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Draft:Evolutionary Approaches to Autism

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Evolutionary Approaches to Autism

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Evolutionary approaches to autism aim to understand the persistence of autism spectrum disorder (ASD) in human populations through the lens of evolutionary biology and psychology. While autism is commonly understood as a neurodevelopmental condition marked by difficulties with social interaction, communication, and a tendency toward repetitive behaviors, its relatively high prevalence—affecting about 1 in 36 children in the U.S.[1]—and strong genetic component pose an evolutionary puzzle. If autism is both highly heritable and linked to characteristics that can limit reproductive success, why hasn’t natural selection phased out the genes involved? Researchers have proposed a range of theories, suggesting that certain autistic traits might offer cognitive or adaptive advantages, or that they result from evolutionary trade-offs in human brain development. Still, these ideas remain largely hypothetical and continue to spark active debate in the scientific community.

Background

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Autism spectrum disorder (ASD) is a highly variable condition, ranging from mild to severe, and is defined by difficulties in social communication alongside restricted interests or repetitive behaviors. A large body of research has shown that autism has a strong genetic basis. Heritability estimates from twin and family studies are generally high—often between 50% and 90%—pointing to a significant role for inherited genetic variation in shaping autism risk.[2][3] Crucially, autism is not linked to a single gene. Instead, it results from a complex mix of genetic influences, including both rare mutations with large effects and common variants that each contribute a small amount. This complexity helps explain why autism-associated traits can persist across generations. Even if more severe forms of ASD reduce an individual’s reproductive success, many genes involved may still be passed on by relatives who carry them in less pronounced forms. In addition, new (de novo) mutations arising each generation introduce further variation, keeping these traits in circulation over time.[4]

Despite the challenges it can pose, autism remains relatively common. Global estimates suggest that roughly 1 in 100 children receive an ASD diagnosis.[5] The consistency of autism-like traits across cultures and throughout history suggests that the underlying predispositions have been part of human variation for a long time—well before autism was formally described. The clinical concept only emerged in the mid-20th century, when Leo Kanner and Hans Asperger introduced it in the 1940s,[6] but the behaviors it describes likely existed long before that. Evolutionary thinking about autism began to take shape more recently, especially in the 1990s and 2000s, as researchers began to ask why natural selection would preserve genes that seem to impair social communication. One clue lies in observations of family members of autistic individuals, who often display traits associated with the so-called “broader autism phenotype”—such as strong attention to detail or aptitude for technical tasks—without meeting the threshold for a diagnosis.[7]

Some early hypotheses suggested that cognitive styles commonly seen in autism might have been useful in ancestral environments. Psychologist Simon Baron-Cohen, for example, proposed that the same traits that make social engagement difficult—like intense focus on patterns or objects—might have been helpful for early humans involved in tasks such as tool-making, hunting, or navigation.[8] In that context, someone less distracted by social cues and more preoccupied with systems might have contributed valuable skills to the group. This idea reflects a broader theme in evolutionary psychiatry: that traits we now classify as disorders may sometimes represent the extreme end of normal variation—potentially beneficial in some settings, even if problematic in others.

The Social Brain Hypothesis and Cognitive Trade-Offs

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One influential framework for thinking about autism from an evolutionary perspective is the social brain hypothesis. This idea holds that the human brain expanded in size and complexity primarily to deal with the demands of social life—navigating relationships, managing group dynamics, and interpreting others’ intentions. Abilities like empathy, theory of mind (the ability to to understand others’ mental states), and effective communication would have been under strong selective pressure in such a context. Since autism affects many of these social capacities, it raises a key question: could strengths in other cognitive domains have offset these challenges in our evolutionary past? Some researchers suggest that autism reflects a kind of cognitive trade-off—where enhanced ability in certain nonsocial areas comes at the cost of social cognition.[9][10] Many people on the spectrum show unusually strong skills in areas like pattern recognition, attention to detail, memory, and systematic reasoning, even as they struggle with spontaneous social understanding. This has led to the idea that autism involves an alternative way of allocating cognitive resources—favoring system-focused thinking over socially oriented processing.

Seen this way, autism represents one end of a broader continuum in the general population. People vary in the degree to which they rely on “mechanistic” thinking (understanding systems, patterns, rules) versus “mentalistic” thinking (intuitively grasping other people’s thoughts and feelings). Autism tends to lie at the far end of the mechanistic side—more “mind mechanics” than “mind reading.”[11] From an evolutionary standpoint, a brain wired for systems rather than people might have been highly useful in certain roles: tool-making, navigation, tracking animals, solving practical problems—domains where focus, precision, and analytical thinking were more valuable than social finesse.

This idea ties into Simon Baron-Cohen’s empathizing–systemizing theory—often known as the “extreme male brain” hypothesis. He argued that autism exaggerates typical male cognitive tendencies, with stronger systemizing and weaker empathizing (on average, across sexes).[12] In prehistoric contexts, someone with a strongly systemizing brain might have excelled at survival tasks, especially those requiring intense concentration and emotional detachment—like hunting or dealing with dangerous tools. Empathizing, though vital for social bonding, might have been less helpful—or even a liability—in high-stress, high-risk situations. Applying the social brain hypothesis to autism highlights a key idea: that human evolution may have favored a mix of cognitive styles. Some brains are wired more for social attunement, others for technical insight—and both may have served useful roles in human communities. Today, this line of thinking feeds into the concept of neurodiversity: the idea that cognitive differences like autism aren’t simply deficits, but part of the natural variation that has helped human groups adapt and thrive.

Alternative Hypotheses on the Evolution of Autism

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Beyond broad trade-off theories, several alternative hypotheses have been proposed to explain why ASD traits persist. These hypotheses are not mutually exclusive; each addresses a different facet of autism’s evolution, from developmental timing and energy use to environmental factors and mating patterns.

Life History Theory Perspective

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Life history theory is an evolutionary framework that explains how organisms allocate energy and effort to growth, survival, and reproduction over their lifespans. It often contrasts “fast” life history strategies (characterized by early maturation, high mating effort, and producing more offspring with less investment in each) with “slow” life history strategies (later maturation, fewer offspring, and high parental investment in each). Intriguingly, researchers have suggested that autism may be associated with a slow life history strategy. Individuals with ASD tend to engage in fewer risky and impulsive behaviors, have lower interest in short-term mating or casual sexual relationships, and often delay milestones like independent living or starting a family. [13] Population studies indicate that, on average, people on the autism spectrum have fewer children than neurotypical peers and often start families later in life, investing substantial time and resources in personal development or specific interests instead.[14]

From an evolutionary perspective, slow strategies are advantageous in stable or predictable environments, where investing heavily in a few offspring (or in one’s own prolonged development) can maximize those offsprings’ success. Fast strategies, conversely, are adaptive in dangerous or unpredictable environments, where “reproduce early and often” hedges against the chance of not surviving long. The fact that autistic-like traits correlate with caution, long-term planning, and reduced reproductive output suggests that ASD might represent an extreme slow strategy that persists because such a strategy was sometimes beneficial in our evolutionary past. Indeed, a recent synthesis classified autism spectrum conditions (along with certain other traits like conscientiousness and risk-aversion) as “slow spectrum” traits in evolutionary terms.[15] Variation in life history strategies within a population is expected – evolution “hedges its bets” by producing both fast and slow strategists so that some will thrive under different condition. In this light, autism could be maintained in the gene pool as part of a diversified bet-hedging strategy: most people follow a moderate strategy, some exhibit fast-strategy traits, and some (including many with ASD) exhibit slow-strategy traits that, while reducing reproductive rate in the current environment, could have been advantageous in contexts where longevity, expertise, or intensive parental care improved fitness. This hypothesis encourages viewing autism not strictly as a defect, but as an alternative developmental trajectory that evolution has not eliminated because it can be adaptive under certain ecological circumstances.

Brain Overgrowth and Energy Allocation Hypothesis

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Another line of reasoning focuses on the biology of brain development in autism, noting that many children with ASD show unusual patterns of brain growth. Studies have found that some infants later diagnosed with autism undergo a period of brain overgrowth in the first 1–2 years of life, resulting in larger-than-average head circumference or brain volume for age.[16] This early overproduction of neurons and connections could be seen as a developmental deviation stemming from the same processes that gave humans our large brains. The "expensive brain" hypothesis posits that there is a trade-off in how energy and resources are used during brain development: growing and maintaining neural tissue is extremely costly in metabolic terms, so an optimal developmental plan requires balancing growth with pruning (the elimination of excess connections) to form efficient networks.[17] In autism, the hypothesis suggests that this balance is shifted – perhaps due to genetic tendencies – toward “too much, too soon” brain growth. The result may be a brain that has an abundance of neural connections or neurons that are not pruned in the typical way. Such a brain might excel at certain kinds of information processing (e.g. low-level perception or memory, supported by dense local connectivity) but struggle with integrating information across distant brain regions (since hyper-development can impair the refinement of long-range networks). In effect, the developing autistic brain may allocate extra energy to building neural tissue, at the cost of efficiency in connectivity and social information processing. This idea is consistent with findings of atypical connectivity in ASD: many neuroimaging studies show that autistic brains tend to be hyper-connected on a local scale and under-connected on a global scale, reflecting an abundance of neural wiring in focal “islands” but less synchronized communication between different functional regions.[18]

Evolutionarily, why would such a costly and unbalanced brain development persist? One explanation is that the genetic variants that nudge the brain toward “overdevelopment” were favored because, in moderation, they contributed to greater intelligence or other advantages. Human brains expanded dramatically in size and capability over the course of evolution, and this likely involved genes that promote neural growth. However, pushing these genes’ effects too far can lead to neurodevelopmental disorders. Recent research supports this pleiotropic trade-off: for instance, the same gene families (NOTCH2NL and those involving Olduvai repeats) that drove the evolutionary enlargement of the human cerebral cortex have been implicated in ASD when present in extra copies.[19] Duplication of such brain-growth genes can cause excessive neuron proliferation and is associated with autism (as well as macrocephaly), whereas deletions of the same genes can cause microcephaly or schizophrenia in other cases. This suggests a delicate evolutionary balancing act. The brain overgrowth hypothesis proposes that autism represents a case where the balance tipped too far: genes that normally give our species a cognitive edge by enlarging and energizing the brain end up overshooting in certain individuals, leading to developmental dysfunction. Those genes remain in the population because, on the whole, they were hugely beneficial to human survival and intelligence, even though in some unlucky combinations they contribute to conditions like ASD. In summary, the brain overgrowth and energy allocation perspective views autism as a costly byproduct of the evolution of our large, energy-hungry brains – a price that evolution is “willing” to pay because the net benefits of a bigger brain outweigh the occasional liabilities.

Maternal Immune Activation Hypothesis

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Not all evolutionary considerations are purely genetic; some involve gene–environment interactions that have been consistent pressures over evolutionary time. One such factor is the maternal immune system. The maternal immune activation (MIA) hypothesis proposes that when a pregnant woman’s immune system is strongly activated – for example, by infections or inflammation – it can disrupt the neurodevelopment of the fetus in ways that increase the risk of autism in the child​.[20] Epidemiologically, studies have noted that children born to mothers who experienced serious viral or bacterial infections, high fever, or autoimmune inflammation during pregnancy have higher rates of ASD (and other neurodevelopmental disorders like schizophrenia) than typical​.[21] In laboratory experiments, exposing pregnant mice to immune challenges (like viral mimics) produces offspring with behavioral abnormalities analogous to autism, indicating a causal link between prenatal immune stress and later social behavior changes.[22]

From an evolutionary standpoint, the MIA hypothesis is often framed as a trade-off between immune defense and brain development. A robust immune response in the mother is crucial for her survival and the protection of the fetus against pathogens – throughout human evolution, maternal infections have been a major threat to both mother and unborn child. Thus, genes that promote strong immune reactions (e.g. fever, inflammation) during pregnancy would be favored because they help eliminate infectious agents. However, these same inflammatory responses can cross the placenta or affect the intrauterine environment, exposing the developing fetal brain to cytokines and other immune molecules that alter how neurons proliferate and connect.[23][24] The result can be subtle changes in brain wiring that predispose the child to autism. Evolution may tolerate this risk because the immediate benefit of fighting off an infection (and ensuring the mother’s and fetus’s survival) is extremely high, whereas the cost – an increased chance of neurodevelopmental issues – is a longer-term consequence that, in evolutionary terms, might be outweighed by survival. In other words, natural selection prioritizes acute survival over optimizing every aspect of brain development

Assortative Mating Hypothesis

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The assortative mating hypothesis offers a more demographic and social explanation for autism’s persistence. This hypothesis suggests that people do not mate randomly with respect to autistic traits; rather, individuals with certain personality or cognitive profiles associated with the broader autism phenotype are more likely to pair up and have children, thereby increasing the odds of those children being on the spectrum.[25] Some supporting evidence for this comes from studies of parents of autistic children: one study found that the mothers and fathers of children with Asperger syndrome both tended to score above average on a test of pattern recognition (the Embedded Figures Test), and many of them worked in technical or scientific fields that require high systemizing ability.[26] Additionally, other research has observed that two parents of an autistic child often share a higher-than-typical number of autistic-like personality traits themselves, suggesting positive correlation (assortment) in their trait profiles[27][28], although another study did not confirm this[29].

Diametrical model of autism and psychosis

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See also Evolutionary approaches to schizophrenia

According to the diametrical model of mental illness, autism and psychotic-spectrum disorders (such as schizophrenia) can be seen as opposite – or diametrically opposed – outcomes of brain development and cognition. This idea, prominently advocated by evolutionary thinkers Bernard Crespi and Christopher Badcock, builds on the observation that many traits in autism seem to be mirror-opposites of traits in schizophrenia. Where autistic individuals often have difficulty attributing intention or mental states to others (sometimes described as mind-blindness), individuals with schizophrenia often over-attribute meaning and intention (leading to paranoia or delusions of reference). Autism is marked by concrete, literal thinking and attention to detail (high mechanistic cognition), whereas psychosis is marked by florid imagination, symbolic or abstract thought gone awry, and hyper-sensitivity to social cues (excess mentalistic cognition).[30][31] The diametrical model encapsulates these contrasts by suggesting that the two conditions lie at opposite ends of a continuum of brain function: one end anchored by an extreme of logical, literal, data-driven processing with minimal intuitive social inference (the autistic end), and the other by an extreme of imaginative, intuitive, socially immersed processing with tenuous grounding in external reality (the psychotic end). Most people, and most of our evolutionary past, operate in the balanced middle – able to mentalize and empathize, but also able to distinguish imagination from reality.

Crespi and Badcock further proposed a potential genetic mechanism for this balancing act: genomic imprinting effects that differentially favor maternal or paternal brain development influences.[32] Genomic imprinting refers to certain genes being expressed only from the mother’s copy or only from the father’s copy. They noted that paternally expressed genes (those where the father’s copy is active) often promote growth of the fetus and selfish resource use, whereas maternally expressed genes tend to limit growth and encourage social attunement (since a mother’s evolutionary interest is to distribute resources among offspring).Autism, in their view, might reflect a bias toward paternal influence: an “extreme of the paternal brain” where growth and mechanistic thinking are emphasized at the expense of social-emotional capacities. Psychosis, conversely, could reflect an extreme of the maternal brain – more sensitive, imaginative, and socially oriented, but at risk of losing touch with concrete reality. Supporting evidence comes from the sex ratio and genetic findings: autism is far more common in males, consistent with an exaggeration of male-typical traits or paternal genetic effects, and many genes implicated in autism are known to be influenced by imprinting or involved in early brain growth control. Meanwhile, conditions on the psychosis spectrum (like schizophrenia) tend to have near-even sex ratios or female slant in certain manifestations, and some genomic regions show opposite effects in autism vs. schizophrenia (for example, certain maternally expressed gene deletions contribute to autism, whereas duplications in the same regions contribute to psychotic features.[33]

Implications for psychiatry and future directions

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Understanding autism through an evolutionary lens has important implications for psychiatry, clinical practice, and future research. Firstly, it reframes ASD from being purely a “disease” or error to being a natural variation in the human condition – a shift that can reduce stigma and promote acceptance.  If autism is seen as part of the spectrum of normal evolutionary variation (albeit an extreme part associated with disability in our current environment), then the goal of interventions shifts from “curing” or eliminating autism to supporting autistic individuals in leveraging their strengths and adapting their environments to their needs. This perspective is highly compatible with the principles of the neurodiversity movement, which calls for respecting neurological differences as one respects ethnic or cultural differences. Clinically, this means focusing on helping autistic people thrive (through skill-building, accommodations, and inclusion) rather than viewing them solely through a deficit model.

In psychiatric taxonomy and genetics, an evolutionary approach encourages looking at dimensions (like life history speed, or mechanistic vs. mentalistic cognition) that cut across traditional diagnostic categories. We see this already in the way autism genetics has revealed overlaps with traits like ADHD, intelligence, and even normal personality variation. It’s possible that future classifications of mental conditions will incorporate evolutionary-strategy dimensions – for instance, identifying a subtype of ASD that represents an extreme slow life history strategy versus another subtype driven by high mutational load. Such distinctions could be clinically useful: a person whose autism arises chiefly from an accumulation of common “high intelligence” alleles might benefit from different support (and have different associated risks, like anxiety or savant skills) compared to a person whose autism is linked to a specific genetic syndrome or prenatal immune challenge.

See also

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References

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  1. ^ CDC (2024-07-19). "Data and Statistics on Autism Spectrum Disorder". Autism Spectrum Disorder (ASD). Retrieved 2025-03-24.
  2. ^ Sandin, Sven; Lichtenstein, Paul; Kuja-Halkola, Ralf; Hultman, Christina; Larsson, Henrik; Reichenberg, Abraham (2017-09-26). "The Heritability of Autism Spectrum Disorder". JAMA. 318 (12): 1182–1184. doi:10.1001/jama.2017.12141. ISSN 0098-7484. PMC 5818813. PMID 28973605.
  3. ^ Franke, Barbara; Fombonne, Eric; Ronald, Angelica (November 2021). "Editorial: The new genetics of autism". Journal of Child Psychology and Psychiatry. 62 (11): 1271–1273. doi:10.1111/jcpp.13527. ISSN 0021-9630. PMID 34708425.
  4. ^ El-Fishawy, Paul; State, Matthew W. (March 2010). "The Genetics of Autism: Key Issues, Recent Findings, and Clinical Implications". Psychiatric Clinics of North America. 33 (1): 83–105. doi:10.1016/j.psc.2009.12.002. PMC 2841771. PMID 20159341.
  5. ^ "Autism". www.who.int. Retrieved 2025-03-24.
  6. ^ Evans, Bonnie (July 2013). "How autism became autism: The radical transformation of a central concept of child development in Britain". History of the Human Sciences. 26 (3): 3–31. doi:10.1177/0952695113484320. ISSN 0952-6951. PMC 3757918. PMID 24014081.
  7. ^ McDonald, T.A. Meridian (January 2021). "The broader autism phenotype constellations–disability matrix paradigm: Theoretical model for autism and the broader autism phenotype". Medical Hypotheses. 146: 110456. doi:10.1016/j.mehy.2020.110456. PMC 8216083. PMID 33412500.
  8. ^ Baron-Cohen, Simon (January 2008). "Autism, Hypersystemizing, and Truth". Quarterly Journal of Experimental Psychology. 61 (1): 64–75. doi:10.1080/17470210701508749. ISSN 1747-0218. PMID 18038339.
  9. ^ Ploeger, Annemie; Galis, Frietson (2020-08-11). "Evolutionary approaches to autism- an overview and integration". McGill Journal of Medicine. 13 (2). doi:10.26443/mjm.v13i2.231. ISSN 1715-8125.
  10. ^ Peng, Ziwen; Chen, Jierong; Jin, Lili; Han, Hongying; Dong, Chenjie; Guo, Ya; Kong, Xuejun; Wan, Guobin; Wei, Zhen (April 2020). "Social brain dysfunctionality in individuals with autism spectrum disorder and their first-degree relatives: An activation likelihood estimation meta-analysis". Psychiatry Research: Neuroimaging. 298: 111063. doi:10.1016/j.pscychresns.2020.111063. PMID 32179248.
  11. ^ Crespi, Bernard; Badcock, Christopher (June 2008). "Psychosis and autism as diametrical disorders of the social brain". Behavioral and Brain Sciences. 31 (3): 241–261. doi:10.1017/S0140525X08004214. ISSN 0140-525X. PMID 18578904.
  12. ^ Baron-Cohen, Simon (1999-06-22). "The Extreme Male-Brain Theory of Autism". Neurodevelopmental Disorders. pp. 390–418. doi:10.7551/mitpress/4945.003.0023. ISBN 978-0-262-28465-3.
  13. ^ Swanepoel, Annie (December 2024). "ADHD and ASD are normal biological variations as part of human evolution and are not "disorders"". Clinical Neuropsychiatry. 21 (6): 451–454. doi:10.36131/cnfioritieditore20240601. ISSN 2385-0787. PMC 11745029. PMID 39839603.
  14. ^ Han, Wen; Chen, Bin-Bin (December 2020). "An evolutionary life history approach to understanding mental health". General Psychiatry. 33 (6): e100113. doi:10.1136/gpsych-2019-100113. ISSN 2517-729X. PMC 7534052. PMID 33089066.
  15. ^ Del Giudice, Marco (2018). Evolutionary psychopathology: a unified approach. New York, NY: Oxford University Press. ISBN 978-0-19-024684-6.
  16. ^ Courchesne, Eric (2003-07-16). "Evidence of Brain Overgrowth in the First Year of Life in Autism". JAMA. 290 (3): 337–344. doi:10.1001/jama.290.3.337. ISSN 0098-7484. PMID 12865374.
  17. ^ Smith, Alastair D; De Lillo, Carlo (2021-10-21). "Sources of variation in search and foraging: A theoretical perspective". Quarterly Journal of Experimental Psychology. 75 (2): 197–231. doi:10.1177/17470218211050314. ISSN 1747-0218. PMID 34609229.
  18. ^ Misra, Vivek (2014-04-01). "The Social Brain Network and Autism". Annals of Neurosciences. 21 (2): 69–73. doi:10.5214/ans.0972.7531.210208. PMC 4117155. PMID 25206065.
  19. ^ Duński, Eryk; Pękowska, Aleksandra (2022-11-21). "Keeping the balance: Trade-offs between human brain evolution, autism, and schizophrenia". Frontiers in Genetics. 13. doi:10.3389/fgene.2022.1009390. ISSN 1664-8021. PMC 9719942. PMID 36479251.
  20. ^ Zawadzka, Aleksandra; Cieślik, Magdalena; Adamczyk, Agata (2021-10-26). "The Role of Maternal Immune Activation in the Pathogenesis of Autism: A Review of the Evidence, Proposed Mechanisms and Implications for Treatment". International Journal of Molecular Sciences. 22 (21): 11516. doi:10.3390/ijms222111516. ISSN 1422-0067. PMC 8584025. PMID 34768946.
  21. ^ Atladóttir, Hjördis Ó.; Thorsen, Poul; Østergaard, Lars; Schendel, Diana E.; Lemcke, Sanne; Abdallah, Morsi; Parner, Erik T. (December 2010). "Maternal Infection Requiring Hospitalization During Pregnancy and Autism Spectrum Disorders". Journal of Autism and Developmental Disorders. 40 (12): 1423–1430. doi:10.1007/s10803-010-1006-y. ISSN 0162-3257. PMID 20414802.
  22. ^ Careaga, Milo; Murai, Takeshi; Bauman, Melissa D. (March 2017). "Maternal Immune Activation and Autism Spectrum Disorder: From Rodents to Nonhuman and Human Primates". Biological Psychiatry. 81 (5): 391–401. doi:10.1016/j.biopsych.2016.10.020. PMC 5513502. PMID 28137374.
  23. ^ Deverman, Benjamin E.; Patterson, Paul H. (October 2009). "Cytokines and CNS Development". Neuron. 64 (1): 61–78. doi:10.1016/j.neuron.2009.09.002. PMID 19840550.
  24. ^ Garay, Paula (2010). "Novel roles for immune molecules in neural development: implications for neurodevelopmental disorders". Frontiers in Synaptic Neuroscience. 2: 136. doi:10.3389/fnsyn.2010.00136. PMC 3059681. PMID 21423522.
  25. ^ Baron-Cohen, Simon (July 2006). "The hyper-systemizing, assortative mating theory of autism". Progress in Neuro-Psychopharmacology and Biological Psychiatry. 30 (5): 865–872. doi:10.1016/j.pnpbp.2006.01.010. PMID 16519981.
  26. ^ Baron-Cohen, Simon; Hammer, Jessica (1997-07-01). "Parents of Children with Asperger Syndrome: What is the Cognitive Phenotype?". Journal of Cognitive Neuroscience. 9 (4): 548–554. doi:10.1162/jocn.1997.9.4.548. ISSN 0898-929X. PMID 23968217.
  27. ^ Virkud, Yamini V.; Todd, Richard D.; Abbacchi, Anna M.; Zhang, Yi; Constantino, John N. (2009-04-05). "Familial aggregation of quantitative autistic traits in multiplex versus simplex autism". American Journal of Medical Genetics Part B: Neuropsychiatric Genetics. 150B (3): 328–334. doi:10.1002/ajmg.b.30810. ISSN 1552-4841. PMC 2819431. PMID 18618672.
  28. ^ Constantino, John N.; Todd, Richard D. (March 2005). "Intergenerational transmission of subthreshold autistic traits in the general population". Biological Psychiatry. 57 (6): 655–660. doi:10.1016/j.biopsych.2004.12.014. PMID 15780853.
  29. ^ Hoekstra, Rosa A.; Bartels, Meike; Verweij, Catharina J. H.; Boomsma, Dorret I. (2007-04-01). "Heritability of Autistic Traits in the General Population". Archives of Pediatrics & Adolescent Medicine. 161 (4): 372–377. doi:10.1001/archpedi.161.4.372. ISSN 1072-4710. PMID 17404134.
  30. ^ Ritsner, Michael S. (2011). Handbook of Schizophrenia Spectrum Disorders, Volume I: Conceptual Issues and Neurobiological Advances. SpringerLink Bücher. Dordrecht: Springer Netherlands. ISBN 978-94-007-0836-5.
  31. ^ Crespi, Bernard; Leach, Emma; Dinsdale, Natalie; Mokkonen, Mikael; Hurd, Peter (May 2016). "Imagination in human social cognition, autism, and psychotic-affective conditions". Cognition. 150: 181–199. doi:10.1016/j.cognition.2016.02.001. PMID 26896903.
  32. ^ Badcock, C.; Crespi, B. (2006-07-01). "Imbalanced genomic imprinting in brain development: an evolutionary basis for the aetiology of autism". Journal of Evolutionary Biology. 19 (4): 1007–1032. doi:10.1111/j.1420-9101.2006.01091.x. ISSN 1010-061X. PMID 16780503.
  33. ^ Crespi, Bernard; Badcock, Christopher (June 2008). "Psychosis and autism as diametrical disorders of the social brain". Behavioral and Brain Sciences. 31 (3): 241–261. doi:10.1017/S0140525X08004214. ISSN 0140-525X. PMID 18578904.
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