medRxiv : the preprint server for health sciences · 2026
Shared genetic and environmental influences between the broad avoidant/restrictive food intake disorder phenotype and neurodevelopmental traits: a twin study.
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Qi Baiyu, Hog Liv, Lichtenstein Paul, Lundström Sebastian, Larsson Henrik, Bulik Cynthia M, Kuja-Halkola Ralf, Taylor Mark J, Dinkler Lisa
Аннотация
IMPORTANCE: Avoidant/restrictive food intake disorder (ARFID) is a feeding and eating disorder characterized by extremely restricted dietary variety and/or quantity resulting in significant physical health impairment and psychosocial dysfunction. ARFID frequently co-occurs with neurodevelopmental conditions, yet the extent to which this co-occurrence reflects shared genetic or environmental influences remains largely unknown, as few twin or genetic studies of ARFID have been conducted.
OBJECTIVE: To examine the extent to which genetic and environmental influences contribute to the association between a broad ARFID phenotype and neurodevelopmental traits.
DESIGN SETTING AND PARTICIPANTS: Population-based twin study using data from the Child and Adolescent Twin Study in Sweden, including 30,374 twins born 1992-2008.
MAIN OUTCOMES AND MEASURES: A broad ARFID phenotype was identified using a composite measure derived from parent reports and national health registers between ages 6 and 12 years. Parents completed measures of neurodevelopmental traits at age 9 or 12 years, including autism (subdomains: social communication problems and restricted/repetitive behaviors), attention-deficit/hyperactivity disorder (ADHD, subdomains: inattention and impulsivity/hyperactivity), tic disorders, learning disorders, oppositional defiant disorder, conduct disorder, obsessive-compulsive disorder (OCD), sensory perception problems, and sleep problems. Phenotypic associations were estimated using polyserial correlations. Bivariate twin models decomposed variance and covariance into genetic and environmental components.
RESULTS: Phenotypic correlations with the broad ARFID phenotype ranged from 0.18 (95% CI: 0.15-0.21) for OCD to 0.36 (95% CI: 0.33-0.38) for autism. Broad genetic correlations (rH; additive plus dominant genetic influences) ranged from 0.27 (95% CI: 0.21-0.33) for conduct disorder to 0.52 (95% CI: 0.44-0.60) for autism-restricted/repetitive behaviors. Genetic factors explained 77% to 95% of all phenotypic correlations. Non-shared environmental correlations were minimal to small, with the largest observed for autism (0.17; 95% CI: 0.08-0.26).
CONCLUSIONS AND RELEVANCE: The broad ARFID phenotype shares substantial genetic influences with a number of neurodevelopmental traits. These findings suggest that the frequent co-occurrence of ARFID with neurodevelopmental traits largely reflects shared genetic influences rather than overlapping environmental influences, supporting the conceptualization of ARFID within a broader neurodevelopmental framework.
OBJECTIVE: To examine the extent to which genetic and environmental influences contribute to the association between a broad ARFID phenotype and neurodevelopmental traits.
DESIGN SETTING AND PARTICIPANTS: Population-based twin study using data from the Child and Adolescent Twin Study in Sweden, including 30,374 twins born 1992-2008.
MAIN OUTCOMES AND MEASURES: A broad ARFID phenotype was identified using a composite measure derived from parent reports and national health registers between ages 6 and 12 years. Parents completed measures of neurodevelopmental traits at age 9 or 12 years, including autism (subdomains: social communication problems and restricted/repetitive behaviors), attention-deficit/hyperactivity disorder (ADHD, subdomains: inattention and impulsivity/hyperactivity), tic disorders, learning disorders, oppositional defiant disorder, conduct disorder, obsessive-compulsive disorder (OCD), sensory perception problems, and sleep problems. Phenotypic associations were estimated using polyserial correlations. Bivariate twin models decomposed variance and covariance into genetic and environmental components.
RESULTS: Phenotypic correlations with the broad ARFID phenotype ranged from 0.18 (95% CI: 0.15-0.21) for OCD to 0.36 (95% CI: 0.33-0.38) for autism. Broad genetic correlations (rH; additive plus dominant genetic influences) ranged from 0.27 (95% CI: 0.21-0.33) for conduct disorder to 0.52 (95% CI: 0.44-0.60) for autism-restricted/repetitive behaviors. Genetic factors explained 77% to 95% of all phenotypic correlations. Non-shared environmental correlations were minimal to small, with the largest observed for autism (0.17; 95% CI: 0.08-0.26).
CONCLUSIONS AND RELEVANCE: The broad ARFID phenotype shares substantial genetic influences with a number of neurodevelopmental traits. These findings suggest that the frequent co-occurrence of ARFID with neurodevelopmental traits largely reflects shared genetic influences rather than overlapping environmental influences, supporting the conceptualization of ARFID within a broader neurodevelopmental framework.