Changes in genetic and environmental influences on disordered eating between early and late adolescence: a longitudinal twin study

We investigated the genetic and environmental contributions to disordered eating (DE) between early and late adolescence in order to determine whether different sources of heritability and environmental risk contributed to these peak times of emergence of eating disorders. Adolescent female twins fr...

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Bibliographic Details
Published in:Psychological medicine 2015-11, Vol.45 (15), p.3249-3258
Main Authors: Fairweather-Schmidt, A. K., Wade, T. D.
Format: Article
Language:English
Subjects:
Adolescent
Adolescent Behavior - physiology
Adult
Australia
Child
Children & youth
Eating disorders
Environment
Feeding and Eating Disorders - etiology
Feeding and Eating Disorders - genetics
Female
Females
Genetic Predisposition to Disease
Genetics
Humans
Longitudinal Studies
Original Articles
Registries
Twins
Young Adult
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Summary:We investigated the genetic and environmental contributions to disordered eating (DE) between early and late adolescence in order to determine whether different sources of heritability and environmental risk contributed to these peak times of emergence of eating disorders. Adolescent female twins from the Australian Twin Registry were interviewed over the telephone with the Eating Disorder Examination (EDE). Data were collected at 12-15 and 16-19 years (wave 1: N = 699, 351 pairs; wave 3: N = 499, 247 pairs). Assessments also involved self-report measures related to negative life events and weight-related peer teasing. Unstandardized estimates from the bivariate Cholesky decomposition model showed both genetic influences and non-shared environmental influences increased over adolescence, but shared environmental influences decreased. While non-shared environmental sources active at ages 12-15 years continued to contribute at 16-19 years, new sources of both additive genetic and non-shared environmental risk were introduced at ages 16-19 years. Weight-related peer teasing in early-mid adolescence predicted increases of DE in later adolescence, while negative life events did not. Two-thirds of the heritable influence contributing to DE in late adolescence was unique to this age group. During late adolescence independent sources of genetic risk, as well as environmental influences are likely to be related in part to peer teasing, appear key antecedents in growth of DE.
ISSN:0033-2917
1469-8978
DOI:10.1017/S0033291715001257