Genetic and environmental influences on thin-ideal internalization across puberty and preadolescent, adolescent, and young adult development.

Thin-ideal internalization (i.e., the acceptance of and adherence to sociocultural beauty ideals for women that focus on thinness) is an important risk factor in the development of body dissatisfaction, disordered eating, and eating disorders (see 1; 2 for reviews of this literature .). Cross-sectional and prospective studies have supported the role of thin-ideal internalization in the development of eating problems (e.g., body dissatisfaction, dieting; 1.), and eating disorder prevention programs that target thin-ideal internalization have been effective in decreasing disordered eating (3.). However, as noted by others (4.), prevention programs could, and should, be improved further, particularly given their potential to decrease the development of eating disorders. Increasing knowledge on the etiology of thin-ideal internalization may be key to developing additional intervention techniques. Unfortunately, risk factors for thin-ideal internalization have been studied less frequently than risk factors for eating pathology (5–8.). Existing research has focused on the role of environmental risk factors that are thought to teach and reinforce beauty ideals of thinness, such as media images, parental and peer influences (5; 6.) Although research has demonstrated that hypothesized media, peer, and parental risk factors are indeed associated with thin-ideal internalization (5; 6.), further research is needed to confirm the direction of these effects, as current studies are limited by cross-sectional designs. In addition to environmental risk factors, twin research has demonstrated that genetic influences explain approximately 40% of the variance in thin-ideal internalization in a sample of post-pubertal adolescent and young adult twins (9.). Thus, genetic influences may explain why, despite almost ubiquitous exposure to the thin-ideal in Western countries, only some women ultimately internalize this ideal and go on to develop disordered eating behaviors (9.). More specifically, in the context of environmental risk factors (e.g., thin-ideal focused media) that nearly all women within Western culture experience, it may be level of genetic risk for thin-ideal internalization that differentiates those women who go on to internalize these ideals, and those who do not. Given that only one twin study of thin-ideal internalization has been conducted, further research is needed to extend knowledge of genetic and environmental effects. In particular, it is necessary to examine etiologic effects across adolescence, a key period for the development of thin-ideal internalization. Indeed, mean levels of thin-ideal internalization have been shown to increase across adolescence (9; 10.). The pubertal period appears to be particularly important in this regard, as girls in pre-to-early puberty report significantly lower levels of thin-ideal internalization than girls in mid-puberty and beyond (11.). These increases in mean levels of thin-ideal internalization may indicate key etiological shifts that should be examined as well. Indeed, related phenotypes, such as disordered eating, show significant etiological changes across this period, such that the heritability of disordered eating is negligible in pre-adolescence and pre-pubertal twins, but is significant (i.e., approximately 50% of variance) in pubertal twins and in twins who are in middle adolescence (i.e., about age 14) or older (i.e., ages 16–40 years; 12; 13; 14.). The effects of the shared environment are opposite of those observed for genetic influences: shared environmental influences account for 40% of the variance in disordered eating in pre-adolescence/pre-puberty, and 10% or less from middle adolescence into middle adulthood and in pubertal twins. These findings have been useful because they have led researchers to develop specific hypotheses regarding mechanisms that may account for differences in heritability across puberty, such as changes in ovarian hormones during puberty (15.). Given that adolescence also seems to be a key developmental period for thin-ideal internalization (11.), developmental twin studies of thin-ideal internalization may help elucidate etiological mechanisms that contribute to risk for thin-ideal internalization across development. The aim of the present study was to investigate the extent to which genetic and environmental influences on thin-ideal internalization differ across age and pubertal development in a large (N=1,064) sample of same-sex female twins (ages 8–25 years). To ensure that effects are specific to thin-ideal internalization, we examined developmental differences in genetic and environmental effects while controlling for disordered eating. Specificity of effects are important to establish given phenotypic and genetic overlap in thin-ideal internalization and disordered eating (16–18.) and the need to identify etiological risk factors that contribute uniquely to thin-ideal internalization.