In addition, other types of dieting/dietary restraint may be involved in gene-environment interactions. Although our measures appeared to ask about both intent to diet and dieting behavior, our factor analysis extracted one homogeneous dietary restraint factor. Given previous research (Stice et al., 2004; 2007), this factor is hypothesized to be akin to an intent to diet rather than objective dietary restraint. However, it may be actual caloric restriction, rather than this intent to diet, that interacts with genotype to increase risk for binge eating. Genetically vulnerable individuals (e.g., those with the “s” allele of the 5-HTTLPR) may be more susceptible to the 5-HT dysregulation that results from dieting (Steiger, 2004), and this may not be captured when using self-report measures of dietary restraint. Thus, future work should attempt to assess caloric intake directly to examine gene-diet interactions.
