TY - JOUR
T1 - Eating disorder symptoms and their associations with anthropometric and psychiatric polygenic scores
AU - Abdulkadir, Mohamed
AU - Hübel, Christopher
AU - Herle, Moritz
AU - Loos, Ruth J.F.
AU - Breen, Gerome
AU - Bulik, Cynthia M.
AU - Micali, Nadia
N1 - Funding Information:
We are extremely grateful to all the families who took part in this study, the midwives for their help in recruiting them, and the whole ALSPAC team, which includes interviewers, computer and laboratory technicians, clerical workers, research scientists, volunteers, managers, receptionists and nurses. This work was supported by the UK Medical Research Council and the Medical Research Foundation (ref: MR/R004803/1). The UK Medical Research Council and Wellcome (Grant ref: 102,215/2/13/2 and 217065/Z/19/Z) and the University of Bristol provide core support for ALSPAC. A comprehensive list of grants funding is available on the ALSPAC website ( http://www.bristol.ac.uk/alspac/external/documents/grant‐acknowledgements.pdf ); This research was specifically funded by the NIHR (CS/01/2008/014), the NIH (MH087786‐01). GWAS data was generated by Sample Logistics and Genotyping Facilities at Wellcome Sanger Institute and LabCorp (Laboratory Corporation of America) using support from 23andMe. NM and CB acknowledge funding from the National Institute of Mental Health (R21 MH115397). CMB is supported by NIMH (R01MH120170; R01MH119084; R01MH118278; U01 MH109528); Brain and Behaviour Research Foundation Distinguished Investigator Grant; Swedish Research Council (Vetenskapsrådet, award: 538‐2013‐8864); CH and CMB are funded by the Lundbeck Foundation (Grant no. R276‐2018‐4581). MH is funded by a fellowship from the Medical Research Council UK (MR/T027843/1). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health and the authors will serve as guarantors for the contents of this paper. The funders were not involved in the design or conduct of the study; collection, management, analysis, or interpretation of the data; or preparation, review, or approval of the manuscript.
Funding Information:
We are extremely grateful to all the families who took part in this study, the midwives for their help in recruiting them, and the whole ALSPAC team, which includes interviewers, computer and laboratory technicians, clerical workers, research scientists, volunteers, managers, receptionists and nurses. This work was supported by the UK Medical Research Council and the Medical Research Foundation (ref: MR/R004803/1). The UK Medical Research Council and Wellcome (Grant ref: 102,215/2/13/2 and 217065/Z/19/Z) and the University of Bristol provide core support for ALSPAC. A comprehensive list of grants funding is available on the ALSPAC website (http://www.bristol.ac.uk/alspac/external/documents/grant-acknowledgements.pdf); This research was specifically funded by the NIHR (CS/01/2008/014), the NIH (MH087786-01). GWAS data was generated by Sample Logistics and Genotyping Facilities at Wellcome Sanger Institute and LabCorp (Laboratory Corporation of America) using support from 23andMe. NM and CB acknowledge funding from the National Institute of Mental Health (R21 MH115397). CMB is supported by NIMH (R01MH120170; R01MH119084; R01MH118278; U01 MH109528); Brain and Behaviour Research Foundation Distinguished Investigator Grant; Swedish Research Council (Vetenskapsr?det, award: 538-2013-8864); CH and CMB are funded by the Lundbeck Foundation (Grant no. R276-2018-4581). MH is funded by a fellowship from the Medical Research Council UK (MR/T027843/1). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health and the authors will serve as guarantors for the contents of this paper. The funders were not involved in the design or conduct of the study; collection, management, analysis, or interpretation of the data; or preparation, review, or approval of the manuscript.
Publisher Copyright:
© 2022 Eating Disorders Association and John Wiley & Sons Ltd.
PY - 2022/5
Y1 - 2022/5
N2 - Background: Eating disorder (ED) symptoms are prevalent in the general population, but their shared genetic underpinnings with psychiatric, metabolic, and anthropometric traits are not known. Here, we examined if polygenic scores (PGSs) of traits associated with anorexia nervosa are also associated with adolescent ED symptoms in the Avon Longitudinal Study of Parents and Children (ALSPAC). Methods: A total of 8654 participants with genotype data and at least one phenotypic measure were included from the ALSPAC study. We associated PGS from 25 traits (16 psychiatric, 4 metabolic, and 5 anthropometric) with eight ED symptoms, including behaviours such as fasting for weight loss and cognitions such as body dissatisfaction. Results: Higher attention deficit hyperactivity disorder PGS and lower educational attainment PGS were associated with fasting for weight loss. Higher insomnia PGS was associated with increased body dissatisfaction. We found no evidence of an association between metabolic trait PGS and any ED symptom. Fat-free mass, fat mass, and body fat percentage PGSs, were positively associated with binge eating, excessive exercise, fasting for weight loss, body dissatisfaction, and weight and shape concern. Conclusions: ED symptoms are genetically associated with psychiatric and anthropometric, but not with metabolic traits. Our findings provide insights for future genetic research investigating on why some individuals with ED symptoms progress to develop threshold EDs while others do not.
AB - Background: Eating disorder (ED) symptoms are prevalent in the general population, but their shared genetic underpinnings with psychiatric, metabolic, and anthropometric traits are not known. Here, we examined if polygenic scores (PGSs) of traits associated with anorexia nervosa are also associated with adolescent ED symptoms in the Avon Longitudinal Study of Parents and Children (ALSPAC). Methods: A total of 8654 participants with genotype data and at least one phenotypic measure were included from the ALSPAC study. We associated PGS from 25 traits (16 psychiatric, 4 metabolic, and 5 anthropometric) with eight ED symptoms, including behaviours such as fasting for weight loss and cognitions such as body dissatisfaction. Results: Higher attention deficit hyperactivity disorder PGS and lower educational attainment PGS were associated with fasting for weight loss. Higher insomnia PGS was associated with increased body dissatisfaction. We found no evidence of an association between metabolic trait PGS and any ED symptom. Fat-free mass, fat mass, and body fat percentage PGSs, were positively associated with binge eating, excessive exercise, fasting for weight loss, body dissatisfaction, and weight and shape concern. Conclusions: ED symptoms are genetically associated with psychiatric and anthropometric, but not with metabolic traits. Our findings provide insights for future genetic research investigating on why some individuals with ED symptoms progress to develop threshold EDs while others do not.
KW - Avon longitudinal study of parents and children (ALSPAC)
KW - anthropometric traits
KW - metabolic traits
KW - psychiatric traits
UR - http://www.scopus.com/inward/record.url?scp=85124738499&partnerID=8YFLogxK
U2 - 10.1002/erv.2889
DO - 10.1002/erv.2889
M3 - Article
C2 - 35178801
AN - SCOPUS:85124738499
SN - 1072-4133
VL - 30
SP - 221
EP - 236
JO - European Eating Disorders Review
JF - European Eating Disorders Review
IS - 3
ER -