Genetic and environmental influences on thin‐ideal internalization across puberty and preadolescent, adolescent, and young adult development. Issue 7 (25th June 2014)

• Record Type: Journal Article
• Authors: Suisman, Jessica L.; Thompson, J. Kevin; Keel, Pamela K.; Burt, S. Alexandra; Neale, Michael; Boker, Steven; Sisk, Cheryl; Klump, Kelly L.; Weissman, Ruth Striegel; Klump, Kelly; Steiger, Howard; Tanofsky‐Kraff, Marian
• Is Part Of: International journal of eating disorders. Volume 47:Issue 7(2014:Nov.)
• Page Start: 773
• Page End: 783
• Publication Date: 2014-06-25
• Subjects: Appetite disorders -- Periodicals; Ingestion disorders -- Periodicals; Eating disorders -- Periodicals; 616.8526
• DOI: 10.1002/eat.22321
• Languages: English
• ISSNs: 0276-3478

Abstract

<abstract abstract-type="main"> <title>ABSTRACT</title> <sec id="eat22321-sec-0001" sec-type="section"> <title>Objective</title> <p>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.</p> </sec> <sec id="eat22321-sec-0002" sec-type="section"> <title>Method</title> <p>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.</p> </sec> <sec id="eat22321-sec-0003" sec-type="section"> <title>Results</title> <p>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.</p> </sec> <sec id="eat22321-sec-0004" sec-type="section"> <title>Discussion</title> <p>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)</p> </sec> </abstract>