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Genetic and environmental influences on thin‐ideal internalization across puberty and preadolescent, adolescent, and young adult development
Author(s) -
Suisman Jessica L.,
Thompson J. Kevin,
Keel Pamela K.,
Burt S. Alexandra,
Neale Michael,
Boker Steven,
Sisk Cheryl,
Klump Kelly L.
Publication year - 2014
Publication title -
international journal of eating disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.785
H-Index - 138
eISSN - 1098-108X
pISSN - 0276-3478
DOI - 10.1002/eat.22321
Subject(s) - internalization , psychology , twin study , developmental psychology , etiology , moderation , demography , biology , genetics , social psychology , heritability , psychiatry , sociology , cell
Objective Mean‐levels of thin‐ideal internalization increase during adolescence and pubertal development, but it is unknown whether these phenotypic changes correspond to developmental changes in etiological (i.e., genetic and environmental) risk. Given the limited knowledge on risk for thin‐ideal internalization, research is needed to guide the identification of specific types of risk factors during critical developmental periods. The present twin study examined genetic and environmental influences on thin‐ideal internalization across adolescent and pubertal development. Method Participants were 1,064 female twins (ages 8–25 years) from the Michigan State University Twin Registry. Thin‐ideal internalization and pubertal development were assessed using self‐report questionnaires. Twin moderation models were used to examine if age and/or pubertal development moderate genetic and environmental influences on thin‐ideal internalization. Results Phenotypic analyses indicated significant increases in thin‐ideal internalization across age and pubertal development. Twin models suggested no significant differences in etiologic effects across development. Nonshared environmental influences were most important in the etiology of thin‐ideal internalization, with genetic, shared environmental, and nonshared environmental accounting for approximately 8%, 15%, and 72%, respectively, of the total variance. Discussion Despite mean‐level increases in thin‐ideal internalization across development, the relative influence of genetic versus environmental risk did not differ significantly across age or pubertal groups. The majority of variance in thin‐ideal internalization was accounted for by environmental factors, suggesting that mean‐level increases in thin‐ideal internalization may reflect increases in the magnitude/strength of environmental risk across this period. Replication is needed, particularly with longitudinal designs that assess thin‐ideal internalization across key developmental phases. © 2014 Wiley Periodicals, Inc. (Int J Eat Disord 2014; 47:773–783)