The hierarchically mechanistic mind: an evolutionary systems theory of the human brain, cognition, and behavior.

The purpose of this review was to integrate leading paradigms in psychology and neuroscience with a theory of the embodied, situated human brain, called the Hierarchically Mechanistic Mind (HMM). The HMM describes the brain as a complex adaptive system that functions to minimize the entropy of our sensory and physical states via action-perception cycles generated by hierarchical neural dynamics. First, we review the extant literature on the hierarchical structure of the brain. Next, we derive the HMM from a broader evolutionary systems theory that explains neural structure and function in terms of dynamic interactions across four nested levels of biological causation (i.e., adaptation, phylogeny, ontogeny, and mechanism). We then describe how the HMM aligns with a global brain theory in neuroscience called the free-energy principle, leveraging this theory to mathematically formulate neural dynamics across hierarchical spatiotemporal scales. We conclude by exploring the implications of the HMM for psychological inquiry.

After phrenology: Time for a paradigm shift in cognitive science.

Anderson (2014) uses an impressive, consolidating review of the literature to argue for major changes in cognitive science. Arguably, however, much of what he proposes is not particularly new. He also neglects important predictive coding approaches that call his perspective of the brain into question, and his misconstrual of evolutionary psychology devalues an influential paradigm that promises to complement his own.

Basic Emotions or Constructed Emotions: Insights From Taking an Evolutionary Perspective.

The ongoing debate between basic emotion theories (BETs) and the theory of constructed emotion (TCE) hampers progress in the field of emotion research. Providing a new perspective, here we aim to bring the theories closer together by dissecting them according to Tinbergen's four questions to clarify a focus on their evolutionary basis. On the basis of our review of the literature, we conclude that whereas BETs focus on the evolution question of Tinbergen, the TCE is more concerned with the causation of emotion. On the survival value of emotions both theories largely agree: to provide the best reaction in specific situations. Evidence is converging on the evolutionary history of emotions but is still limited for both theories-research within both frameworks focuses heavily on the causation. We conclude that BETs and the TCE explain two different phenomena: emotion and feeling. Therefore, they seem irreconcilable but possibly supplementary for explaining and investigating the evolution of emotion-especially considering their similar answer to the question of survival value. Last, this article further highlights the importance of carefully describing what aspect of emotion is being discussed or studied. Only then can evidence be interpreted to converge toward explaining emotion.

Two Different Mismatches: Integrating the Developmental and the Evolutionary-Mismatch Hypothesis.

Evolutionary psychology aims to understand the origins of the human mind, including disease. Several theories about the origins of disease have been proposed. One concerns a developmental mismatch-a mismatch might occur at the individual level between the environment experienced during childhood and the environment the adult finds herself in, possibly resulting in disease. A second theory concerns the idea of an evolutionary mismatch-humans are adapted to ancestral conditions so they might now experience a mismatch with their modern environment, possibly resulting in disease. A third theory-differential susceptibility-outlines how genetic and epigenetic differences influence the extent to which humans are susceptible to rearing, including positive and negative experiences. Because of these differences, some individuals are more prone to develop disease than others. We review empirical studies that substantiate these theories and argue that an overarching theory that integrates these three lines into one provides a more accurate understanding of disease from an evolutionary perspective.

Emotion recognition in nonhuman primates: How experimental research can contribute to a better understanding of underlying mechanisms.

Recognising conspecifics' emotional expressions is important for nonhuman primates to navigate their physical and social environment. We address two possible mechanisms underlying emotion recognition: emotional contagion, the automatic matching of the observer's emotions to the emotional state of the observed individual, and cognitive empathy, the ability to understand the meaning and cause of emotional expressions while maintaining a distinction between own and others' emotions. We review experimental research in nonhuman primates to gain insight into the evolution of emotion recognition. Importantly, we focus on how emotional contagion and cognitive empathy can be studied experimentally. Evidence for aspects of cognitive empathy in different nonhuman primate lineages suggests that a wider range of primates than commonly assumed can infer emotional meaning from emotional expressions. Possibly, analogous rather than homologous evolution underlies emotion recognition. However, conclusions regarding its exact evolutionary course require more research in different modalities and species.

The social instability stress paradigm in rat and mouse: A systematic review of protocols, limitations, and recommendations.

BACKGROUND: Social stress is an important environmental risk factor for the development of psychiatric disorders, including depression and anxiety disorders. Social stress paradigms are commonly used in rats and mice to gain insight into the pathogenesis of these disorders. The social instability stress (SIS) paradigm entails frequent (up to several times a week) introduction of one or multiple unfamiliar same-sex home-cage partners. The subsequent recurring formation of a new social hierarchy results in chronic and unpredictable physical and social stress. PURPOSE: We compare and discuss the stress-related behavioral and physiological impact of SIS protocols in rat and mouse, and address limitations due to protocol variability. We further provide practical recommendations to optimize reproducibility of SIS protocols. METHODS: We conducted a systematic review in accordance with the PRISMA statement in the following three databases: PubMed, Web of Science and Scopus. Our search strategy was not restricted to year of publication but was limited to articles in English that were published in peer-reviewed journals. Search terms included "social* instab*" AND ("animal" OR "rodent" OR "rat*" OR "mice" OR "mouse"). RESULTS: Thirty-three studies met our inclusion criteria. Fifteen articles used a SIS protocol in which the composition of two cage mates is altered daily for sixteen days (SIS16D). Eleven articles used a SIS protocol in which the composition of four cage mates is altered twice per week for 49 days (SIS49D). The remaining seven studies used SIS protocols that differed from these two protocols in experiment duration or cage mate quantity. Behavioral impact of SIS was primarily assessed by quantifying depressive-like, anxiety-like, social-, and cognitive behavior. Physiological impact of SIS was primarily assessed using metabolic parameters, hypothalamus-pituitary-adrenal axis activity, and the assessment of neurobiological parameters such as neuroplasticity and neurogenesis. CONCLUSION: Both shorter and longer SIS protocols induce a wide range of stress-related behavioral and physiological impairments that are relevant for the pathophysiology of depression and anxiety disorders. To date, SIS16D has only been reported in rats, whereas SIS49D has only been reported in mice. Given this species-specific application as well as variability in reported SIS protocols, additional studies should determine whether SIS effects are protocol duration- or species-specific. We address several issues, including a lack of consistency in the used SIS protocols, and suggest practical, concrete improvements in design and reporting of SIS protocols to increase standardization and reproducibility of this etiologically relevant preclinical model of social stress.

Nonlinear epigenetic variance: review and simulations.

We present a review of empirical evidence that suggests that a substantial portion of phenotypic variance is due to nonlinear (epigenetic) processes during ontogenesis. The role of such processes as a source of phenotypic variance in human behaviour genetic studies is not fully appreciated. In addition to our review, we present simulation studies of nonlinear epigenetic variance using a computational model of neuronal network development. In each simulation study, time series for monozygotic and dizygotic twins were generated and analysed using conventional behaviour genetic modelling. In the results of these analyses, the nonlinear epigenetic variance was subsumed under the non-shared environmental component. As is commonly found in behaviour genetic studies, observed heritabilities and unique environmentabilities increased with time, whereas common environmentabilities decreased. The fact that the phenotypic effects of nonlinear epigenetic processes appear as unsystematic variance in conventional twin analyses complicates the identification and quantification of the ultimate genetic and environmental causes of individual differences. We believe that nonlinear dynamical system theories provide a challenging perspective on the development of individual differences, which may enrich behaviour genetic studies.

Why did the savant syndrome not spread in the population? A psychiatric example of a developmental constraint.

A developmental constraint is a mechanism that limits the possibility of a phenotype to evolve. There is growing evidence for the existence of developmental constraints in the biological literature. We hypothesize that a developmental constraint prevents the savant syndrome, despite its positive aspects, from spreading in the population. Here, the developmental constraint is the result of the high interactivity among body parts in an early stage in embryological development, namely early organogenesis or the phylotypic stage. The interactivity during this stage involves all components of the embryo, and as a result mutations that affect one part of the embryo also affect other parts. We hypothesize that a mutation, which gives rise to the development of the positive aspects of the savant syndrome (e.g., an impressive memory capacity), will virtually always have a deleterious effect on the development of other phenotypic traits (e.g., resulting in autism and/or impaired motor coordination). Thus, our hypothesis states that the savant syndrome cannot spread in the population because of this developmental constraint. The finding that children with savant syndrome often have autism and physical anomalies, which are known to be established during early organogenesis, supports our hypothesis.

The dot-probe task to measure emotional attention: A suitable measure in comparative studies?

For social animals, attending to and recognizing the emotional expressions of other individuals is of crucial importance for their survival and likely has a deep evolutionary origin. Gaining insight into how emotional expressions evolved as adaptations over the course of evolution can be achieved by making direct cross-species comparisons. To that extent, experimental paradigms that are suitable for investigating emotional processing across species need to be developed and evaluated. The emotional dot-probe task, which measures attention allocation toward emotional stimuli, has this potential. The task is implicit, and subjects need minimal training to perform the task successfully. Findings in nonhuman primates, although scarce, show that they, like humans, have an attentional bias toward emotional stimuli. However, the wide literature on human studies has shown that different factors can have important moderating effects on the results. Due to the large heterogeneity of this literature, these moderating effects often remain unnoticed. We here review this literature and show that subject characteristics and differences in experimental designs affect the results of the dot-probe task. We conclude with specific recommendations regarding these issues that are particularly relevant to take into consideration when applying this paradigm to study animals.

Emotion processing deficits: a liability spectrum providing insight into comorbidity of mental disorders.

Epidemiological studies have revealed that mental disorders are highly comorbid; almost half of the people with a mental disorder also meet the criteria of another disorder. The explanation of this high comorbidity has remained a scientific puzzle. We propose 'disrupted emotion processing' as a liability spectrum that underlies many different mental disorders. Emotion processing deficits have been reported in different disorders and result in difficulties in regulating emotions and at the perceptual level in attentional biases and impaired recognition of emotional expressions. This article provides a detailed overview of the literature on disrupted emotion processing in clinical groups on the behavioral and neurological level. In the discussion, the similarities and differences between these disorders are discussed in the context of common neuro-endocrine, genetic and environmental factors and ideas are put forward on how future research may advance. Most importantly, more interdisciplinary research is needed in which different techniques, tasks and clinical populations are combined to get a better understanding of disrupted emotion processing as a liability spectrum underlying various different mental disorders.

Stochastic catastrophe analysis of switches in the perception of apparent motion.

Dynamical phenomena such as bistability and hysteresis have been found in a number of studies on perception of apparent motion. We show that new developments in stochastic catastrophe theory make it possible to test models of these phenomena empirically. Catastrophe theory explains discontinuous changes in responses caused by continuous changes in experimental parameters. We propose catastrophe models for two experimental paradigms on perception of apparent motion and present experiments that support these models. We test these models by using an algorithm for fitting stochastic catastrophe models. We derive from catastrophe theory the prediction that a dynamical phenomenon called divergence is necessary when hysteresis is found. This new prediction is supported by the data.

Cognition and the evolution of music: pitfalls and prospects.

What was the role of music in the evolutionary history of human beings? We address this question from the point of view that musicality can be defined as a cognitive trait. Although it has been argued that we will never know how cognitive traits evolved (Lewontin, 1998), we argue that we may know the evolution of music by investigating the fundamental cognitive mechanisms of musicality, for example, relative pitch, tonal encoding of pitch, and beat induction. In addition, we show that a nomological network of evidence (Schmitt & Pilcher, 2004) can be built around the hypothesis that musicality is a cognitive adaptation. Within this network, different modes of evidence are gathered to support a specific evolutionary hypothesis. We show that the combination of psychological, medical, physiological, genetic, phylogenetic, hunter-gatherer, and cross-cultural evidence indicates that musicality is a cognitive adaptation.

Evolutionary approaches to autism- an overview and integration.

Autism is a highly heritable neurodevelopmental disorder, which greatly reduces reproductive success. The combination of high heritability and low reproductive success raises an evolutionary question: why was autism not eliminated by natural selection? We review different perspectives on the evolution of autism and propose an integration which emphasizes epistatic interactions between the effects of genes during development. It is well-established that autism is a polygenic disorder, and that the genes contributing to autism interact. If a disorder is polygenic, it is likely that the genes underlying the disorder are also involved in traits that are beneficial for the individual. For example, it is possible that genes involved in the development of autism are also involved in the development of intelligence. As intelligence is positively correlated with reproductive success, genes involved in autism can possibly spread in the population. We propose that in most individuals, the interactions between genes result in normal or high intelligence and the absence of autism. However, in some unlucky situations, often in combination with spontaneous negative mutations, the interactions between genes can lead to the development of autism (or other pathologies). Thus, the combination of high heritability and low reproductive success in autism can be explained from an evolutionary developmental perspective that emphasizes the role of epistatic interactions in polygenic disorders.

Evo Devo and cognitive science.

Evo Devo (evolutionary developmental) biology forges a synthesis of evolutionary and developmental processes. Evo Devo is the result of collaborative work of evolutionary and developmental biologists after the discovery of regulatory genes that human beings share with many other animals, including fruit flies, frogs, and rats. Compared to traditional evolutionary biologists, Evo Devo biologists focus on processes underlying the generation of evolutionary novelties, rather than on how natural selection changes gene frequencies in populations and how organisms are adapted to their environment. Evo Devo biologists try to answer questions such as: How do novel structures arise? Which mechanisms facilitate or constrain evolutionary change? In this article we argue that insights from Evo Devo research can contribute to the understanding of the evolution and development of cognition, and of the origin of neurocognitive disorders. We discuss three major Evo Devo topics: modularity, evolvability, and developmental constraints. We argue that each of these topics are relevant for research in cognitive science, and we argue that interdisciplinary research is necessary in order to unravel the evolutionary and developmental mechanisms of cognitive traits and disorders. WIREs Cogni Sci 2011 2 429-440 DOI: 10.1002/wcs.137 For further resources related to this article, please visit the WIREs website.

The association between autism and errors in early embryogenesis: what is the causal mechanism?

The association between embryonic errors and the development of autism has been recognized in the literature, but the mechanism underlying this association remains unknown. We propose that pleiotropic effects during a very early and specific stage of embryonic development-early organogenesis-can explain this association. In humans early organogenesis is an embryonic stage, spanning Day 20 to Day 40 after fertilization, which is characterized by intense interactivity among body parts of the embryo. This implies that a single mutation or environmental disturbance affecting development at this stage can have several phenotypic effects (i.e., pleiotropic effects). Disturbances during early organogenesis can lead to many different anomalies, including limb deformities, craniofacial malformations, brain pathology, and anomalies in other organs. We reviewed the literature and found ample evidence for the association between autism and different kinds of physical anomalies, which agrees with the hypothesis that pleiotropic effects are involved in the development of autism. The proposed mechanism integrates findings from a variety of studies on autism, including neurobiological studies and studies on physical anomalies and prenatal influences on neurodevelopmental outcomes. The implication is that the origin of autism can be much earlier in embryologic development than has been frequently reported.

Identification of everyday objects on the basis of silhouette and outline versions.

Line drawings of everyday objects were modified into silhouettes by filling-in the complete area enclosed by boundary contours, and outline versions were created by extracting the contours from the silhouettes. A large number of participants was asked to try to identify these silhouette and outline versions in experiment 1. Identifiability ranged from 0% to 100% correct responses with a large range in-between. Several kinds of errors and several reasons for difficulties with identification emerged in our data set. In experiment 2, we compared the original identification rates to those of inverted silhouettes (white figures on a black background), and in experiment 3 we compared the original identification rates of objects with filled-in holes or background parts to those of versions without filling-in. These stimuli and identification norms are useful for additional research on priming and context effects of object identification, neuropsychological deficits of object identification, and all kinds of studies with silhouettes where the role of top down knowledge could be of interest.

Linking dynamical perceptual decisions at different levels of description in motion pattern formation: psychophysics.

The relationship between local-level motion detection and higher level pattern-forming mechanisms was investigated with the motion quartet, a bistable stimulus for which either horizontal or vertical motion patterns are perceived. Local-level perturbations in luminance contrast affected the stability of the perceived patterns and, thereby, the size of the pattern-level hysteresis obtained by gradually changing the motion quartet's aspect ratio. Briefly eliminating luminance contrast (so nonmotion was perceived during the perturbation) eliminated pattern-level hysteresis, and briefly increasing luminance contrast (so motion was perceived during the perturbation) increased pattern-level hysteresis. Partially reducing luminance contrast resulted in bistability during the perturbation; pattern-level hysteresis was maintained when motion was perceived, and eliminated when nonmotion was perceived. The results were attributed to local motion/nonmotion perceptual decisions in area V1 affecting the magnitude of the activation feeding forward to motion detectors in area MT, where the stability of pattern-level perceptual decisions is determined by activation-dependent, future-shaping interactions that inhibit soon-to-be-stimulated detectors responsive to competing motion directions.