A neurodevelopmental model of eating disorder risk in midlife to older adulthood.

Prior research suggests that rapid neurobiological changes and their interaction with psychosocial stressors serve as major precipitants of disordered eating in adolescence. However, there has been little discussion of how similar processes may facilitate disordered eating in later life, which is similarly associated with rapid biosocial change. We present a novel framework for the increased risk of eating pathology in midlife into older adulthood, suggesting testable mechanistic pathways to guide future research. First, we review critical neurobiological and cognitive alterations that occur during this unique developmental stage and link them to established risk and maintenance factors for disordered eating in younger populations. Second, we discuss how neurobiological aging processes interact with aging-related psychosocial and biological stressors to increase vulnerability for disordered eating. We then outline the following directions for future research in middle-aged and older adults: 1) directly investigate the influence of brain changes, and their interactions with age-related environmental and hormonal influences, on eating disorder behavior; 2) distinguish pathways from neurodevelopmental changes to eating pathology that differ as a function of aspects of identity, comorbidity, or specific developmental period; 3) establish the neurodevelopmental risk factors influencing risk for different eating disorder phenotypes; and 4) identify potential neural targets for prevention and treatment of eating disorders as vulnerable individuals age. Finally, we advocate for enhanced awareness of how neurobiological changes in midlife and older adulthood may increase the risk of eating pathology, and for a multidisciplinary approach that considers biological and environmental vulnerabilities in treating disordered eating in this population.