Disordered Eating Symptoms Scale

2015 ◽  
Author(s):  
Annie Shearer ◽  
Jody Russon ◽  
Joanna Herres ◽  
Tita Atte ◽  
Tamar Kodish ◽  
...  
2015 ◽  
Vol 129 (1) ◽  
pp. 18-36 ◽  
Author(s):  
Kristen M. Culbert ◽  
S. Marc Breedlove ◽  
Cheryl L. Sisk ◽  
Pamela K. Keel ◽  
Michael C. Neale ◽  
...  

2019 ◽  
Vol 53 (3) ◽  
pp. 391-403
Author(s):  
Ruofan Ma ◽  
Kevin P. Capobianco ◽  
NiCole T. Buchanan ◽  
Zhiyuan Hu ◽  
Jonathan M. Oakman

2013 ◽  
Vol 44 (5) ◽  
pp. 1029-1041 ◽  
Author(s):  
S. E. Racine ◽  
K. M. Culbert ◽  
S. A. Burt ◽  
K. L. Klump

BackgroundAdvanced paternal age at birth has been linked to several psychiatric disorders in offspring (e.g. schizophrenia) and genetic mechanisms are thought to underlie these associations. This study is the first to investigate whether advanced paternal age at birth is associated with eating disorder risk using a twin study design capable of examining both phenotypic and genetic associations.MethodIn a large, population-based sample of female twins aged 8–17 years in mid-puberty or beyond (n = 1722), we investigated whether advanced paternal age was positively associated with disordered eating symptoms and an eating disorder history [i.e. anorexia nervosa (AN), bulimia nervosa (BN) or binge eating disorder (BED)] in offspring. Biometric twin models examined whether genetic and/or environmental factors underlie paternal age effects for disordered eating symptoms.ResultsAdvanced paternal age was positively associated with disordered eating symptoms and an eating disorder history, where the highest level of pathology was observed in offspring born to fathers ⩾40 years old. The results were not accounted for by maternal age at birth, body mass index (BMI), socio-economic status (SES), fertility treatment or parental psychiatric history. Twin models indicated decreased genetic, and increased environmental, effects on disordered eating with advanced paternal age.ConclusionsAdvanced paternal age increased risk for the full spectrum of eating pathology, independent of several important covariates. However, contrary to leading hypotheses, environmental rather than genetic factors accounted for paternal age–disordered eating associations. These data highlight the need to explore novel (potentially environmental) mechanisms underlying the effects of advanced paternal age on offspring eating disorder risk.


2020 ◽  
Vol 66 (3) ◽  
pp. 366-371
Author(s):  
Vivienne M. Hazzard ◽  
Alison L. Miller ◽  
Katherine W. Bauer ◽  
Bhramar Mukherjee ◽  
Kendrin R. Sonneville

2018 ◽  
Vol 27 (1) ◽  
pp. 34-51 ◽  
Author(s):  
Rejane Augusta de Oliveira Figueiredo ◽  
Sabina Simola-Ström ◽  
Rasmus Isomaa ◽  
Elisabete Weiderpass

2014 ◽  
Vol 44 (11) ◽  
pp. 2271-2286 ◽  
Author(s):  
K. M. Culbert ◽  
S. A. Burt ◽  
C. L. Sisk ◽  
J. T. Nigg ◽  
K. L. Klump

BackgroundTestosterone may be a biological factor that protects males against eating disorders. Elevated prenatal testosterone exposure is linked to lower levels of disordered eating symptoms, but effects emerge only after mid-puberty. Whether circulating levels of testosterone account for decreased risk for disordered eating in boys after mid-puberty is currently unknown; however, animal data support this possibility. In rodents, prenatal testosterone's masculinizing effects on sex-differentiated behaviors emerge during puberty when circulating levels of testosterone increase and ‘activate’ the expression of masculinized phenotypes. This study investigated whether higher levels of circulating testosterone predict lower levels of disordered eating symptoms in adolescent boys, and in particular whether effects are associated with advancing pubertal maturation.MethodParticipants were 213 male twins from the Michigan State University Twin Registry. The Minnesota Eating Behavior Survey and Eating Disorder Examination Questionnaire assessed several disordered eating symptoms. The Pubertal Development Scale assessed pubertal status. Afternoon saliva samples were assayed for testosterone using enzyme immunoassays.ResultsConsistent with animal data, higher levels of circulating testosterone predicted lower levels of disordered eating symptoms in adolescent boys and effects emerged with advancing puberty. Results were not accounted for by several important covariates, including age, adiposity, or mood/anxiety symptoms.ConclusionsFindings suggest that elevated circulating testosterone may be protective and underlie decreased risk for eating pathology in males during/after puberty, whereas lower levels of testosterone may increase risk and explain why some, albeit relatively few, males develop eating disorders.


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