts, on neonatal jaundice and on asthma, to show that some evolutionary medicine practitioners have allowed their fervent panselectionism to directly shape their recommendations for clinical practice. I argue that this escalation of panselectionism’s influence is inappropriate under Williams’ and Nesse original stated standards, despite being inspired by their program. I also show that the examples’ conflation of clinical and evolutionary considerations is inappropriate even under Christopher Boorse’s controversial evolution-rooted concepts of disease and health. (shrink)

Division of labour is a marked feature of multicellular organisms. Margulis proposed that the ancestors of metazoans had only one microtubule organizing center (MTOC), so they could not move and divide simultaneously. Selection for simultaneous movement and cell division had driven the division of labour between cells. However, no evidence or explanation for this assumption was provided. Why could the unicellular ancetors not have multiple MTOCs? The gain and loss of three possible strategies are discussed. It was found that the (...) advantage of one or two MTOC per cell is environment-dependent. Unicellular organisms with only one MTOC per cell are favored only in resource-limited environments without strong predatory pressure. If division of labour occurring in a bicellular organism just makes simultaneous movement and cell division possible, the possibility of its fixation by natural selection is very low because a somatic cell performing the function of an MTOC is obviously wasting resources. Evolutionary biologists should search for other selective forces for division of labour in cells. (shrink)

The language of evolutionary biology and psychology is built on concepts applicable in the first instance to individual strategic rationality but extended to the level of genetic explanation. Current discussions of mental disorders as evolutionary adaptations would apply that extended language back to the individual level, with potentially problematic moral/political implications as well as possibilities of confusion. This paper focuses on one particularly problematic area: the explanation of women's greater tendency to depression. The suggestion that there are "good evolutionary reasons" (...) for depression makes sense, and might be helpful to note in therapy, as implying that the tendency is not a defect. However, evolutionary adaptiveness should not be confused with individual or psychological adaptiveness. Besides making reference to an earlier environment, it presupposes a strategic standpoint that may not accord with the legitimate interests of the individual, as this example makes vivid. (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)

Müller's target article aims to summarize approaches to the question of how language elements (phonemes, morphemes, etc.) and rules are laid down in the brain. However, it suffers from being too vague about basic assumptions and empirical predictions of neurobiological models, and the empirical evidence available to test the models is not appropriately evaluated. (1) In a neuroscientific model of language, different cortical localizations of words can only be based on biological principles. These need to be made explicit. (2) Evidence (...) for and against word class differences could be evaluated more rigorously. (3) All (and only) humans are able to learn languages with complex syntactic structures; it is, therefore, not appropriate to deny innateness and universality of syntactic principles. The real question appears to be the following: Which neurobiological principles are the linguistic principles based on? (shrink)

Minimizing the costs that others impose upon oneself and upon those in whom one has a fitness stake, such as kin and allies, is a key adaptive problem for many organisms. Our ancestors regularly faced such adaptive problems (including homicide, bodily harm, theft, mate poaching, cuckoldry, reputational damage, sexual aggression, and the infliction of these costs on one's offspring, mates, coalition partners, or friends). One solution to this problem is to impose retaliatory costs on an aggressor so that the aggressor (...) and other observers will lower their estimates of the net benefits to be gained from exploiting the retaliator in the future. We posit that humans have an evolved cognitive system that implements this strategy – deterrence – which we conceptualize as a revenge system. The revenge system produces a second adaptive problem: losing downstream gains from the individual on whom retaliatory costs have been imposed. We posit, consequently, a subsidiary computational system designed to restore particular relationships after cost-imposing interactions by inhibiting revenge and motivating behaviors that signal benevolence for the harmdoer. The operation of these systems depends on estimating the risk of future exploitation by the harmdoer and the expected future value of the relationship with the harmdoer. We review empirical evidence regarding the operation of these systems, discuss the causes of cultural and individual differences in their outputs, and sketch their computational architecture. (shrink)

Our aim in this chapter is to draw lessons from current theory on the evolution of human cooperation for the management of contemporary commons. Evolutionary theorists have long been interested in cooperation but social scientists have documented patterns of cooperation in humans that present unusual problems for conventional evolutionary theory (and for rational choice explanations as well). Humans often cooperate with nonrelatives and are prone to cooperate in one-shot games. Cooperation is quite dependent on social institutions. We believe that this (...) last fact is the critical clue to understanding human cooperation. Models of cultural evolution suggest that group selection is a more potent force on culture than on genes. Evolutionary theory is in essence a theory of preferences in terms of rational actor theory and is thus complementary to the bounded rational choice models that underpin so much theorizing in the social sciences. Thus, the theory suggests a source for prosocial impulses, and leads to predictions about the limits of human altruism and constraints likely to be imposed upon the evolution of social institutions. We also consider the dynamics of genes as they coevolved with increasingly sophisticated cultural institutions over the long course of human evolution in the Pleistocene. We hypothesize that the long exposure of human populations to group selected cultural norms and preferences is likely to have resulted in an innate psychology adapted to living in egalitarian, cooperative societies of a few hundred to a few thousand people. We call this the tribal social instincts hypothesis. The evolution of complex societies in the past few thousand years constitutes a series of natural experiments that test this hypothesis. If it is correct, the institutions of complex societies must somehow take advantage of the prosocial elements of the tribal instincts while finessing the problem that the tribal social instincts are ill adapted to life in large, hierarchical, inegalitarian societies with extensive dominance of subordinates by elites.. (shrink)

Although natural selection might be expected to reduce the incidence and severity of disease, disease persists. Natural selection leads to increases in the mean fitness of populations and so will reduce the frequency of disease-associated alleles, but other evolutionary processes, such as mutation and gene flow, may introduce or increase the frequency of these deleterious alleles. The pleiotropic actions of genes and the epistatic interactions between them complicate the relationship between genotype and phenotype, and may result in the preservation of (...) disease-associated alleles. Deleterious alleles may also be maintained because of linkage to beneficial alleles. The inability of natural selection to eliminate diseases of aging is a reminder that fitness – success in producing progeny, or in contributing genes to the population gene pool – is not equivalent to the absence of disease. Nutritional or psychosocial cues may lead to life history strategies that maximize survival to reproductive maturity at the expense of disease later in life. Natural selection acts on genes, cells, and groups, as well as on organisms; the outcome of evolution reflects selection at different levels of biological organization. Finally, the human environment is constantly changing, largely because of the evolution of our parasites and because of changes in cultural beliefs and practices; genetic evolution is comparatively slow and lags behind environmental change. An evolutionary nosology complements traditional medical nosologies and enhances our understanding of the persistence of disease and the meaning of human variation. (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)

Müller argues that general cognitive skills and linguistic skills are not necessarily independent. However, cross-linguistic evidence from an inherited specific language disorder affecting productive rules suggests significant degrees of modularity, innateness, and universality of language. Confident claims about the overall nature of such a complex system still await more interdisciplinary research.

Much good work has been done on the evolution of human morality by focusing on how “selfish genes‘ can give rise to altruistic human beings. A richer research program is needed, however, to take into account the ambivalence of naturally evolved biopsychological motivators and the historical pluralism of human morality in religious systems. Such a program is described here. A first step is to distinguish the ultimate cause of natural selection from proximate causes that are the results of natural selection. (...) Next, some proximate causes are suggested as possible conditions of biological and emotional valuing as well as of customary social morality and individual rational ethical thought. Finally, different moral perspectives of Confucianism, Hinduism, Buddhism, and Christianity are briefly presented in order to illustrate how one might inquire about the selection of a variety of biopsychological and cultural proximate causes that enable the evolution of a plurality of religious moral systems. (shrink)