Genetic and environmental influences on thin-ideal internalization.

Psychosocial perspectives on the development of eating disorders and disordered eating symptoms (e.g., body dissatisfaction, weight preoccupation) often center on sociocultural factors such as thin-ideal images that are perpetuated by the mass media within Western cultures1–3. Typically, these theories place an emphasis on thin-ideal internalization (i.e., the acceptance and adherence to sociocultural beauty standards of thinness), which is hypothesized to be a primary mechanism that links exposure to mass media and the development of eating pathology3–4. For example, the Tripartite Model2; 5 of body dissatisfaction and eating disturbance postulates that the sociocultural emphasis on thinness is reinforced and perpetuated by three primary factors: the media (i.e., television, advertisements, magazines), parents (e.g., parental focus on weight/dieting) and peers (e.g., peer discussions about dieting, weight-based teasing). According to the Tripartite Model, the reinforcement of the thin-ideal by these primary factors leads to thin-ideal internalization, as well as social comparison (i.e., evaluating and comparing oneself to others, including individuals displayed in the media). It is through the development of thin-ideal internalization and social comparison that body dissatisfaction, disordered eating, and eating disorders are thought to emerge. Empirical support for the Tripartite Model, including the significance of thin-ideal internalization as a central factor in this model, has begun to emerge, as structural equation modeling results have generally demonstrated good fits to Tripartite Model data6–9. Moreover, research continues to demonstrate robust associations between thin-ideal internalization and disordered eating10–13, and interventions that decrease thin-ideal internalization have also been shown to decrease body dissatisfaction14–15. Taken together, it is clear that thin-ideal internalization is an important component in the pathway from sociocultural risk factors to the development of eating pathology. Despite these promising findings, additional research is needed to more fully understand risk factors for the development of thin-ideal internalization. Theories such as the Tripartite Model inherently suggest that risk factors (e.g., exposure to media, behaviors of peers and family) are environmental in nature, and that these environmental factors account for the variance in thin-ideal internalization. One additional component that is strikingly absent from current theoretical models and research is the possibility that genetic influences contribute to the variance in thin-ideal internalization. This possibility is supported by the fact that despite almost ubiquitous exposure to thin-ideal images in Western countries, only some women ultimately internalize this ideal and go on to develop disordered eating behaviors. Individual difference factors, such as genetic risk, may predict which of these women are more likely to internalize the thin-ideal and which are not. The presence of significant genetic influences on eating disorders, and disordered eating symptoms (e.g., dietary restraint, drive for thinness, weight preoccupation, body dissatisfaction, shape/weight concerns) lend additional credence to the possibility that genetic factors may contribute to thin-ideal internalization16–21. The fact that thin-ideal internalization is a pre-cursor to many of these symptoms (rather than a correlate of, or proxy for, the symptoms;10; 22 further highlights the need to clarify genetic and environmental influences on thin-ideal internalization specifically. Twin studies are a powerful approach for determining the degree to which variance in a trait is accounted for by genetic versus environmental factors. The classical twin design allows for the investigation of additive genetic effects, or genetic influences on a trait are due to the additive effects of multiple genetic loci. Twin designs also allow the variance in a trait to be parsed into two forms of environmental effects; the shared and nonshared environment. Shared environmental factors (C) are environmental influences that are common to siblings raised in the same family and make them more similar to each another. These influences are generally conceptualized as family-wide or culture-wide factors, such as parenting style, socioeconomic status, and exposure to certain cultural beliefs/practices. Nonshared environmental factors (E), on the other hand, are environmental influences that are unique to siblings reared in the same family that make them more dissimilar from one another. Examples of nonshared environmental factors include differential experiences between siblings such as peer groups, extracurricular activities, or traumatic life events. To date, twin and adoption studies of post-pubertal adolescents and adults have demonstrated little-to-no effect of the shared environment on eating disorders and disordered eating symptoms, but a rather large and significant effect of nonshared environmental factors23–25. Importantly, the current conceptualization of the etiology of thin-ideal internalization would suggest a significant effect of the shared environment, as the exposure to media (i.e., almost all women are exposed to high levels of thin-ideal media) and parental attitudes/beliefs (e.g., emphasis on thinness) are likely common to siblings reared in the same family. However, as noted above, it is also possible that genetic factors contribute to this variance and predict which girls/women internalize the shared beauty ideals and which are relatively immune to the environmental effects. Moreover, it may be that the sociocultural influences act in a nonshared rather than shared environmental fashion. For example, siblings may experience differential exposure to cultural and family pressures for thinness that lead to differential internalization of thin-ideal messages. A prototypical example in this regard is the situation in which parental reinforcement of the thin-ideal in only one child (e.g., encouraging a heavier child to lose weight) might lead to thin-ideal internalization in only one sibling. These types of environmental effects would load onto the nonshared rather than shared environment, since they would make siblings’ thin-ideal internalization different rather than similar to each other. Clarification of the extent to which genetic, shared environmental, and/or nonshared environmental factors contribute to thin-ideal internalization is needed to identify more specific risk factors and the ways in which they are most likely to operate. Consequently, the aim of the present study was to investigate the extent to which genetic and environmental influences contribute to the variance in thin-ideal internalization in a large sample of female adolescent and young adult twins.