Abstract Introduction Gender Dysphoria (GD) is characterized by a marked incongruence between an individual’s experienced gender and the one assigned at birth. Autism Spectrum Disorder (ASD) is a neurodevelopmental condition marked by social communication difficulties, restricted interests, and repetitive behaviours. Recent evidence suggests an increased prevalence of ASD among individuals with GD, with studies estimating comorbidity rates between 6–26%. This overlap has raised questions regarding potential shared biological, psychological, and social mechanisms. Objective To review current evidence on the association between Gender Dysphoria and Autism Spectrum Disorder, exploring possible biological, psychological, and social mechanisms, and outlining implications for clinical and mental health care in transgender individuals. Methods A narrative review of the literature was conducted, focusing on historical, diagnostic, and theoretical perspectives regarding GD and ASD. Diagnostic criteria from DSM and ICD editions were compared, and multiple explanatory models, biological, psychological, and social, were analyzed based on recent systematic reviews and meta-analyses. Results Fifteen major theories were identified to explain the association between GD and ASD. Biological hypotheses include prenatal hormonal exposure, birth weight variations, genetic predisposition, and the “Extreme Male Brain” theory. Psychological models emphasize atypical gender development, rigidity, sensory processing differences, and theory of mind alterations. Social explanations involve minority stress, experiences of feeling different, and resistance to social norms. Despite numerous hypotheses, empirical evidence remains inconsistent, and methodological limitations are frequent, such as lack of standardized diagnostic tools and statistical analysis. Conclusions Individuals with co-occurring GD and ASD present higher vulnerability to stigmatization and mental health problems, including anxiety and somatization disorders. Current research mainly focuses on prevalence rather than causation, leaving explanatory mechanisms uncertain. It is unlikely that a single theory accounts for the overlap; rather, different models may apply to different individuals. Theories of “Weakened Sexual Dimorphism” and “Resistance to Social Norms” appear most promising. Future studies should move beyond establishing associations to explore the clinical implications and specific support needs of this population. Disclosure No
Pires et al. (Mon,) studied this question.
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