The existing GxE typology emphasizes two main interactive models: diathesis-stress and differential susceptibility (Ellis et al. 2011). These models are described graphically in Fig. 1. First, latent genetic risks for obesity may not manifest for individuals within relatively healthy social environments; risky social environments may be required to observe otherwise small genetic associations. Loos and Bouchard (2003) described environments with limited access to healthy food outlets or spaces in which to exercise regularly as “obesogenic,” and these environments “trigger” (Shanahan and Hofer 2005) otherwise latent genetic risks. In this manner, the environment is characterized as a fundamental cause (Link and Phelan 1995) of obesity although the genetic factors remain central to the etiology of physical weight gain. This social triggering mechanism in the diathesis-stress (or dual risk) model is the dominant GxE paradigm in biological, behavioral, and social science research and is supported by recent work of Rokholm et al. (2011).
