Differential susceptibility, a reconceptualization of the diathesis-stress model of psychopathology, describes gene-environment interactions that reflect individual differences in responsiveness to environmental influences, both detrimental and beneficial. This model has been described metaphorically by the classification of orchids, which thrive under optimal care but wither under adverse conditions, and dandelions, which weather broad environmental circumstances but are less responsive to careful cultivation. Etiological research in the field of eating disorders has largely focused on the identification of specific behavioral phenotypes, temperamental traits, genotypes and neurobiological processes that confer risk. In this article, we propose that these putative vulnerability factors represent phenotypes and endophenotypes of a genetic predisposition towards environmental sensitivity. We assert that this sensitivity not only transmits eating disorder risk but also confers resilience, depending on the circumstances. In particular, we propose that differential susceptibility can be used as a framework to organize disparate temperamental and neurobiological findings and their complex interplay with various developmental, environmental and sociocultural influences to increase eating disorder risk and treatment responsiveness. Finally, we assert that viewed through the lens of differential susceptibility, sensitivity can be leveraged to refine our interventions and develop novel treatment and prevention strategies to support favorable outcomes for individuals with eating disorders.
Keywords: diathesis-stress; differential susceptibility; eating disorders; sensory processing sensitivity; vantage sensitivity.
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