Animal models have proven to be exceptionally informative in defining neuropeptide regulation of appetite and energy homeostasis (Gao and Horvath 2007, Berthoud 2012, Williams and Elmquist 2012). More recent studies using a range of animal models and molecular tools are elucidating how epigenetic changes resulting from specific prenatal and postnatal dietary environments or experiences affect metabolic processes and appetite regulation (Levin 2008, Zambrano and Nathanielsz 2013, Burdge and Lillycrop 2014). Taken together, these approaches are helping to define possible treatment interventions for eating disorders in people (Casper, Sullivan, and Tecott 2008, Foltin 2012, van Gestel et al. 2014, Lutter, Croghan, and Cui 2016). The choice of animal used is best dictated by the question being addressed. Because of similarities in physiology and neurobiology, studies of captive nonhuman primates have begun to contribute significantly to our understanding of appetite regulation (see Wilson et al. 2014 for a review). Importantly, the use of nonhuman primate models provides the unique opportunity to extend analyses beyond a focus on the homeostatic regulation of appetite. This is particularly relevant given the well-established notion that a number of psychosocial factors influence food intake in people (Bruce and Ricciardelli 2015), including chronic stressor exposure (Tsenkova, Boylan, and Ryff 2013), even in children (Nguyen-Rodriguez, Unger, and Spruijt-Metz 2009). While the importance of psychosocial factors can be modeled in nonprimate animals (Tamashiro, Hegeman, and Sakai 2006), socially housed nonhuman primates share many characteristics in addition to physiology and neurobiology, with humans increasing the translational value of these pre-clinical studies.