ABSTRACT
I describe an integrative social‐evolutionary model for the adaptive significance of the human oxytocinergic system. The model is based on a role for this hormone in the generation and ...maintenance of social familiarity and affiliation across five homologous, functionally similar, and sequentially co‐opted contexts: mothers with offspring, female and male mates, kin groups, individuals with reciprocity partners, and individuals within cooperating and competing social groups defined by culture. In each situation, oxytocin motivates, mediates and rewards the cognitive and behavioural processes that underlie the formation and dynamics of a more or less stable social group, and promotes a relationship between two or more individuals. Such relationships may be positive (eliciting neurological reward, reducing anxiety and thus indicating fitness‐enhancing effects), or negative (increasing anxiety and distress, and thus motivating attempts to alleviate a problematic, fitness‐reducing social situation). I also present evidence that testosterone exhibits opposite effects from oxytocin on diverse aspects of cognition and behaviour, most generally by favouring self‐oriented, asocial and antisocial behaviours. I apply this model for effects of oxytocin and testosterone to understanding human psychological disorders centrally involving social behaviour. Reduced oxytocin and higher testosterone levels have been associated with under‐developed social cognition, especially in autism. By contrast, some combination of oxytocin increased above normal levels, and lower testosterone, has been reported in a notable number of studies of schizophrenia, bipolar disorder and depression, and, in some cases, higher oxytocin involves maladaptively ‘hyper‐developed’ social cognition in these conditions. This pattern of findings suggests that human social cognition and behaviour are structured, in part, by joint and opposing effects of oxytocin and testosterone, and that extremes of such joint effects partially mediate risks and phenotypes of autism and psychotic‐affective conditions. These considerations have direct implications for the development of therapies for alleviating disorders of social cognition, and for understanding how such disorders are associated with the evolution of human cognitive‐affective architecture.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
2.
Pattern Unifies Autism Crespi, Bernard
Frontiers in psychiatry,
02/2021, Volume:
12
Journal Article
Peer reviewed
Open access
Autism is a highly heterogeneous condition, genetically and phenotypically. This diversity of causation and presentation has impeded its definition, recognition, assessment, and treatment. Current ...diagnostic criteria for autism involve two domains, restricted interests and repetitive behavior (RRBs) and social deficits, whose relationship remains unclear. I suggest that the large suite of traits associated with autism can be usefully conceptualized under the single rubric of "pattern," a term that connects autism with basic brain and cognitive functions and structures its phenotypes within a single theoretical framework. Autism thus involves increases and enhancements to pattern perception, pattern recognition, pattern maintenance, pattern generation, pattern processing, and pattern seeking. RRBs result from increased and imbalanced pattern-related perception and cognition, and social alterations result in part from the usual lack of clear pattern in social interactions, combined with the interference of RRBs with social development. This framework has strong implications for assessment of social and non-social autism-related traits, personalized therapy, and priorities for research.
A suite of recent studies has reported positive genetic correlations between autism risk and measures of mental ability. These findings indicate that alleles for autism overlap broadly with alleles ...for high intelligence, which appears paradoxical given that autism is characterized, overall, by below-average IQ. This paradox can be resolved under the hypothesis that autism etiology commonly involves enhanced, but imbalanced, components of intelligence. This hypothesis is supported by convergent evidence showing that autism and high IQ share a diverse set of convergent correlates, including large brain size, fast brain growth, increased sensory and visual-spatial abilities, enhanced synaptic functions, increased attentional focus, high socioeconomic status, more deliberative decision-making, profession and occupational interests in engineering and physical sciences, and high levels of positive assortative mating. These findings help to provide an evolutionary basis to understanding autism risk as underlain in part by dysregulation of intelligence, a core human-specific adaptation. In turn, integration of studies on intelligence with studies of autism should provide novel insights into the neurological and genetic causes of high mental abilities, with important implications for cognitive enhancement, artificial intelligence, the relationship of autism with schizophrenia, and the treatment of both autism and intellectual disability.
Recent advances in genetics, and new applications of evolutionary biology, are transforming psychology and psychiatry. The purpose of this article is to review and synthesize the progress in these ...two areas that is most salient to the practice of clinical psychology. First, I describe how the results of genome-wide studies have elucidated the genetic architectures of psychiatric disorders. These genetic results can be applied to generate polygenic risk scores, identify rare causal mutations, evaluate gene by environment interactions, and help determine the specific causes of psychiatric disorders for each individual, all of which can help to guide therapies and treatments. Second, I explain how evolutionary theory, applied to human development, the human psyche, and mental disorders, leads to novel insights relevant to therapy. Evolutionary thinking for psychiatry and psychology is consilient with contemporary schools of thought in clinical psychology, but also provides novel, non-intuitive, and clinically-useful insights. Effects of the genome in development, and functioning of the adult psyche, are both usefully conceived as dynamical, non-linear systems, regulated by feedbacks, that can become disordered in predictable yet individualistic ways. The merging of genetic, neurological, psychological, and evolutionary approaches is set to transform clinical psychology and psychiatry, but requires increased emphasis on cross-disciplinary thinking and research.
•Advances in integrating evolution and genetics with clinical psychology are described.•Genomics provides insights into mental disorders that are relevant to therapy.•Evolutionary thinking clarifies the clinical treatment of mental disorders.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Neural exaptations represent descent via transitions to novel neural functions. A primary transition in human cognitive and neural evolution was from a predominantly socially oriented primate brain ...to a brain that also instantiates and subserves science, technology, and engineering, all of which depend on mathematics. Upon what neural substrates and upon what evolved cognitive mechanisms did human capacities for science, technology, engineering, and mathematics (STEM), and especially its mathematical underpinnings, emerge? Previous theory focuses on roles for tools, language, and arithmetic in the cognitive origins of STEM, but none of these factors appears sufficient to support the transition.
In this article, I describe and evaluate a novel hypothesis for the neural origins and substrates of STEM-based cognition: that they are based in human kinship systems and human maximizing of inclusive fitness.
The main evidence for this hypothesis is threefold. First, as demonstrated by anthropologists, human kinship systems exhibit complex mathematical and geometrical structures that function under sets of explicit rules, and such systems and rules pervade and organize all human cultures. Second, human kinship underlies the core algebraic mechanism of evolution, maximization of inclusive fitness, quantified as personal reproduction plus the sum of all effects on reproduction of others, each multiplied by their coefficient of relatedness to self. This is the only "natural" equation expected to be represented in the human brain. Third, functional imaging studies show that kinship-related cognition activates frontal-parietal regions that are also activated in STEM-related tasks. In turn, the decision-making that integrates kinship levels with costs and benefits from alternative behaviors has recently been shown to recruit the lateral septum, a hub region that combines internal (from the prefrontal cortex, amygdala, and other regions) and external information relevant to social behavior, using a dedicated subsystem of neurons specific to kinship.
Taken together, these lines of evidence suggest that kinship systems and kin-associated behaviors may represent exaptations for the origin of human STEM.
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.
A remarkable suite of forms of genomic conflict has recently been implicated in speciation. We propose that these diverse roles of genomic conflict in speciation processes can be unified using the ...concept of ‘conflictual speciation’. Conflictual speciation centers on the evolution of reproductive isolation as a byproduct of antagonistic selection among genomic elements with divergent fitness interests. Intragenomic conflicts are expected to readily generate Dobzhansky–Muller incompatibilities, due to population-specific interactions between opposing elements, and thus they could be especially important in speciation. Moreover, selection from genomic conflicts should be relatively unrelenting across ecological and evolutionary time scales. We explain how intragenomic conflicts can promote, or sometimes constrain, speciation, and describe evidence relating conflicts to the evolution of reproductive isolation.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Asexuality is rare in animals in spite of its apparent advantage relative to sexual reproduction, indicating that it must be associated with profound costs
1–9. One expectation is that reproductive ...advantages gained by new asexual lineages will be quickly eroded over time
3, 5–7. Ancient asexual taxa that have evolved and adapted without sex would be “scandalous” exceptions to this rule, but it is often difficult to exclude the possibility that putative asexuals deploy some form of “cryptic” sex, or have abandoned sex more recently than estimated from divergence times to sexual relatives
10. Here we provide evidence, from high intraspecific divergence of mitochondrial sequence and nuclear allele divergence patterns, that several independently derived
Timema stick-insect lineages have persisted without recombination for more than a million generations. Nuclear alleles in the asexual lineages displayed significantly higher intraindividual divergences than in related sexual species. In addition, within two asexuals, nuclear allele phylogenies suggested the presence of two clades, with sequences from the same individual appearing in both clades. These data strongly support ancient asexuality in
Timema and validate the genus as an exceptional opportunity to attack the question of how asexual reproduction can be maintained over long periods of evolutionary time.
► The genus
Timema comprises at least seven independently derived asexual lineages ► Nuclear alleles in asexuals display higher divergence levels than in sexual species ► At least two asexual lineages have persisted for more than 1,000,000 generations
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
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Trade-offs between advantageous but conflicting properties (e.g., speed vs. accuracy) are ubiquitous in cognition, but the relevant literature is conceptually fragmented, scattered ...across disciplines, and has not been organized in a coherent framework. This paper takes an initial step toward a general theory of cognitive trade-offs by examining four key properties of goal-directed systems: performance, efficiency, robustness, and flexibility. These properties define a number of basic functional trade-offs that can be used to map the abstract “design space” of natural and artificial cognitive systems. Basic functional trade-offs provide a shared vocabulary to describe a variety of specific trade-offs including speed vs. accuracy, generalist vs. specialist, exploration vs. exploitation, and many others. By linking specific features of cognitive functioning to general properties such as robustness and efficiency, it becomes possible to harness some powerful insights from systems engineering and systems biology to suggest useful generalizations, point to under-explored but potentially important trade-offs, and prompt novel hypotheses and connections between disparate areas of research.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
10.
The hallmarks of autism Crespi, Bernard J.
Frontiers in psychiatry,
08/2022, Volume:
13
Journal Article
Peer reviewed
Open access
I suggest that the current study of autism is problematic, due to: (1) its failure to pursue a medical model of disease causation, with protocols for differential diagnoses of causes; (2) a notable ...incidence of unrecognized false positive diagnoses in children; (3) the conceptual equating of autism with sets of traits that have been shown to be genetically and phenotypically unrelated to one another; and (4) the expansion of use of the terms “autism” and “autism traits” to psychiatric conditions that have no substantive etiological or symptomatic overlap with autism. These problems can be alleviated by, like Kanner, considering autism as a syndrome, a constellation of traits, conceptualized as differences rather than deficits, some set of which is found in each affected individual to some degree. The original, prototypical form of autism can be delineated based on the “hallmarks” of autism: a set of core traits, originally explicated by Kanner, that defines a relatively-homogeneous group, and that connects with the larger set of autism symptoms. The hallmarks of autism provide a touchstone for research that is unambiguous, historically continuous to the present, and linked with major theories for explaining the causes and symptoms of autism. Use of the hallmarks of autism does not impact recognition and treatment of individuals with DSM diagnosed autism, or individuals with the many disorders that involve social deficits. This perspective is compatible with the research domain criteria approach to studying autism,
via
analyses of autism's constituent traits and the differential diagnosis of its individual-specific causes.
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