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The Evolutionary Etiologies of Autism Spectrum and Psychotic Affective Spectrum Disorders

May 2016

May 2016

DOI:10.1007/978-3-319-29716-3_20

In book: Evolutionary Thinking in Medicine (pp.299-327)

Authors:

Bernard J Crespi

Simon Fraser University

Risks of human psychiatric conditions have evolved, and their symptoms represent perturbations to adaptive cognitive and affective systems. Evolutionary considerations are useful in this context because they direct us to the identification of specific human adaptations that become dysregulated in disease, though either underdevelopment or overdevelopment. Autism is thus conceptualized in terms of underdeveloped social cognition, such that the highly elaborated human social brain does not complete its usual developmental trajectory. Psychotic affective conditions, mainly schizophrenia, bipolar disorder, and depression, are, in contrast to autism, conceptualized in terms of dysfunctionally overdeveloped aspects of social cognition, such that they are caused by opposite neural system alterations to those producing autism. The hypothesis that autism and psychotic affective conditions represent diametric disorders is supported by a wide range of convergent evidence from genetics, development, neuroscience, psychology, and cognitive science. The diametric model provides for reciprocal illumination of the causes of these conditions and makes specific recommendations for research strategies and the development of novel treatments.

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"Evolutionary thinking in medicine: from research to policy and practice", Oxford University Press,

edited by A. Alvergne, C. Jenkinson and C. Faurie. April 2016.

The Evolutionary Etiologies of Autism Spectrum and Psychotic-Affective Spectrum Disorders

Bernard J Crespi

Department of Biological Sciences

Simon Fraser University

Burnaby British Columbia, Canada V5A 1S6

crespi@sfu.ca

Abstract

Risks of human psychiatric conditions have evolved, and their symptoms represent perturbations to

adaptive cognitive and affective systems. Evolutionary considerations are useful in this context

because they direct us to the identification of specific human adaptations that become dysregulated

in disease, though either underdevelopment or overdevelopment. Autism is thus conceptualized in

terms of underdeveloped social cognition, such that the highly-elaborated human social brain does

not complete its usual developmental trajectory. Psychotic-affective conditions, mainly schizophrenia,

bipolar disorder, and depression, are, in contrast to autism, conceptualized in terms of dysfunctionally

over-developed aspects of social cognition, such that they are caused by opposite neural-system

alterations to those producing autism. The hypothesis that autism and psychotic-affective conditions

represent diametric disorders is supported by a wide range of convergent evidence from genetics,

development, neuroscience, psychology, and cognitive science. The diametric model provides for

reciprocal illumination of the causes of these conditions, and makes specific recommendations for

research strategies and the development of novel treatments.

Lay Summary

The mental and behavioral traits that have evolved in humans, such as complex sociality, make us

vulnerable to corresponding mental disorders, such as disorders that involve too little, or too much,

social thinking. Autism can be considered as a disorder where complex sociality does not develop,

while schizophrenia, bipolar disorder, and depression can be considered as the opposite:

pathologically over-developed social thought and behavior, as seen for example in paranoia and

hearing voices. Evolutionary biology is fundamentally important in understanding, defining and

treating mental disorders because it helps us to determine what the brain has evolved to do, which

informs us about the different ways that brain functions can become dysregulated in disease.

I. Introduction

The standard medical model and the reification of psychiatric disorders

The standard medical model for understanding and treating disease focuses on determining its

proximate physiological and developmental causes, in terms of how functional systems have become

dysregulated (Nesse and Stein 2012). High blood glucose levels, for example, may be due to type 1

diabetes, which results from specific, well-characterized physiological and molecular-biological

causes, and, as a result, can be unambiguously diagnosed. Understanding the normal functioning of

blood glucose regulation, or any other physiological system, thus represents a key precondition to

determining etiology and effective treatments.

How can the standard medical model be applied to psychiatric disorders? Diabetes is real, meaning

here that its presence can be objectively and unequivocally quantified. By contrast, psychiatric

disorders like autism and schizophrenia are not real, because the causes and patterns of brain

functions that underlie them are only dimly understood. Psychiatric disorders are, instead, abstract,

heuristic, descriptive constructs that are more or less useful for guiding research, diagnoses, and

treatments. The clearest evidence for such artificiality is the Diagnostic and Statistical Manual of

Mental Disorders (DSM) criteria for diagnosing psychiatric disorders, which comprise detailed lists of

symptoms, some set of which are considered necessary and sufficient to infer the presence of

disease.

Despite these considerations, it is commonplace for psychiatric conditions to be reified - that is -

considered as real, for research, medical and societal purposes (Crespi 2011). Such pragmatic

reification can be considered as innocuous, but it is not: it constrains and biases how researchers

think about mental disorders, and their associated research agendas, and leads to misconceptions of

psychiatric disorders as objectively-defined, purely-pathological 'diseases' that people 'have',

comparable in some fundamental way to diseases like diabetes, cancer, or atherosclerosis that can

be objectively and physiologically quantified in terms of their causes and effects.

Under current paradigms, determining the 'causes' of mental disorders often becomes conflated with

characterizing mental pathologies or deficits, at levels from genes, to neurodevelopment and

function, to cognitive functions, and to deleterious environments. By contrast, according to the

standard medical model, mental disorders should instead be conceptualized, and analyzed, in terms

of what functional mental systems have become dysregulated, and what forms such dysregulations

take. In this regard, for example, to better-understand autism we must also better-understand the

development of neurotypical social cognition, and to understand bipolar disorder and depression, we

must also understand the adaptive functions of normal, contextual variation in mood.

The evolution of mental adaptations

Adaptive functions of the human mind and brain, like those of glucose regulation, have, of course,

evolved. Most generally, this meaning of 'adaptive' means that such systems show, and have for

many, many past generations shown, genetically-based variation among individuals that has

influenced survival and reproduction. Such variation has thus been subject to natural selection,

which leads, across generations, to increases in, or maintenance of, the adaptive 'fit' or 'match'

between organismal phenotypes and aspects of their environments. For example, the beaks of

Darwin’s finches are ‘fit’ in their sizes and shapes for different food sources. Similarly, specific

regions of the human neocortex adaptively function to recognize individual faces (the fusiform gyrus),

or to infer the thoughts and intentions of other humans (the medial prefrontal cortex). Specific mental

adaptations, like the insulin pathway, are real and quantifiable, and the subject of intense interest in

disciplines such as cognitive neuroscience.

Natural selection of human physiology and morphology is expected, under basic evolutionary

considerations, to have led to maximization of functional robustness, homeostatic ability, and

efficiency, as well as optimal flexibility under variable circumstances, all in the service of survival and

reproduction. But what, then, is natural selection – the driver of adaptation – expected to maximize

with regard to human cognition, emotion and behavior? We usually think of mental disorders as

centrally involving unhappiness, of the subject as well as their social circle, which motivates the

seeking of help from the medical community. However, natural selection is by no means expected to

maximize happiness, simply because increased happiness is by no means a primary means or route

to increased survival and reproduction (Nesse 2004). Instead, natural selection is predicted, by basic

theory, to maximize condition-dependent human striving for the goals that have led, across many

past generations in relevant environments, to high survival and reproduction, relative to other

humans.

In the context of striving, human emotional systems have evolved to motivate and modulate goal

seeking, dynamically across different circumstances. Such motivation is mediated by the human

‘liking’ and ‘wanting’ reward systems, as well as by unhappiness or dissatisfaction with current

situations. Human cognitive systems, by contrast, represent sets of evolved mechanisms for

information processing, causal thinking, and decision-making that subserve identification of

appropriate goals, and tactics for reaching them. Both emotional and cognitive systems develop

across infancy, childhood and adolescence, whereby genes, environments, and gene by environment

interactions mediate neurodevelopment. To understand human psychiatric disorders from an

evolutionary perspective, it thus becomes necessary to connect these psychological trajectories and

adaptations with their corresponding maladaptations (lacks of fit of phenotypes to the environment),

expressed as developmental, emotional, and cognitive dysfunctions that revolve around human

striving and cognition. What adaptations, then, are dysregulated in major human mental disorders,

and how?

Evolutionary biology is useful in medicine for two main reasons: (1) it teaches us how to think about

human medically-relevant phenotypes, and diagnoses, in novel, productive ways, and (2) it indicates

specific new data to collect, and new approaches for therapies. In this chapter, I focus on the

evolutionary biology of psychiatric disorders centrally involving social cognition, affect, and

development. I first describe the primary types of causes of mental disorders, from evolutionary-

medical thinking. Next, I describe autism spectrum disorders, and psychotic-affective spectrum

disorders, in the context of these causes, with reference to recent findings in genetics, neuroscience,

and psychology, and in the contexts of which human-evolved adaptations have been subject to what

forms of alteration in each case. Third, I describe and evaluate hypotheses for the relationships of

these disorders with one another - relationships that define evolved axes of human development,

affect and cognition that structure variation in adaptive and maladaptive human mental functioning.

Finally, I make specific suggestions for research and clinical therapies that follow directly from these

considerations.

II. Research Findings

The evolutionary causes of psychiatric disorders represent the 'ultimate' sources of these conditions,

which indicate why, given their evolutionary history, humans exhibit particular forms of mental

disorders with particular symptoms and severities. Each of the six main causes described below

centers on explanations for deviations from mental adaptation and health, in the context of how

maladaptations can arise, and be maintained, in populations.

(1) Deleterious alleles. Mutations generate novel alleles that usually cause reduced genetic function,

because the perturbations randomly alter a system that would otherwise develop reasonably well.

Highly-penetrant mutations, with large effects, are especially likely to be highly deleterious, and

considerable evidence attests to important roles for de novo, deleterious mutations, such as copy

number variants or changes to highly conserve amino acid residues, in the causes of mental illness

(e. g., Malhotra and Sebat 2012). Highly deleterious alleles that are associated with relatively-severe

mental illnesses include, for example, monogenic causes of autism or schizophrenia, that evolve

under mutation-selection balance: rare mutations arise, and are selected against because their

bearers exhibit greatly-reduced reproduction.

Rare, deleterious alleles such as copy number variants have been estimated to account for a small

percentage of cases of major mental illness (Escudero and Johnstone 2014). Most inferred 'risk

alleles' for mental disorders, such as those identified with genome-wide association studies are,

however, relatively common (at frequencies above 1% or 5%), and have small effects on risk through

one dimension of their multifaceted impacts on neurodevelopment, neuronal function, and other

systems. The degree to which such alleles can be considered as deleterious to health overall - given

all of their effects - remains an open question; for example, neurodegenerative disease risk trades off

with cancer risk, such that higher risks in one domain of disease may commonly entail lower risks in

another (Plun-Favreau et al. 2010). Presumably, if psychiatric risk alleles were purely deleterious,

they would indeed not be common in populations. Risk alleles may also exhibit positive effects, on

health and reproduction, when expressed in genetic relatives of individuals with mental illness (Power

et al. 2013); these findings indicate that 'risk' alleles do not simply confer increased risk of disease,

but may, depending on context, confer benefits as well. Such considerations can help to explain the

high heritabilities of psychiatric conditions including autism, bipolar disorder and schizophrenia, on

the order of 50-80% (e. g., Singh et al. 2014).

(2) Mismatched environments. Populations and individuals are always adapted to past

environments, and if environments change more rapidly than they can be tracked by selection and

genetic response to selection, then populations will be maladapted. Human environments have

changed radically over the past few hundred years, which is expected to lead to higher risk of

psychiatric disorders to the extent that the novel environments include risk factors such as increased

social stress and isolation, or toxins such as lead and mercury that degrade neurodevelopment. For

example, some of the highest rates of schizophrenia are found among visible-minority (e. g., different

skin color) immigrants, who appear to be subject to relatively-severe psychosocial stresses due to

their novel, challenging environments (Bourque et al. 2012).

(3) Extremes of adaptations. Some psychiatric conditions, such as Generalized Anxiety Disorder, or

some manifestations of Obsessive-Compulsive Disorder such as excessive hygienic behavior, clearly

represent extremes of normally-adaptive behavior: anxiety functions to modulate arousal and

attention under challenging conditions (Stein 2013), and hygiene reduces risks of infection (Curtis

2014). This conceptual framework has been generalized to connect normal personality variation

along a spectrum to personality disorders and to severe psychiatric disorders, by demonstrating

which aspects of personality are amplified, reduced, or otherwise distorted to generate mental

dysfunction (Trull and Widiger 2013). This approach has successfully described continua in

personality traits from normal to maladaptive extremes, although the adaptive significance, in terms

of fitness-related benefits and costs of personality variation among normal individuals, remains

largely unstudied. Maladaptive extremes can also be considered more directly in the context of

human evolutionary history, in that the evolution of human-specific traits, such as large brain size and

language, has generated potential and scope for loss of these specific traits, as in microcephaly and

Specific Language Impairment, as well as potential and scope for dysfunctional over-development,

as in macrocephaly and the disordered and exaggerated components of speech in schizophrenia

(Crespi 2008; Crespi and Leach 2014).

(4) Tradeoffs. Tradeoffs have been well-characterized for developmental and physiological

phenotypes, whereby, for example, increased resource allocation in one domain takes away from

another. For neurological and psychological phenotypes, however, conceptual paradigms based on

tradeoffs have yet to be developed, despite evidence for tradeoffs of verbal-social with visual-spatial

skills (Johnson and Bouchard 2007), empathic with systemizing (rule-based) interests and abilities

(Nettle 2007), neural flexibility with stability (Liljenstrom 2003), as well as tradeoffs between neural

activation of the internally, self-directed default mode network, and the outwardly-focussed task-

positive network (Jack et al. 2013). Cognitive and emotional tradeoffs are important because they

structure the brain's functional architecture, and generate coincidences of relative strengths with

relative deficits; for example, Kravariti et al. (2006) found that having closer relatives with

schizophrenia was strongly associated with better verbal skills relative to visual-spatial skills.

Tradeoffs are stronger under resource-related constraints, which may commonly follow from

dysfunctional neurodevelopment, and their extremes are expected to characterize some psychiatric

conditions. Autism, for example, has been strongly associated with a combination of high systemizing

and low empathizing, whereas some combination of dysfunctionally high empathizing and low

systemizing appears to characterize some psychotic-affective conditions (Brosnan et al. 2010),

especially borderline personality disorder and depression (Dinsdale and Crespi 2013).

(5) Conflicts. Genetically-based conflicts, whereby two parties exhibit different optima for some

genetically-based phenotype, generate risk of maladaptation because one party may more or less

'lose' the conflict, resources are wasted on conflictual interactions, and conflict mechanisms generate

novel targets for dysregulation and disease (Crespi et al. 2014). The forms of evolutionary-genetic

conflict most salient to psychiatric conditions include parent-offspring conflict (e. g., Crespi 2010),

genomic imprinting conflict (Crespi and Badcock 2008; Haig 2014), and sexual conflict (Haig et al.

2014). Dysregulated genomic imprinting, for example, underlies the expression of Prader-Willi

syndrome, one of the strongest genetic causes of psychosis (Soni et al. 2008), and this syndrome

represents only an extreme case of such psychiatric effects (Crespi 2008). Similarly, a recent

epidemiological study of over two million individuals demonstrated that unaffected sisters (but not

brothers) of individuals with schizophrenia and bipolar disorder exhibit higher fertility than controls, a

pattern that is uniquely predicted by a hypothesis of 'sexually-antagonistic' alleles that impose costs

on males but benefit females (Power et al. 2013).

(6) Defenses mistaken as symptoms. This last 'cause' of disease is only apparent: some psychiatric

symptoms represent conditionally-adaptive defenses for alleviating problematic conditions, rather

than deleterious manifestations of disease. Thus, in the same way that fever represents a

conditionally-adaptive bodily response to infection, with health benefits that usually outweigh its

costs, some psychiatric symptoms can be interpreted as conferring benefits, relative to their absence

or reduction. Examples of such phenomena include: (a) repetitive behavior in autism, which serves to

dampen excessively-high levels of autonomic and sensory arousal (Hirstein et al. 2001), (b)

dissociation, as a psychological mechanism to reduce deleterious effects of trauma (Russo et al.

2014), (c) delusion formation in psychosis, as a means to mentally cope with the exaggerated and

disordered perceptions of salience (causal meaning) (Kapur 2003), and (d) mild depression (low

mood), as a conditionally-adaptive response to circumstances that favor disengagement from failing

or unreachable goals - which escalates to full depression if useless goal-seeking persists (Nesse and

Jackson 2011). The danger of conceptualizing defenses, like fever, as purely-deleterious symptoms

is that treating them is expected to make the situation specifically worse unless the underlying cause

of the disorder (and defense) is addressed, such as the sensory hyper-sensitivity in autism, the

trauma in dissociation, or the challenging life-events and personal motivational structure that underlie

liability to low mood and depression.

These six causes of etiology and symptoms of psychiatric conditions converge in their emphases on

determining what evolved genetic, developmental, neural, cognitive and emotional systems are

altered, and how they are altered, in psychiatric conditions. These causes also provide our

framework for determining how nominal, DSM-designated psychiatric conditions are related to one

another in their causes, as independent and separate, partially overlapping, or diametric to one

another in the same general way as the development or activity of any biological system or pathway

can be altered in two opposite directions.

Autism spectrum conditions

Autism is defined, and commonly reified, as a combination of deficits in social reciprocity and

communication with high levels of restricted interests and repetitive behavior (Figure 1). The degree

to which this combination represents a cohesive syndrome, with causally-shared rather than

independent symptoms and causal factors, remains unclear (Brunsdon and Happé 2014). Beyond

these two commonalities, autism presents diverse features, with overall intellectual abilities varying

from very low to above average, cognitive enhancements (above neurotypical) in sensory and visual-

spatial abilities in a substantial fraction of individuals, and a sex ratio that is highly male-biased

overall but much less so among more severely-affected individuals (Baron-Cohen et al. 2011).

The most straightforward connection between the major features of autism, and human evolution, is

that our evolutionary history has been characterized by elaboration of the 'social brain': the

distributed, integrated set of neural systems that subserve the acquisition, processing, and use of

social information. It is these social brain phenotypes that are specifically underdeveloped in autism.

As such, autism can be conceptualized as the expression of maladaptive extremes of social-brain

under-development, which, in principle, may be caused in a proximate way by reduction or loss of

any of the myriad systems that is necessary or sufficient for human social brain development. Autism

thus exhibits many single-gene, syndromic causes due to deleterious mutation, but it is also

commonly underlain by combined effects from the hundreds or thousands of genes bearing alleles

that affect social-brain development (Heil and Schaaf 2013). As such, there can be no primary,

proximate physiologically-based cause of autism (as there may be, for example, for type 1 diabetes),

and the search for causes becomes a differential characterization, subdivision, and prioritization of

the diverse genetic, epigenetic, and environmental influences that converge on under-development of

the social brain.

As social cognition is under-developed under all psychologically-based theories for autism, it can also

be conceptualized, and studied, in terms of developmental heterochrony, whereby child cognitive

development is not completed in autism, and childhood characteristics, including reduced social

cognition, are retained into adulthood (Woodard and van Reet 2011; Crespi 2013). In this context,

other human-elaborated traits including highly-developed, regulated social striving and goal-seeking,

guided by perceived reward-associated or cost-associated (aversive) salience (inferred, causative

meaning) of social stimuli, remain underdeveloped as well on the autism spectrum. External stimuli

may thus have salience predominantly in terms of perceived sensations, or specific, highly-restricted

non-social interests, especially foci of highly selective attention (Ploog 2010). Frith (2012) indeed

sees a weak drive to discern meaning in the world as epitomizing the weak central coherence theory

of autism, which has been supported by a wide range of evidence.

A central, unresolved question in the study of autism is whether a single, central psychological or

cognitive-level factor can explain the apparently inexplicable combination of reduced sociality with

restricted interests and repetitive behavior. In the context of social brain under-development,

increased restricted interests and repetitive behaviors, and sensory, visual-spatial, and mechanistic-

cognition enhancements in autism, can be explained by several hypotheses.

First, increases in asocial phenotypes may pre-empt the development of social phenotypes, such as

by directing perceived salience, interests, and brain specializations along asocial paths. Such

effects, which are notably represented by a theory for autism etiology based on enhanced perceptual

functioning (Mottron et al. 2006) may be mediated by over-developments of sensory perception and

mechanistic, systemizing cognition (Baron-Cohen et al. 2011).

Second, increased asocial cognition may itself be a direct result of reduced social cognition, as a

compensatory or tradeoff-based neurodevelopmental mechanism akin to the over-development of

non-visual senses among the blind.

Third, some such asocial cognition and behavior, and phenotypes such as insistence on sameness

and stimulus over-selectivity, may, as noted above, represent defenses that aid in coping with

challenging symptoms such as increased perceptual sensitivity or avoidance of stress from dealing

with inexplicable social-cognitive tasks.

Finally, one possible resolution, based on reduced expression of a phenotype virtually unique to

humans, is that autism is, in part, underpinned psychologically by under-developed imagination,

defined as 'the faculty or action of forming new ideas, or images or concepts of external objects not

present to the senses'. This hypothesis, originally described by Rutter (1972), and Wing and Gould

(1979) can, in principle, jointly explain social and asocial alterations in autism, including reduced

pretend play, reduced social imagination as expressed in theory of mind, restriction of interests and

repetition of behavior, and insistence on sameness.

Determining the degree to which of these hypotheses is correct, in general or for any particular

individual, is crucially important to autism therapy, especially to prevent enhancements or

conditionally-adaptive defenses of autistic individuals from being treated as deleterious symptoms.

Psychotic-affective spectrum conditions

Psychotic-affective spectrum conditions include a set of DSM disorders, mainly schizophrenia,

bipolar disorder, and depression, that broadly overlap in their symptoms, neurological and

psychological correlates, and genetic and environmental risk factors (Doherty and Owen 2014)

(Figure 1). All of these conditions exhibit substantial genetic components, and mediation in part by

rare, penetrant risk factors, although most genetic risk appears to be underlain by many alleles each

of small effect.

Schizophrenia, as well as other conditions that involve psychosis, can be understood most directly

and simply in terms of dysfunction of the human adaptive system for assigning salience (causal

meaning) to external, as well as internally-generated, stimuli (Kapur 2003; Winton-Brown et al. 2014).

Salience assignment, which is underpinned by a dedicated neural system involving the anterior

cingulate cortex and insula, is fundamental to cognition, behavior, and goal-seeking, in that it

mediates subjective causal understanding of perceptual inputs. Psychosis thus involves over-

developed and inappropriate salience, usually in the contexts of social interactions, agency,

intentionality, self-other associations, and other aspects of mentalistic (social and mind-related)

thought, apparently due to the primacy of social cognition in human goal-directed behavior (Crespi

and Badcock 2008). Paradigmatic manifestations of psychosis thus involve paranoia, other social

delusions, megalomania, belief that events always refer to the self, alterations to self-other

distinctions, and assignment of mind, agency and intentions to inappropriate subjects and inanimate

objects. Such reality distortions are mediated by top-down cognitive processes, and they can be

considered as attempts to 'make sense' of the excessively-high and inappropriate salience

assignment, for external stimuli, that is driven by hyper-dopaminergic neurotransmission (Kapur

2003; Cook et al. 2012; Howes and Murray 2014). Hallucinations, in turn, can be understood as

misinterpreted and exaggerated internal perceptions, mediated by over-developed salience of

internal representations, such that given certain neurophysiological alterations, thought, inner

speech, and imagination come to be considered as external percepts. Like delusions, hallucinations

are usually expressed as social phenomena, especially auditory hallucinations.

Schizophrenia is predominantly considered as a disorder of cognition, whereby the causal meanings

that guide striving become over-developed and dysfunctionally over-mentalistic. Bipolar disorder and

depression, by contrast, represent mainly disorders of emotion, the set of neural and hormonal

systems that motivate and modulate striving and goal-seeking across different contexts.

Understanding such mood disorders requires consideration of the adaptive significance of condition-

dependent variation in human emotions, especially with regard to the social interactions that

permeate human thought and behavior (Nesse and Ellsworth 2009). In this context, considerable

evidence indicates that low mood is normally adaptive in situations where individuals benefit by

disengaging from unreachable or unprofitable goals, as it facilitates such disengagement and

motivates alternative behavioral patterns of goal-seeking that should be more advantageous (Keller

and Nesse 2005). High, positive mood, in comparison, represents an emotional mechanism whereby

human reward systems motivate continuation of beneficial behavior, because one's goals are being

reached. Depression, then, can be conceptualized and studied as overly-low and overly-stable mood,

a maladaptive extreme of an adaptation, whereby individuals fail to disengage from deleterious

thought patterns and striving (Nesse 2004; Keller and Nesse 2005). Conversely, mania represents an

emotional opposite to depression, as the expression of inability to emotionally restrain high mood and

intensity of striving, even if and when its consequences become detrimental (Johnson 2005; Johnson

et al. 2012a). Behaviors associated with mania and hypomania can, moreover, be directly

interpreted in the context of extreme striving for social dominance, power, and influence, which, if

successful, leads to substantial benefits (Johnson and Carver 2012; Johnson et al. 2012b). This

evolutionary perspective can explain shifts between mania and depression in bipolar disorder, in that

mania is expected to foster pursuit of goals that become more and more risky, unreachable or

unsuccessful, eventually prompting the generation of mixed states, and descent into depression.

In bipolar disorder, then, cognitive salience systems, and choices of goals, commonly remain

functional, but the homeostatic regulation of the emotions that underlie goal pursuit becomes

dysregulated, towards overly low or overly high moods and their sequelae. Moreover, like

schizophrenia, mania and depression both centrally involve extremes of social, mentalistic thought

and behavior, here in the contexts of guilt, shame, embarrassment, perceived social defeat, and

social rumination in depression, and social-dominance pursuit and pride in mania. Affective

psychoses, which comprise psychosis with incongruence of mood, may thus be mediated by self-

punishment driven, or reward-driven, over-attributions of social salience, in the context of

emotionality that becomes sufficiently strong to dysregulate salience. These considerations can help

to explain well-documented, otherwise-inexplicable associations of bipolar disorder with high social

motivation and achievement (Coryell et al. 1989; Johnson et al. 2012a; Higler et al. 2014). Moreover,

bipolar disorder, as well as schizophrenia and schizotypy, have been associated across a wide

diversity of studies with increased social imagination, divergent thinking, creativity, and goal

attainment, especially in the arts and humanities (Nettle 2002, 2006; Burns 2004; Simeonova et al.

2005; Carson 2011; Bilder and Knudsen 2014). Imagination can indeed be considered, under

Bayesian models of cognition and learning, as directly associated with causal cognition and inference

of meaning, such that salience, causal thinking, and imagination should tend to increase, or

decrease, in concert with one another (Walker and Gropnik 2013).

The relationship between autism spectrum and psychotic-affective spectrum disorders

Bleuler invented the term 'autism' to describe withdrawal from reality and social interactions in

schizophrenia, but Kanner was careful to point out that his conceptualization of autism referred to

children who had never participated in social life (Kanner 1965). The relationship between autism

and schizophrenia, and psychotic-affective disorders more generally, has since been considered in

terms of two main hypotheses, (1) partial overlap, with some degree of shared social-cognitive

deficits and genetic risk factors; (2) a diametric (opposite) relationship, based, at a psychological

level, on under-development of social cognition and affect in autism, normality at the center, and

dysfunctional forms of their over-development in psychotic-affective conditions (Crespi et al. 2010)

(Figure 2). The partial overlap hypothesis is data-driven and motivated primarily by the prominence of

social deficits especially in autism and schizophrenia. By contrast, the diametric hypothesis follows

directly from evolutionary and neurodevelopmental considerations, under the premises that human

evolution has been characterized primarily by elaboration of social cognition (generating increased

scope for altered development of specific phenotypes), and that the neurodevelopmental systems

that underlie it, like all biological systems, can vary and be perturbed in two opposite directions

towards lower or higher expression (Figure 2).

A central prediction of the diametric hypothesis is that autism, and psychotic-affective conditions

(especially schizophrenia, for which most of the relevant data is available) should exhibit opposite

phenotypes and genetic risk factors. A suite of such evidence is described in Table 1, which provides

support for the diametric hypothesis from diverse and independent sources of data. The partial-

overlap hypothesis is consistent with the sharing of deficits, especially in social cognition, between

autism and schizophrenia, but such deficits can also be considered as deriving from opposite

alterations both of which reduce performance on standard tests. Genetic risk factors, such as some

genomic copy-number variants and some SNPs, have also been associated with both autism

spectrum disorders and schizophrenia (Crespi et al. 2010). Such findings, however, are subject to the

caveat that premorbidity to schizophrenia in children and young adolescents, in the form of social

deficits and associated developmental problems, can be realistically diagnosed only as autism

spectrum since there is not (and never has been) a diagnostic category for schizophrenia

premorbidity (Crespi and Crofts 2012). This structural limitation in the DSM is expected to lead to a

non-negligible incidence of false-positive diagnoses of autism among children who are actually

premorbid for schizophrenia, especially among individuals harboring relatively-penetrant genetic risk

factors such as copy number variants. Patterns of diagnoses for well-studied CNVs indeed fit with

expectations from such false positive diagnoses (Crespi and Crofts 2012).

The diametric hypothesis for autism and psychotic-affective disorders is novel and controversial, and

has just begun to be subject to systematic, large-scale testing of its predictions (e. g., Byars et al.

2014). However, to the extent that it is correct, the study of human disorders involving social

cognition should be revolutionized, and provided its first solid grounding in basic evolutionary

principles.

III. Implications for policy and practice

Risks for human mental disorders have evolved. Evolutionary conceptualizations of autism and

psychotic-affective disorders lead directly to novel, specific implications for understanding, studying

and treating these conditions.

First, autism, schizophrenia, bipolar disorder, and depression cannot justifiably be considered as

'diseases' under standard medical models of disease, because the neural-system adaptations

subject to maladaptive alteration in each case remain inadequately understood. Instead, these

conditions currently represent broad-scale, heuristic descriptions for suites of related psychological

and behavioral problems, none of which has currently-specifiable genetic or neurological causes in

the same way as do diseases like cancer or diabetes, and all of which grade smoothly in their

symptoms into normality. As such, schizophrenia and related psychotic and affective disorders can

best be considered as 'syndromes': groups of symptom dimensions that cluster in different

combinations across different individuals (van Os 2009). Risks and symptoms for these psychiatric

conditions have, however, evolved in close conjunction with the evolution of complex human social

cognition, affect and behavior, which provides the basis for an ultimate understanding, and nosology,

of psychiatric maladaptations. In this context, DSM descriptions of autism or a psychotic-affective

condition should represent starting points for differential diagnosis of their genetic, social and

environmental causes, for each specific individual. Such causes are expected to involve some

combination of effects from deleterious mutations, evolutionarily-novel environments, extremes of

adaptations, tradeoffs, genomic conflicts, and evolved defenses.

Second, autism can be considered, from an evolutionary perspective, in terms of under-development

of social cognition and affect, centrally involving some combination, and causal conjunction, of

reduced social development with increased non-social perception, attention, and cognition. Such

social and non-social alterations may have diverse proximate causes, but they appear to commonly

converge, psychologically, on reductions in imagination, which can explain both lower levels of

sociality and increases in restricted interests and repetitive behavior. This conceptualization of autism

is fully compatible with previously-developed psychological models founded on reduced central

coherence (Happé and Frith 2006), lower empathizing and higher systemizing (Baron-Cohen et al.

2011), and enhanced perceptual function (Mottron et al. 2006).

Third, psychotic-affective disorders can be considered as centrally involving dysfunctionally over-

developed social cognition, affect, and behavior, expressed as social hyper-salience in aspects of

psychosis, dysregulated social goal motivation and dominance-seeking in mania, and extremes of

negative social emotionality in depression. Each of these disorders, which grade into one another,

can best be understood in the individual-level contexts of the developmental causes of negatively-

valenced and imaginative social salience, and the motivational structure of one's past, current and

future imagined life goals, especially regarding regulation of, and impediments to, success in striving.

This framework is fully compatible with current psychological, neurological, cognitive-science-level

accounts of psychotic-affective conditions (e. g., Kapur 2003; Johnson et al. 2012a,b; Winton-Brown

et al. 2014), but grounds them in evolutionary considerations, and in their relationship to the autism

spectrum.

Fourth, autism and psychotic-affective conditions can be considered and analyzed as diametric

(opposite) disorders with regard to social development, cognition, affect, and behavior. This

diametric model provides for comprehensive, reciprocal illumination of the diagnoses, causes and

treatments of these disorders, such that insights derived from studying one set of disorders can be

applied directly to the other. Most generally, cognitive-behavioral treatments for autism should

especially focus on enhancing phenotypes that are over-developed in psychotic-affective conditions,

including social imagination, flexible and social salience, and social motivation and goal-seeking. By

contrast, treatments for psychotic-affective conditions, in addition to focusing more directly on the

adaptive, dynamic regulation of social-cognitive salience and mood-directed striving, should involve

therapies to make perception, cognition, affect and behavior relatively 'more autistic'. Similar

considerations apply to pharmacological effects: for example, valproate during fetal development

represents a well-established human cause, and animal model, of autism (Markram and Markram

2010), but valproate is also used to treat bipolar disorder and schizophrenia (Haddad et al. 2009);

comparably, mGlur5 pathway antagonists are being used to treat fragile X syndrome and autism

(Lozano et al. 2014), whereas mGlur5 agonists are being developed to treat schizophrenia (Matosin

and Newell 2013).

The findings and inferences described here emphasize that evolutionary approaches in medicine,

and psychiatry, can offer specific, well-rationalized hypotheses, and can help to direct research and

treatments along novel and promising paths. Such progress should lead, eventually, to the

integration of psychiatry with the standard medical model of disease, as dovetailing evolutionary and

proximate approaches to the study of brain development and function uncover the adaptive

significance of psychological, cognitive, and affective phenotypes, and their neurological and genetic

foundations.

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Figure 1. Phenotypes that describe (a) the autism spectrum and (b) the psychotic-affective spectrum,

based on DSM-V diagnoses, evolutionary considerations, and the hypothesized relationships

between the two sets of disorders.

Figure 2. The autism spectrum and the psychotic-affective spectrum can be conceptualized as

diametric disorders, with regard to the direction of alterations in uniquely-human or human-elaborated

phenotypes that comprise their core features.

Table 1. Diametric genetic risk factors, phenotypes, and correlates of autism spectrum and psychotic affective spectrum conditions.

For phenotypes with large sets of evidence, only recent articles or reviews are cited. Crespi and Badcock (2008) present additional

evidence, from less-recent literature.

Trait Autism spectrum Psychotic-affective spectrum Comments

Copy number

variants

Duplications of 22q11.2 increase

autism risk (Crespi and Crofts

2012; Rees et al. 2014)

Duplications of 22q11.2

decrease schizophrenia risk;

deletions of 22q11.2 greatly

increase schizophrenia risk

(Rees et al. 2014)

Deletions of 22q11.2 suggested

to increased ASD risk but

pattern not found in ASD CNV

cohorts (Crespi and Crofts 2102)

Copy number

variants

Duplications of 1q21.1 increase

autism risk, increase head size

(Brunetti-Pierri et al. 2008;

Crespi and Crofts 2012)

Deletions of 1q21.1 increase

schizophrenia risk, reduce head

size (Brunetti-Pierri et al. 2008;

Rees et al. 2014b)

Deletions may increase autism

risk, or be false positive (Crespi

and Crofts 2012)

Copy number

variants

Deletions of 16p11.2 increase

autism risk, increase head size

(Qureshi et al. 2014)

Duplications of 16p11.2 increase

schizophrenia risk, reduce head

size (Rees et al. 2014b; Qureshi

et al. 2014)

Duplications may increase

autism risk, or be false positive

(Crespi and Crofts 2012)

Copy number

variants

Duplications of 15q11.2 (BP1-

BP2) increase autism risk

(Chaste et al. 2014)

Deletions of 15q11.2 (BP1-BP2)

increase schizophrenia risk

(Rees et al. 2014b)

Deletions and duplications of

CYFIP1, a key gene in this CNV

region, cause opposite

alterations to dendritic spine

complexity (Pathania et al. 2014)

Birth size (weight,

length)

Smaller size protects against

autism; larger size increases

autism risk (Byars et al. 2014)

Larger size protects against

schizophrenia; smaller size

increases schizophrenia risk

(Byars et al. 2014)

Each of the patterns of risk has

been replicated across many

other studies

Brain size Larger brain size in children with

autism (Courchesne et al. 2011;

Baribeau and Anagnostou 2014)

Smaller brain size in

schizophrenia (Haijma et al.

2013)

Autism involves faster brain

growth in early childhood, in

particular

Neurological

function

Congenital blindness increases

risk of autism (Hobson and

Bishop 2003; Ek et al. 2005)

Congenital blindness protects

against schizophrenia (Landgraf

and Osterheider 2013;

Silverstein et al. 2013)

Neurological

function

Sensory abilities increased in

autism (Brown et al. 2003;

Mottron et al. 2006, 2013;

Heaton et al. 2008a,b; Dohn et

al. 2012; Falter et al. 2013;

Tavassoli et al. 2014)

Sensory abilities decreased in

schizophrenia; sensory

deprivation induces features of

psychosis (Bates 2005; Leitman

et al. 2005, 2010; Force et al.

2008; Javitt 2009a,b; Mason and

Brady 2009; Daniel et al. 2014)

Strong, highly consistent pattern

in schizophrenia; substantial

although somewhat mixed

evidence in autism

Neurological

function

Prepulse inhibition increased in

autism (Kohl et al. 2014; Madsen

et al. 2014)

Prepulse inhibition decreased

(Swerdlow et al. 2014)

Findings highly consistent for

schizophrenia, variable for

autism

Neurological

function

Mismatch negativity increased in

autism (Orekhova and

Stroganova 2014)

Mismatch negativity decreased

in schizophrenia (Nagai et al.

2013; Todd et al. 2013)

Findings highly consistent for

schizophrenia, variable for

autism

Neurological

function

Mirror neuron system activation

decreased in autism (Oberman

et al. 2005; Kana et al. 2011)

Mirror neuron system activation

increased in actively psychotic

individuals with schizophrenia

(McCormick et al. 2012)

Same protocol used to measure

mirror neuron function, in autism

and schizophrenia (McCormick

et al. 2012); other studies of

schizophrenia usually show

reduced activation (Mehta et al.

2014) but do not involve actively-

psychotic subjects

Neurological

function

Default mode system activation

reduced in autism, in association

with reduced self-referential and

imaginative cognition (Kennedy

et al. 2006; Buckner et al. 2008;

Iocaboni 2006; Kennedy and

Courchesne 2008)

Default system over-activated in

schizophrenia, in association

with reality distortion and

increased imaginative cognition

(Buckner et al. 2008); also less

deactivation of this system

(Landin-Romero et al. 2014)

Some studies of autism show

reduced deactivations of default

system, that may be associated

with reduced activation (Buckner

et al. 2008); Immordino-Yang et

al. (2012) also contrast autism

and schizophrenia as opposite

with regard to the default

network

Neurological

function

Reduced connectivity within

default mode in autism (van dem

Hagen et al. 2012; Jung et al.

2014)

Increased connectivity within

default mode in schizophrenia

(Whitfield-Gabrieli et al. 2009;

Tang et al. 2013; Li et al. 2015)

Some mixed results in both

autism and schizophrenia, but

two reviews support opposite

nature of the alterations (Broyd

et al. 2009; Karbasforoushan

and Woodward 2012)

Neurological

function

Increased local brain

connectivity, decreased long-

range connectivity, in

association with early brain

overgrowth (Baribeau et al.

2013)

Decreased local brain

connectivity, increased long-

range connectivity, in

association with increased

cortical thinning, in childhood-

onset schizophrenia (Baribeau et

al. 2013)

Findings based on review of

neuroimaging findings (Baribeau

et al. 2013)

Neurological

function

Temporal-parietal junction region

shows reduced activation in

autism, underlies mentalizing

reductions (Lombardo et al.

2011; Kana et al. 2014)

Temporal-parietal junction region

shows increased activation in

schizophrenia, underlies some

psychotic symptoms (Wible

2012)

Emotionality and

motivation

Reduced social motivation in

autism (Chevallier et al. 2012)

Increased social motivation in

mania, hypomania (Johnson et

al. 2012a,b)

Motivation in general decreased

in negative symptom

schizophrenia, depression

Emotionality and

motivation

Cognitive empathic abilities

reduced in autism (Baron-Cohen

2010)

Some cognitive empathic

abilities enhanced in borderline

personality disorder and

subclinical depression (Harkness

et al. 2011; Dinsdale and Crespi

2013)

Cognitive empathic abilities

lower in schizophrenia, bipolar

disorder and depression, in

association with general

cognitive deficits (e. g., Baez et

al. 2013; Konstantakopoulos et

al. 2014

Emotionality and

motivation

Reduced social emotion in

autism (Kasari et al. 2001)

Increased social emotion

expression in bipolar disorder

and depression (e. g., guilt,

shame, embarrassment, pride)

(Kim et al. 2011; Johnson and

Carver 2012)

Reduced general expressed

emotionality in negative

symptom schizophrenia

Cognitive function Decreased inattentional

blindness in autism

(Swettenham et al. 2014)

Increased inattentional blindness

in schizophrenia (Hanslmayr et

al. 2012)

Cognitive function Over-selective attention (Ploog

2010; Reed and McCarthy 2012)

Reductions in selective attention

in schizophrenia and positive

schizotypy (Morris et al. 2013;

Granger et al. 2012)

Cognitive function Enhanced Stroop task

performance in autism (Adams

and Jarrold 2009)

Decreased Stroop task

performance in schizophrenia,

by meta-analysis (Westerhausen

et al. 2011)

Results mixed for autism, highly

consistent for schizophrenia

Cognitive function Enhanced Iowa Gambling Task

performance in high-functioning

autism (South et al. 2013)

Reduced Iowa Gambling Task

performance in schizophrenia, in

most studies (Adida et al. 2011

Results mixed for autism,

consistent for schizophrenia

Cognitive function Reduced susceptibility to rubber

hand illusion in autism and in

healthy high-ASD trait

individuals (Cascio et al. 2012;

Paton et al. 2012; Palmer et al.

2013)

Increased susceptibility to rubber

hand illusion in schizophrenia

(Park and Nasrallah 2014)

Same general pattern also found

for visual illusions, with some

inconsistencies (Crespi 2013)

Cognitive function Literal word interpretation,

under-interpretation of social

relevance, in autism (Chance

2014)

Over-interpretation of word

meaning and social relevance in

schizophrenia (Chance 2014)

Cognitive function Decreased induction of false

memories (Beversdorf et al.

2000; Hiller et al. 2007)

Increased induction of false

memories associated with

psychosis phenotypes (Corlett et

al. 2009; Kanemoto et al. 2013;

Grant et al. 2014)

Results somewhat mixed (some

non-significant) for autism

Cognitive function Semantic memory network

states overly rigid in autism

(Faust and Kenett 2014)

Semantic memory network

states chaotic in schizophrenia

(Faust and Kenett 2014)

Cognitive function Working memory deficits in

autism (Kercood et al. 2014);

extraordinary working memory

enhancements in child prodigies,

who score above autism range

in Attention to Detail on Autism

Quotient test, and exhibit high

rates of autism in their families

(Tuthsatz and Urbach 2012)

Large working memory deficits in

schizophrenia; highly consistent

finding (Lee and Park 2005;

Silver Feldman 2014)

Findings of Tuthsatz and Urbach

(2012) would benefit from

replication; areas of excellence

in child prodigies notably overlap

with those found in savantism in

autism (Treffert 2009)

Cognitive function Hyperlexia found predominantly

in autism (Cardoso-Martins and

da Silva 2010; Samson et al.

2012; Mottron et al. 2013)

Dyslexia associated with

schizophrenia and schizotypy

(Revheim et al. 2006, 2014;

Arnott et al. 2011)

Williams and Casanova (2010)

contrast autism and dyslexia for

cortical microstructure

Cognitive function More-deliberative decision-

related processing in autism

(Brosnan et al. 2014)

'Jumping to conclusions'

associated with delusions in

schizophrenia (Speechley et al.

2010; Langdon et al. 2014)

Cognitive function Bias towards hypo-priors in

Bayesian models of perception

and cognition (Pellicano and

Burr 2012; Lawson et al. 2014)

Bias towards hyper-priors in

Bayesian models of perception

and cognition (Cook et al. 2012;

Pellicano and Burr 2012)

Cognitive function Reduced inference of intentions

in autism (Ciaramidaro et al.

2014)

'Hyper-intenionality' in

schizophrenia and schizotypy

(Backasch et al. 2013; Moore

and Pope 2014

Bara et al. (2011) contrast

autism and schizophrenia

directly in this regard

Cognitive function Reduced theory of mind in

autism spectrum children by

ToM Storybooks test (Blijd-

Hoogewys et al. 2008)

'Hyper-Theory-of Mind' in

children with more psychotic

experiences by ToM Storybooks

test (Clemmensen et al. 2014)

Cognitive function Theory of mind abilities reduced

in autism, using MASC test, due

to combination of hypo-

mentalizing, lack of mentalizing,

and hyper-mentalizing (Dziobek

et al. 2006; Lahera et al. 2014)

Theory of mind abilities reduced

in association with positive

symptoms of schizophrenia,

using MASC test, due to hyper-

mentalizing (Montag et al. 2011;

Fretland et al. 2015); hyper-

mentalizing also found in

borderline personality disorder

using MASC (Sharp et al. 2011)

Cognitive function Reduced salience of social

stimuli, and overly-specific and

inflexible salience of primary

perceptual and non-social stimuli

(Bird et al. 2006; Sasson and

Touchstone 2014)

Over-developed and arbitrary

salience in prodrome and

psychosis, mainly involving

social phenomena (van Os

2009; Winton-Brown et al. 2013;

Howes and Murray 2014)

Cognitive function Decreased perception of

biological motion, entities, in

autism; fail to see humans who

are there (Blake Turner Smoski

2003)

Increased and false perception

of biological motion, entities, in

schizophrenia; see humans in

random dots (Kim Park Blake

2011)

Cognitive function Selectively enhanced visual-

spatial abilities in autism

(Almeida et al. 2013; Kana et al

2013).

Reduced visual-spatial skills,

relative to verbal skills, positively

associated with genetic liability

to schizophrenia (Kravariti et al.

2006; also see O'Connor et al.

2012)

Cognitive function Enhanced Embedded Figures

Test performance among

healthy individuals with more

autistic traits (Russell-Smith et

al. 2010)

Reduced Embedded Figures

Test performance among

healthy individuals with more

positively-schizotypal traits

(Russell-Smith et al. 2010)

Behavior Reduced imagination and

creativity in autism (Craig and

Baron-Cohen 1999; King et al.

2014)------------------------------------

-------------------

Increased imagination and

creativity, in schizophrenia,

schizotypy, and bipolar disorder

and in relatives (Jamison 1993;

Nettle 2001; Nelson and

Rawlings 2008; Claridge and

McDonald 2009; Kaufman 2014)

---------------------------

The literature relating psychotic-

affective spectrum phenotypes

and conditions to aspects of

increased imagination and

creativity is large and diverse;

reduced imagination has been

considered as a diagnostic

criterion for autism

Behavior Reduced pretend play and social

play in autism (Jarrold et al.

2003; Hobson et al. 2013)

Higher levels of dissociation,

hallucination, psychotic-affective

psychopathology associated with

presence of childhood imaginary

companions (Bonne et al.1999;

Gleason et al. 2003; McLewin

and Muller 2006; Fernyhough et

al. 2007)

-------------------------------------------

---

Social correlates Autism associated with technical

professions in fathers, mothers

and grandfathers (Wheelwright

and Baron-Cohen 2001; Spek

and Velderman 2013; Dickerson

et al. 2014)

Schizophrenia, schizotypy,

bipolar disorder, and depression

associated with careers and

interests in arts, humanities and

literature (Nettle and Clegg

2006; Rawlings and Locarnini

2008)

Social correlates Autism in family associated with

technical college majors

(Campbell and Wang

2012)---------

Bipolar disorder, depression in

family associated with arts and

humanities majors (Campbell

and Wang 2012)

----------------------------------

Insufficient data on

schizophrenia for analysis, in

this study

Social correlates Autism associated with higher

socioeconomic status (Durkin et

al. 2010; Leonard et al. 2011)

Schizophrenia associated with

lower socioeconomic status

(Werner et al. 2007)

Insights into the Neuro-Pharmacological Treatment of Schizophrenia: Past, Present, and Future

Chapter

Full-text available

Jan 2023

Schizophrenia is the seventh largest cause of impairment in people aged from 15 to 44 years around the world. This is the long-term psychological disorder marked by illusions, thinking and attention difficulties, absence of desire along with that the majority will have significant and long-term social impairments. Generally, schizophrenia is associated with positive as well as negative or cognitive symptoms. The conventional antipsychotics are used to treat the positive symptoms but the negative symptoms are rarely treated. There were no effective drugs for the treatment of schizophrenia before the introduction of antidopaminergic psychotropic drugs in the 1950s. Here, we described the key meta-analytic evidence on the efficacy of antipsychotics in the acute treatment of schizophrenia, particularly clozapine in treatment-resistant patients. In this chapter, primarily we have focused on the neuropharmacological treatment options available for schizophrenia and how has the treatment changed over time. An improved understanding of how conventional antipsychotic drugs convey their therapeutic effect during the treatment and what are the cutting-edge alternatives that are available in order to mitigate the drawbacks of traditional neuroleptics.

Imaginative Culture and Human Nature: Evolutionary Perspectives on the Arts, Religion, and Ideology

Book

Full-text available

Nov 2022

This is a collection of 21 articles published as an eBook in Frontiers in Psychology. This Research Topic aims to demonstrate that imaginative culture is an important functional part of evolved human behavior—diverse in its manifestations but unified by species-typical sets of biologically grounded motives, emotions, and cognitive dispositions. The topic encompasses four main areas of research in the evolutionary human sciences: (1) evolutionary psychology and anthropology, which have fashioned a robust model of evolved human motives organized systemically within the phases and relationships of human life history; (2) research on gene-culture coevolution, which has illuminated the mechanisms of social cognition and the transmission of cultural information; (3) the psychology of emotions and affective neuroscience, which have gained precise knowledge about the evolutionary basis and neurological character of the evolved emotions that give power to the arts, religion, and ideology; and (4) cognitive neuroscience, which has identified the Default Mode Network as the central neurological location of the human imagination. By integrating these four areas of research and by demonstrating their value in illuminating specific kinds of imaginative culture, this Research Topic aims at incorporating imaginative culture within an evolutionary conception of human nature.

Autistic-Like Traits and Positive Schizotypy as Diametric Specializations of the Predictive Mind

Article

Jul 2022
PERSPECT PSYCHOL SCI

Brett Andersen

According to the predictive-processing framework, only prediction errors (rather than all sensory inputs) are processed by an organism’s perceptual system. Prediction errors can be weighted such that errors from more reliable sources will be more influential in updating prior beliefs. It has previously been argued that autism-spectrum conditions can be understood as resulting from a predictive-processing mechanism in which an inflexibly high weight is given to sensoryprediction errors that results in overfitting their predictive models to the world. Deficits in executive functioning, theory of mind, and central coherence are all argued to flow naturally from this core underlying mechanism. The diametric model of autism and psychosis suggests a simple extension of this hypothesis. If people on the autism spectrum give an inflexibly high weight to sensory input, could it be that people with a predisposition to psychosis (i.e., people high in positive schizotypy) give an inflexibly low weight to sensory input? In this article I argue that evidence strongly supports this hypothesis. An inflexibly low weight given to sensory input can explain such disparate features of positive schizotypy as increased exploratory behavior, apophenia, hyper theory of mind, hyperactive imagination, attentional differences, and having idiosyncratic worldviews.

Why iPlay: The Relationships of Autistic and Schizotypal Traits With Patterns of Video Game Use

Article

Full-text available

Feb 2022

Video games are popular and ubiquitous aspects of human culture, but their relationships to psychological and neurophysiological traits have yet to be analyzed in social-evolutionary frameworks. We examined the relationships of video game usage, motivations, and preferences with autistic and schizotypal traits and two aspects of neurophysiology, reaction time and targeting time. Participants completed the Autism Quotient, Schizotypal Personality Questionnaire, a Video Game Usage Questionnaire, and two neurophysiological tasks. We tested in particular the hypotheses, motivated by theory and previous work, that: (1) participants with higher autism scores would play video games more, and participants with higher schizotypy scores would play video games less; and (2) autism and positive schizotypy would be associated with opposite patterns of video game use, preferences and motivations. Females, but not males, with higher autism scores played more video games, and exhibited evidence of relatively male-typical video game genre preferences and motivations. By contrast, positive schizotypy was associated with reduced video game use in both genders, for several measures of game use frequency. In line with previous findings, males played video game more than females did overall, preferred action video games, and exhibited faster reaction and targeting times. Females preferred Puzzle and Social Simulation games. Faster reaction and targeting times were associated with gaming motives related to skill development and building behavior. These findings show that gaming use and patterns reflect aspects of psychology, and gender, related to social cognition and imagination, as well as aspects of neurophysiology. More generally, the results suggest that video game use is notably affected by levels of autistic and schizotypal traits, and that video games may provide an evolutionarily novel medium for imaginative play in which immersive play experiences can be decoupled from social interaction.

Serpent Handling: Toward a Cognitive Account – Honoring the Scholarship of Ralph W. Hood Jr.

Article

Full-text available

Jul 2021

The ritual handling of serpents remains an unnoticed cultural form for the explanatory aims and theoretical insights desired by cognitive scientists of religion. In the current article, we introduce the Hood and Williams archives at The University of Tennessee at Chattanooga that contains data culled from Hood's 40-plus year career of studying serpent handlers. The archives contain hundreds of hours of interviews and recordings of speaking in tongues, handling fire, drinking poison, and taking up serpents by different congregants and congregations. The archive remains a rich but untapped source of data for building, testing, and refining cognitive theories of ritual in general, and serpent handling in specific. We connect Hood's work to current cognitive theories and engage critically with research on the social functions of ritual. Finally, we discuss several further reasons to pay more attention to SHS communities and practices in cognitive theories of ritual.

Social and endogenous motivations in the emergence of canonical babbling in infants at low and high risk for autism

Preprint

Full-text available

May 2021

There is a growing body of research emphasizing the role of social and endogenous motivations in human development. The present study evaluated canonical babbling across the second-half year of life using all-day recordings of 98 children with typical or elevated likelihoods of autism i.e., at “low risk” or “high risk”, respectively. Canonical babbling ratios (CBRs) were calculated from human coding along with Likert-scale ratings on vocal turn taking and vocal play in each segment. We observed no main effect of risk on CBRs. CBRs were significantly elevated during high vocal play. High turn taking yielded a weaker significant effect. We conclude that both social and endogenous motivations may drive infants’ tendencies to produce their most advanced vocal forms.

Evolutionary Psychology and Psychiatry

Chapter

Full-text available

Dec 2020

In an ideal world, psychiatry would be appropriately informed by evolutionary theory and we expect that this will happen one day. In this chapter salient evolutionary contributions regarding the definition and demarcation of mental disorder are considered as well as evolutionary proposals for rethinking the classification of mental disorder. Although evolutionary analysis of mental disorders rests on a set of principles shared with the rest of medicine, these principles remain unfamiliar to the majority of psychiatrists. We examine these principles and advocate consideration of the phylogenetic or ultimate causes of disorders and how Tinbergen’s four questions may be applied to psychiatry. Leading evolutionary literature on a number of psychiatric conditions is explored including: schizophrenia spectrum disorders, depression, alcohol and drug addictions, eating disorders and others. Some preliminary evolutionary thoughts on placebo responses, pharmacological treatments and future research are also presented in brief. Mainstream psychiatry, like the rest of medicine, continues to focus on proximate causation of disease and disorder. Evolutionary science has not permeated the syllabus of most undergraduate or postgraduate medical and psychiatric education, with a few notable exceptions. Consequently, most psychiatrists have scant understanding of even the basics of evolution let alone its impact on the behavioural sciences. Therefore, the majority of psychiatrists and other mental health professionals remain largely unaware of the potential of Darwinian theory to further our understanding of human vulnerability to mental disorder. Evolutionary work consequently has not yet significantly influenced the mainstream research agenda in mental health nor has it had much impact on clinical practice. Various barriers to the incorporation and dissemination of evolutionary thinking into psychiatry are discussed, some of which are shared by the rest of medicine. Finally, we contemplate the potential contributions evolutionary science can generate for both theory and practice of psychiatry and advocate for pertinent areas of evolutionary biology to be taught at both the undergraduate and postgraduate levels as a basic science.

Is It Schizophrenia or Not? Different Biological Characterization

Chapter

Jan 2023

Videsha Bansal

Schizophrenia (SZD) is one of the chronic disorders but is not very common. The symptoms of SZD are broadly divided into two types: positive and negative symptoms. Still SZD is hard to diagnose at an initial level because it shares some similar characteristics with other disorders like Alzheimer’s (AD), Parkinson’s (PD), or chronic and manic depression. Characterizing it from other mental disorders is one of the most vital works. In this chapter, we have covered five major mental disorders which share some or the other common characteristics. We have selected SZD, AD, PD, chronic depression, and Bi-polar disorder. Starting from their definition to its severity, we have highlighted different characteristics like biological, psychological, and cognitive characteristics of SZD, and how it is different from other disorders. Wherever possible we have also linked more than two disorders and ways to differentiate them from each other. We have also discussed the clinical methods to diagnose each selected mental disorder and is there an effective way to treat it or not. This chapter sheds a limited light on each selected disorder.

Introduction to Evolutionary Psychiatry

Chapter

Full-text available

Sep 2022

Evolutionary psychiatry attempts to explain and examine the development and prevalence of psychiatric disorders through the lens of evolutionary and adaptationist theories. In this edited volume, leading international evolutionary scholars present a variety of Darwinian perspectives that will encourage readers to consider 'why' as well as 'how' mental disorders arise. Using insights from comparative animal evolution, ethology, anthropology, culture, philosophy and other humanities, evolutionary thinking helps us to re-evaluate psychiatric epidemiology, genetics, biochemistry and psychology. It seeks explanations for persistent heritable traits shaped by selection and other evolutionary processes, and reviews traits and disorders using phylogenetic history and insights from the neurosciences as well as the effects of the modern environment. By bridging the gap between social and biological approaches to psychiatry, and encouraging bringing the evolutionary perspective into mainstream psychiatry, this book will help to inspire new avenues of research into the causation and treatment of mental disorders.

The Puzzle of the Unbalanced Mind

Article

Full-text available

Dec 2001
Psychol Today

Randolph M Nesse

Why do genes for mental disorders persist? This article argues it is because traits with a cliff-edged fitness function are shaped to a performance peak where some individuals fall off.

Movie for the Assessment of Social Cognition (MASC): Spanish Validation

Article

Full-text available

Feb 2014
J AUTISM DEV DISORD

We present the Spanish validation of the "Movie for the Assessment of Social Cognition" instrument (MASC-SP). We recruited 22 adolescents and young adults with Asperger syndrome and 26 participants with typical development. The MASC-SP and three other social cognition instruments (Ekman Pictures of Facial Affect test, Reading the Mind in the Eyes Test, and Happé's Strange Stories) were administered to both groups. Individuals with Asperger syndrome had significantly lower scores in all measures of social cognition. The MASC-SP showed strong correlations with all three measures and relative independence of general cognitive functions. Internal consistency was optimal (0.86) and the test-retest was good. The MASC-SP is an ecologically valid and useful tool for assessing social cognition in the Spanish population.

The autism and schizophrenia associated gene CYFIP1 is critical for the maintenance of dendritic complexity and the stabilization of mature spines.

Article

Full-text available

Jun 2014

Copy number variation (CNV) at the 15q11.2 region has been identified as a significant risk locus for neurological and neuropsychiatric conditions such as schizophrenia (SCZ) and autism spectrum disorder (ASD). However, the individual roles for genes at this locus in nervous system development, function and connectivity remain poorly understood. Haploinsufficiency of one gene in this region, Cyfip1, may provide a model for 15q11.2 CNV-associated neuropsychiatric phenotypes. Here we show that altering CYFIP1 expression levels in neurons both in vitro and in vivo influences dendritic complexity, spine morphology, spine actin dynamics and synaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor lateral diffusion. CYFIP1 is highly enriched at synapses and its overexpression in vitro leads to increased dendritic complexity. Neurons derived from Cyfip1 heterozygous animals on the other hand, possess reduced dendritic complexity, increased mobile F-actin and enhanced GluA2-containing AMPA receptor mobility at synapses. Interestingly, Cyfip1 overexpression or haploinsufficiency increased immature spine number, whereas activity-dependent changes in spine volume were occluded in Cyfip1 haploinsufficient neurons. In vivo, Cyfip1 heterozygous animals exhibited deficits in dendritic complexity as well as an altered ratio of immature-to-mature spines in hippocampal CA1 neurons. In summary, we provide evidence that dysregulation of CYFIP1 expression levels leads to pathological changes in CNS maturation and neuronal connectivity, both of which may contribute to the development of the neurological symptoms seen in ASD and SCZ.

Evolutionary foundations for psychiatric diagnosis: making DSM-V valid1

Chapter

Full-text available

Mar 2011

The Oxford Handbook of the Development of Imagination

Article

Apr 2013

Children are widely celebrated for their imaginations, but developmental research on this topic has often been fragmented or narrowly focused on fantasy. However, there is growing appreciation for the role that imagination plays in cognitive and emotional development, as well as its link with children’s understanding of the real world. With their imaginations, children mentally transcend time, place, and/or circumstance to think about what might have been, plan and anticipate the future, create fictional relationships and worlds, and consider alternatives to the actual experiences of their lives. The Oxford Handbook of the Development of Imagination provides a comprehensive overview of this broad new perspective by bringing together leading researchers whose findings are moving the study of imagination from the margins of mainstream psychology to a central role in current efforts to understand human thought. The topics include fantasy-reality distinctions, pretend play, magical thinking, narrative, anthropomorphism, counterfactual reasoning, mental time travel, creativity, paracosms, imaginary companions, imagination in non-human animals, the evolution of imagination, autism, dissociation, and the capacity to derive real life resilience from imaginative experiences. Many of the chapters include discussions of the educational, clinical, and legal implications of the research findings and special attention is given to suggestions for future research.

Creativity and Psychopathology: A Shared Vulnerability Model

Article

Mar 2011

Shelley H Carson

Creativity is considered a positive personal trait. However, highly creative people have demonstrated elevated risk for certain forms of psychopathology, including mood disorders, schizophrenia spectrum disorders, and alcoholism. A model of shared vulnerability explains the relation between creativity and psychopathology. This model, supported by recent findings from neuroscience and molecular genetics, suggests that the biological determinants conferring risk for psychopathology interact with protective cognitive factors to enhance creative ideation. Elements of shared vulnerability include cognitive disinhibition (which allows more stimuli into conscious awareness), an attentional style driven by novelty salience, and neural hyperconnectivity that may increase associations among disparate stimuli. These vulnerabilities interact with superior meta-cognitive protective factors, such as high IQ, increased working memory capacity, and enhanced cognitive flexibility, to enlarge the range and depth of stimuli available in conscious awareness to be manipulated and combined to form novel and original ideas.

The brain's default network: Anatomy, function and relevance to disease

Article

Jan 2008

Psychosis and autism as diametrical disorders of the social brain

Article

Jan 2008

The Evolutionary Biology of Human Neurodevelopment: Evo-Neuro-Devo Comes of Age

Chapter

Nov 2015

This chapter discusses the field of evo-neuro-devo, an emerging discipline that focuses on how human neurodevelopment, and risk for psychiatric conditions mediated by neurodevelopment. It overviews segregating genetic variation, and de novo (new germline) mutations, provide novel insights into human neurodevelopmental gene functions, including effects from pleiotropy, polygenic inheritance, and developmental-genetic convergence. The chapter addresses how are the causes and phenotypes of the primary human neurodevelopmental conditions, especially autism and schizophrenia, related to recent neurodevelopmental and cognitive changes in human evolutionary history. It focuses on how genetic factors that cause changes in the rate and timing patterns of neurodevelopmental events, and associated psychological phenotypes, are involved in autism spectrum conditions and schizophrenia. The chapter describes a "developmental heterochronic" model for helping to explain the genetic bases of these two conditions, and connect the model with heterochronic change in human ancestry.

Jumping to delusions in early psychosis

Article

Aug 2006

R. Langdon

Creativity and Mental Illness

Book

Aug 2014

James C. Kaufman

Are creative people more likely to be mentally ill? This basic question has been debated for thousands of years, with the 'mad genius' concept advanced by such luminaries as Aristotle. There are many studies that argue the answer is 'yes', and several prominent scholars who argue strongly for a connection. There are also those who argue equally strongly that the core studies and scholarship underlying the mad genius myth are fundamentally flawed. This book re-examines the common view that a high level of individual creativity often correlates with a heightened risk of mental illness. It reverses conventional wisdom that links creativity with mental illness, arguing that the two traits are not associated. With contributions from some of the most exciting voices in the fields of psychology, neuroscience, physics, psychiatry, and management, this is a dynamic and cutting-edge volume that will inspire new ideas and studies on this fascinating topic.

The Evolutionary Etiologies of Autism Spectrum and Psychotic Affective Spectrum Disorders

Abstract

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