Thin-ideal internalization has received increasing support as an important risk factor in the development of disordered eating attitudes/behaviors and eating disorders. However, relatively little is known about the etiology of thin-ideal internalization itself. The current research used a series of studies to better understand risk factors for thin-ideal internalization during adolescence. Study 1 investigated whether known phenotypic changes in thin-ideal internalization across adolescence correspond to developmental changes in etiological (i.e., genetic and environmental) risk. Participants included 846 female twins (ages 8-25 years) from the Michigan State University Twin Registry (MSUTR). 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. Phenotypic analyses generally indicated significant increases in thin-ideal internalization across age and pubertal development. With few exceptions, twin models suggested no significant differences in etiologic effects across development. At all developmental phases, environmental influences were most important in the etiology of thin-ideal internalization, with genetic, shared environmental, and nonshared environmental influences accounting for roughly 10%, 30%, and 60%, respectively, of the total variance. Findings suggest that despite mean-level increases in thin-ideal internalization across development, the relative influence of genetic versus environmental risk does not shift across this period, with the majority of variance accounted for by environmental factors. Results suggest that early risk factors for thin-ideal internalization are likely to be important across development, and mean-level increases in thin-ideal internalization may reflect increases in the magnitude/strength of environmental risk across this period.Study 2 examined if affiliation with body-conscious peer groups may influence thin-ideal internalization through socialization processes (e.g., conversations focused on thinness) versus selection processes (e.g., selection into body-conscious peer groups) using co-twin control methodology. Participants included 392 female twins (ages 8-15) from the MSUTR. Thin-ideal internalization and peer group characteristics were assessed via self-report questionnaires. Co-twin control analyses examined whether twin discordance in exposure to weight-focused peers predicted within-twin pair discordance in thin-ideal internalization. Within co-twin control analyses, predictive effects in monozygotic (MZ) and dizygotic (DZ) twins suggest socialization effects, as increased exposure to weight-focused peers would be associated with increased risk for thin-ideal internalization in one co-twin relative to the other, regardless of the degree of genetic and/or environmental sharing. Analyses suggested a role for socialization, as increased exposure to weight-focused peers predicted increased thin-ideal internalization in MZ twin pairs. Results in DZ twins were less consistent, but overall were similar to results in MZ twins. Findings supported etiological theories that suggest socialization processes in the association between weight-focused peers and thin-ideal internalization. Longitudinal and observational research is needed to confirm causal effects and identify peer socialization processes that increase thin-ideal internalization risk.
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