Mapping the genetic landscape of the age at onset and severity of eating disorder symptoms
6 affiliations
- 1Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, UK
- 2UK National Institute for Health and Social Care Research (NIHR) Biomedical Research Centre for Mental Health, South London and Maudsley Hospital, London, UK
- 3Department of Clinical, Educational, and Health Psychology, University College London, London, United Kingdom
- 4Department of Psychology, Humboldt-Universität zu Berlin, Berlin, Germany
- 5National Centre for Register-based Research, Aarhus University, Aarhus, Denmark
- 6Clinic for Child and Adolescent Psychiatry, Psychotherapy and Psychosomatics, German Red Cross Hospitals Westend, Berlin, Germany
Abstract
Background: Eating disorder treatment is most successful when delivered at first onset, underscoring the importance of early intervention. Genetic factors may contribute to earlier onset, but molecular genetic research into symptom onset and severity remains limited.
Aims: We investigated (1) age at onset of behavioural symptoms and low weight, including sex differences, (2) the SNP-based heritability and cross-trait polygenic associations of symptoms, onset, and severity.
Method: Participants (n = 24,973) of genetically-derived European ancestry were from the NIHR BioResource, including the Genetic Links to Anxiety and Depression Study, Eating Disorders Genetics Initiative UK, and COVID-19 Psychiatry and Neurological Genetics Study. Symptoms were assessed with the ED100K questionnaire. We described sex-stratified onset of binge eating, low weight, self-induced vomiting, laxatives, diuretics, excessive exercise, and fasting. SNP-based heritability was estimated using GCTA-GREML. We tested associations with 26 polygenic scores (PGS), which were calculated using SBayesRC.
Results: Symptom median onset ranged from 16-20 years: vomiting (16), fasting and excessive exercise (17), binge eating (18), laxatives (19), diuretics (20), and low weight (20). Males were disproportionately likely to report adult onset. In females, behavioural symptoms and low weight showed substantial heritability (SNP-based h2 = 0.31–0.78), but onset and cognitive symptoms appeared to be less heritable. PGS analyses identified distinct pathways: in females, higher childhood obesity PGS was linked to earlier binge eating onset (~7 months), and higher educational attainment PGS to earlier low weight onset (~6 months).
Conclusions: Eating disorder symptoms begin in adulthood as frequently as adolescence, challenging stereotypes and underscoring investment needed in adult services, particularly for men. While symptoms were strongly heritable, onset and cognitive symptoms showed limited genetic contribution. Symptom-level PGS analyses highlight distinct biological and developmental pathways. Larger sample sizes and more accurate phenotyping are needed.
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BibTeX
@article{davies2026mapping,
title = {{Mapping the genetic landscape of the age at onset and severity of eating disorder symptoms}},
author = {Helena L. Davies and Abigail R. ter Kuile and Zain-Ul-Abideen Ahmad and Sang Hyuck Lee and Rujia Wang and Jessica Mundy and Jonathan Coleman and Carlotta Sampels and Saakshi Kakar and Emily Kelly and Chelsea Mika Malouf and Gursharan Kalsi and Moritz Herle and Gerome Breen and Christopher Hübel},
journal = {The British journal of psychiatry : the journal of mental science},
year = {2026},
month = oct,
doi = {10.1192/bjp.2026.10763},
url = {https://europepmc.org/article/PMC/PMC7619679},
note = {CC BY},
}
RIS
TY - JOUR
TI - Mapping the genetic landscape of the age at onset and severity of eating disorder symptoms
AU - Helena L. Davies
AU - Abigail R. ter Kuile
AU - Zain-Ul-Abideen Ahmad
AU - Sang Hyuck Lee
AU - Rujia Wang
AU - Jessica Mundy
AU - Jonathan Coleman
AU - Carlotta Sampels
AU - Saakshi Kakar
AU - Emily Kelly
AU - Chelsea Mika Malouf
AU - Gursharan Kalsi
AU - Moritz Herle
AU - Gerome Breen
AU - Christopher Hübel
PY - 2026
DA - 2026/10/07
JO - The British journal of psychiatry : the journal of mental science
DO - 10.1192/bjp.2026.10763
UR - https://europepmc.org/article/PMC/PMC7619679
AB - Background: Eating disorder treatment is most successful when delivered at first onset, underscoring the importance of early intervention. Genetic factors may contribute to earlier onset, but molecular genetic research into symptom onset and severity remains limited. Aims: We investigated (1) age at onset of behavioural symptoms and low weight, including sex differences, (2) the SNP-based heritability and cross-trait polygenic associations of symptoms, onset, and severity. Method: Participants (n = 24,973) of genetically-derived European ancestry were from the NIHR BioResource, including the Genetic Links to Anxiety and Depression Study, Eating Disorders Genetics Initiative UK, and COVID-19 Psychiatry and Neurological Genetics Study. Symptoms were assessed with the ED100K questionnaire. We described sex-stratified onset of binge eating, low weight, self-induced vomiting, laxatives, diuretics, excessive exercise, and fasting. SNP-based heritability was estimated using GCTA-GREML. We tested associations with 26 polygenic scores (PGS), which were calculated using SBayesRC. Results: Symptom median onset ranged from 16-20 years: vomiting (16), fasting and excessive exercise (17), binge eating (18), laxatives (19), diuretics (20), and low weight (20). Males were disproportionately likely to report adult onset. In females, behavioural symptoms and low weight showed substantial heritability (SNP-based h2 = 0.31–0.78), but onset and cognitive symptoms appeared to be less heritable. PGS analyses identified distinct pathways: in females, higher childhood obesity PGS was linked to earlier binge eating onset (~7 months), and higher educational attainment PGS to earlier low weight onset (~6 months). Conclusions: Eating disorder symptoms begin in adulthood as frequently as adolescence, challenging stereotypes and underscoring investment needed in adult services, particularly for men. While symptoms were strongly heritable, onset and cognitive symptoms showed limited genetic contribution. Symptom-level PGS analyses highlight distinct biological and developmental pathways. Larger sample sizes and more accurate phenotyping are needed.
SN - 0007-1250
SN - 1472-1465
ER -