Etiological influences on continuity and co‐occurrence of eating disorders symptoms across adolescence and emerging adulthood

2019 
OBJECTIVE: The role of common and symptom-specific genetic and environmental influences in maintaining eating disorder symptoms across development remains unclear. This study investigates the continuity and change of etiological influences on drive for thinness, bulimia, and body dissatisfaction symptoms and their co-occurrence, across adolescence and emerging adulthood. METHOD: In total, 2,629 adolescent twins (mean age = 15.20, SD = 1.95) reported eating disorders symptoms across three waves of data collection. Biometric common pathways model was fitted to estimate genetic and environmental contributions to the continuity of each symptom over time, as well as time- and symptom-specific influences. RESULTS: Drive for thinness and body dissatisfaction symptoms showed a pattern of high continuity across development and high correlations with each other, whereas bulimia symptoms were moderately stable and less associated with the other two symptoms. Latent factors reflecting continuity of each symptom were largely under genetic influence (Al  = 0.60-0.82). New genetic influences contributing to change in the developmental course of symptoms were observed in emerging adulthood. Genetic influences correlated considerably between the three symptoms. Non-shared environmental influences were largely time-and symptom-specific, but some contributed moderately to the continuity across development (El  = 0.18-0.40). The etiological overlap was larger between drive for thinness and body dissatisfaction symptoms than with bulimia symptoms. DISCUSSION: The results provide preliminary evidence that stable as well as newly emerging genetic influences contribute to the co-occurrence of drive for thinness, bulimia, and body dissatisfaction symptoms across adolescence and emerging adulthood. Conversely, environmental influences were less stable and contributed to change in symptoms over time.
    • Correction
    • Source
    • Cite
    • Save
    • Machine Reading By IdeaReader
    74
    References
    4
    Citations
    NaN
    KQI
    []