Thursday, May 9, 2024
5/9/2024
PROJECT SUMMARY Binge eating (BE) occurs in most eating disorders and at significant rates in the community, including among children and adolescents. The chronic course of BE and significant psychiatric and medical morbidity further attest to its public health significance. Critically, although males account for up to one-half of BE cases, there is a paucity of research exploring risk for BE in males and studies exploring biological factors are nearly non- existent. Adrenal and gonadal androgens are one set of male-specific biological factors that may be critical given that they drive sexual differentiation and pubertal development in males, they cause changes in palatable food intake in animals, and they are potent regulators of gene transcription within neurobiological systems relevant to BE. Moreover, animal studies and our preliminary human data show that lower levels of androgens (e.g., testosterone) are predictive of higher phenotypic levels of BE and stronger genetic influences on BE in males during puberty, but no large-scale study has examined these biological processes. Larger-scale studies that span the full range of pubertal maturation (e.g., adrenarche through gonadarche) and comprehensively assess adrenal and gonadal androgens are a necessary next step that will enhance scientific Rigor and provide critical Reproducibility and translational data. The long-term objective of the proposed work is to identify the role of androgens on phenotypic and genetic risk for BE in boys during puberty. The Specific Aims are to: 1) examine whether lower levels of adrenal and/or gonadal androgens contribute to BE in boys during puberty; and 2) examine if genetic factors are mechanisms that drive phenotypic effects of adrenal and gonadal androgens on BE in boys during puberty. Participants will include 1,000 same-sex male twins (ages 7- 17) recruited through the Michigan State University Twin Registry. Questionnaires and interviews will be administered to the twins and at least one parent to assess BE, other mood/behavioral symptoms (e.g., mood, anxiety), and the physical changes of puberty. Salivary samples will be collected and assayed for adrenal and gonadal androgen levels. Multilevel structural equation models will be used to examine the phenotypic effects of adrenal and gonadal androgens on BE during puberty. Latent twin moderation models will examine the extent to which lower levels of adrenal and gonadal androgens are associated with stronger genetic effects on BE during puberty. All analyses will also explore whether observed effects are independent of other factors (i.e., adiposity, anxiety, depression) that change during puberty and are associated with androgens and BE. Findings from our innovative, multi-method project have the potential to significantly increase understanding of the causes of BE in boys by identifying androgens as novel neurobiological factors that contribute to BE. Greater insight into etiological mechanisms of BE in boys will narrow the search for putative neurobiological systems and genes and contribute to improved treatment and prevention of these syndromes.
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