Abstract
The goal of the current study was to examine whether genetic and environmental influences on an important risk factor for disordered eating, weight and shape concern, remained stable over adolescence. This stability was assessed in 2 ways: whether new sources of latent variance were introduced over development and whether the magnitude of variance contributing to the risk factor changed. We examined an 8-item WSC subscale derived from the Eating Disorder Examination (EDE) using telephone interviews with female adolescents. From 3 waves of data collected from female-female same-sex twin pairs from the Australian Twin Registry, a subset of the data (which included 351 pairs at Wave 1) was used to examine 3 age cohorts: 12 to 13, 13 to 15, and 14 to 16 years. The best-fitting model contained genetic and environmental influences, both shared and nonshared. Biometric model fitting indicated that nonshared environmental influences were largely specific to each age cohort, and results suggested that latent shared environmental and genetic influences that were influential at 12 to 13 years continued to contribute to subsequent age cohorts, with independent sources of both emerging at ages 13 to 15. The magnitude of all 3 latent influences could be constrained to be the same across adolescence. Ages 13 to 15 were indicated as a time of risk for the development of high levels of WSC, given that most specific environmental risk factors were significant at this time (e.g., peer teasing about weight, adverse life events), and indications of the emergence of new sources of latent genetic and environmental variance over this period.
Published Version
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