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This page is an AI-assisted Turkish summary of the study presented at the 26th World Congress of Psychiatry. The study belongs to the presenting authors; please refer to the original source when citing it.

EV0494

OXTR gene polymorphisms as a potential contributor to the overlap between restrictive eating disorders and autism spectrum disorder: preliminary findings

OXTR GENE POLYMORPHISMS AS POTENTIAL CONTRIBUTORS TO THE OVERLAP BETWEEN RESTRICTIVE EATING DISORDERS AND AUTISM SPECTRUM DISORDER - PRELIMINARY FINDINGS

In a preliminary sample of 10 adolescents diagnosed with both anorexia nervosa and autism spectrum disorder, the rs53576 A allele was present in all participants, whereas the rs2254298 A allele was less common; these findings are descriptive and do not demonstrate causality.

The aim is to investigate the potential contribution of oxytocin receptor (OXTR) gene polymorphisms to the overlap between restrictive eating disorders and autism spectrum disorder (ASD). This preliminary report includes the first 10 participants diagnosed with both anorexia nervosa (AN) and ASD from a cohort launched in November 2025 at the Medical University of Silesia, with a target sample size of 200; children and adolescents diagnosed with AN, OSFED, ARFID, and/or ASD were recruited following stabilization during inpatient care and from outpatient clinics, and EAT-26, BDI-II, TAS-20, CAT-Q, and STAI were administered, together with ADOS-2 where applicable. The protocol specified the collection of 25 mL of venous blood using EDTA, an RNA stabilizer, and aprotinin, with storage at -20 degrees; only OXTR rs53576 and rs2254298 were analyzed in this report, using descriptive statistics (median, interquartile range, minimum and maximum values, genotype counts and percentages). In the sample, the median age was 15.0 [14.0 to 16.0], current body mass index was 14.9 kg/m2 [14.3 to 15.9], lowest weight during the illness was 34.0 kg [33.0 to 37.1], and highest lifetime weight was 49.0 kg [43.5 to 52.0]. Median scale scores were reported as 24.0 [17.8 to 31.0] for EAT-26, 56.0 [46.0 to 60.0] for TAS-20 (n = 9), 83.0 [74.8 to 98.0] for CAT-Q, 26.0 [10.8 to 34.3] for BDI-II, 51.5 [37.3 to 52.8] for STAI X-1, and 50.5 [36.8 to 61.3] for STAI X-2. Regarding genotype distribution, for rs53576, 8 participants (80%) had the AA genotype and 2 participants (20%) had the AG genotype, with all 10 participants (100%) carrying the A allele and an A allele frequency of 18/20 (0.90); for rs2254298, 6 participants (60%) had the GG genotype and 4 participants (40%) had the AG genotype, with 4 participants (40%) carrying the A allele and an A allele frequency of 4/20 (0.20). The authors note that these descriptive preliminary findings cannot establish shared genetic causality or clinical utility, and that larger, controlled cohorts are needed to evaluate associations between AN and ASD.

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