Changing perspectives on autism: Overlapping contributions of evolutionary psychiatry and the neurodiversity movement

Perspectives on autism and psychiatric conditions are affected by a mix of scientific and social influences. Evolutionary psychiatry (EP) and the neurodiversity movement are emerging paradigms that reflect these distinct influences, with the former grounded in scientific theory and the latter driven by political and social principles. Despite their separate foundations, there is a significant overlap between EP and neurodiversity that has not been explored. Specifically, both paradigms reframe disorders as natural cognitive differences rather than disease; expand the concept of "normal" beyond that implied in modern psychiatry; focus on relative strengths; recognize that modern environments disadvantage certain individuals to cause functional impairment; emphasize cognitive variation being socially accommodated and integrated rather than treated or cured; and can help reduce stigmatization. However, in other ways, they are distinct and sometimes in conflict. EP emphasizes scientific explanation, defines "dysfunction" in objective terms, and differentiates heterogenous cases based on underlying causes (e.g. autism due to de novo genetic mutations). The neurodiversity movement emphasizes social action, removes barriers to inclusion, promotes inclusive language, and allows unrestricted identification as neurodivergent. By comparing and contrasting these two approaches, we find that EP can, to some extent, support the goals of neurodiversity. In particular, EP perspectives could be convincing to groups more responsive to scientific evidence and help achieve a middle ground between neurodiversity advocates and critics of the movement

Genetic and endocrine correlates of variation in human sociality

Hormones play evolutionarily ancient roles in social behaviour; yet the degree to which hormone systems influence human socio-emotional behaviour remains unclear. It is hypothesized that (i) hormone-associated genes linked to psychiatric conditions contribute to variation in social traits among non-clinical populations, and (ii) changes in endogenous hormone levels coordinate adaptive social behaviour with stimuli in the environment. Consistent with the first hypothesis, a vasopressin receptor polymorphism linked to autism was significantly associated with autistic-like traits in healthy individuals. Consistent with the second hypothesis, an empathy-inducing stimulus was found to mediate a trade-off in hormone levels, with oxytocin increasing and testosterone decreasing. Furthermore, a common polymorphism in the general transcription factor II-I gene, which is linked to Williams syndrome, was associated with oxytocin response to the empathy-inducing stimulus and social anxiety among healthy individuals. Together, these findings highlight the diverse ways through which hormone systems contribute to variation in human sociality

Effects of oxytocin administration on salivary sex hormone levels in autistic and neurotypical women

Abstract: Background: Oxytocin administration, which may be of therapeutic value for individuals with social difficulties, is likely to affect endogenous levels of other socially relevant hormones. However, to date, the effects of oxytocin administration on endogenous hormones have only been examined in neurotypical individuals. The need to consider multi-hormone interactions is particularly warranted in oxytocin trials for autism due to evidence of irregularities in both oxytocin and sex steroid systems. Methods: In this double-blind cross-over study, saliva samples were collected from 16 autistic and 29 neurotypical women before and after intranasal administration of 24 IU oxytocin or placebo. Oestradiol, testosterone, and oxytocin levels were quantified in saliva samples. Participants also completed the Autism-Spectrum Quotient (AQ) and Empathy Quotient (EQ) questionnaires. Results: Distinct patterns of change in testosterone and oestradiol levels pre- to-post-administration were observed in autistic relative to neurotypical women (ANCOVA, p < 0.05 main effect of Group), controlling for sample collection time. The mean percent change oestradiol was + 8.8% for the autism group and − 13.0% for the neurotypical group (t = 1.81, p = 0.08), while the mean percent change testosterone was + 1.1% in the autism group and − 12.6% in the neurotypical group (t = 1.26, p = 0.22). In the oxytocin condition, the mean percent change oestradiol was + 12.6% in the autism group and − 6.9% in the neurotypical group (t = 1.78, p = 0.08), while the mean percent change testosterone was + 14.4% in the autism group and − 15.2% in the neurotypical group (t = 3.00, p = 0.006). Robust regression confirmed that group differences in percent change hormone levels were not driven by a small number of influential individuals. Baseline hormone levels did not differ between groups when considered individually. However, baseline testosterone relative to oestradiol (T:E2 ratio) was higher in autistic women (p = 0.023, Cohen’s d = 0.63), and this ratio correlated positively and negatively with AQ and EQ scores, respectively, in the combined sample. Limitations: Further studies with larger and more diverse autistic sample are warranted to confirm these effects. Conclusions: This study provides the first evidence that oxytocin influences endogenous testosterone levels in autistic individuals, with autistic women showing increases similar to previous reports of neurotypical men. These findings highlight the need to consider sex steroid hormones as a variable in future oxytocin trials

Changing perspectives on autism: Overlapping contributions of evolutionary psychiatry and the neurodiversity movement

Publication status: PublishedFunder: Fondation Pierre Mercier; doi: http://dx.doi.org/10.13039/501100022761Funder: Universität Zürich; doi: http://dx.doi.org/10.13039/501100006447AbstractPerspectives on autism and psychiatric conditions are affected by a mix of scientific and social influences. Evolutionary psychiatry (EP) and the neurodiversity movement are emerging paradigms that reflect these distinct influences, with the former grounded in scientific theory and the latter driven by political and social principles. Despite their separate foundations, there is a significant overlap between EP and neurodiversity that has not been explored. Specifically, both paradigms reframe disorders as natural cognitive differences rather than disease; expand the concept of “normal” beyond that implied in modern psychiatry; focus on relative strengths; recognize that modern environments disadvantage certain individuals to cause functional impairment; emphasize cognitive variation being socially accommodated and integrated rather than treated or cured; and can help reduce stigmatization. However, in other ways, they are distinct and sometimes in conflict. EP emphasizes scientific explanation, defines “dysfunction” in objective terms, and differentiates heterogenous cases based on underlying causes (e.g. autism due to de novo genetic mutations). The neurodiversity movement emphasizes social action, removes barriers to inclusion, promotes inclusive language, and allows unrestricted identification as neurodivergent. By comparing and contrasting these two approaches, we find that EP can, to some extent, support the goals of neurodiversity. In particular, EP perspectives could be convincing to groups more responsive to scientific evidence and help achieve a middle ground between neurodiversity advocates and critics of the movement.</jats:p

CD38 genetic variation is associated with increased personal distress to an emotional stimulus

AbstractGenetic variation in CD38—a putative oxytocin pathway gene—has been linked to higher oxytocin levels, empathy, and sensitive parenting, but also to more negative interpersonal outcomes (e.g., alienation from friends and family, poorer romantic relationship quality). To reconcile these seemingly contradictory findings, we drew upon the idea that CD38 variation may heighten social-emotional sensitivity and, consequently, make individuals prone to negative emotions in distressing interpersonal situations. To test this hypothesis, we performed a secondary analysis of a dataset including participants’ (n = 171; 94 females) empathic concern (“sympathetic”) and distress-related (“anxious”) responses to an emotional video. Distress responses were higher for the CD38 rs3796863 AA/AC group vs. the CC group (p = 0.03, η2 = 0.027); however, there was no significant effect of genotype for empathic concern responses to the video or for indices of trait empathy. These findings provide preliminary evidence that, in the face of an interpersonal stressor, CD38 genetic variation may predict more self-focused, aversive emotional reactions. More broadly, this finding highlights the need to adopt a more nuanced perspective in which the influence of oxytocin system variation (assessed by oxytocin-related genetic variation) should be considered in light of the social context.</jats:p

CD38 genetic variation is associated with increased personal distress to an emotional stimulus

Abstract Genetic variation in CD38—a putative oxytocin pathway gene—has been linked to higher oxytocin levels, empathy, and sensitive parenting, but also to more negative interpersonal outcomes (e.g., alienation from friends and family, poorer romantic relationship quality). To reconcile these seemingly contradictory findings, we drew upon the idea that CD38 variation may heighten social-emotional sensitivity and, consequently, make individuals prone to negative emotions in distressing interpersonal situations. To test this hypothesis, we performed a secondary analysis of a dataset including participants’ (n = 171; 94 females) empathic concern (“sympathetic”) and distress-related (“anxious”) responses to an emotional video. Distress responses were higher for the CD38 rs3796863 AA/AC group vs. the CC group (p = 0.03, η2 = 0.027); however, there was no significant effect of genotype for empathic concern responses to the video or for indices of trait empathy. These findings provide preliminary evidence that, in the face of an interpersonal stressor, CD38 genetic variation may predict more self-focused, aversive emotional reactions. More broadly, this finding highlights the need to adopt a more nuanced perspective in which the influence of oxytocin system variation (assessed by oxytocin-related genetic variation) should be considered in light of the social context

Procyshyn 2017 GTF2I Oxytocin Electronic Supplementary Materials from The Williams syndrome prosociality gene GTF2I mediates oxytocin reactivity and social anxiety in a healthy population

Supplementary Tables S1 - S4, Supplementary Figure S

Procyshyn 2017 GTF2I Oxytocin DataSet from The Williams syndrome prosociality gene GTF2I mediates oxytocin reactivity and social anxiety in a healthy population

Demographic data, anxiety score, oxytocin measurements, GTF2I genotyping dat

Procyshyn 2017 GTF2I Oxytocin Electronic Supplementary Materials from The Williams syndrome prosociality gene GTF2I mediates oxytocin reactivity and social anxiety in a healthy population

Supplementary Tables S1 - S4, Supplementary Figure S