Binge eating (BE) is a core symptom of multiple eating disorders and disproportionately affects females during/after puberty. Gonadal hormones (estrogen, progesterone, testosterone) are sex-differentiated and have been posited as key biological contributors to BE risk. This review synthesizes recent findings from animal and human studies regarding gonadal hormone influences on the etiology BE in females during puberty and adulthood.
Recent findings
Estrogen may exert organizational effects (i.e., long-lasting) during puberty that shape responsivity to activational effects (i.e., transient) of gonadal hormones on BE in late adolescence/adulthood. In adulthood, estradiol appears to be protective against BE, while progesterone antagonizes this effect. Emerging data also implicate testosterone as an additional hormonal risk factor for BE in women, particularly under conditions of lower estradiol. However, not all females exposed to these high-risk gonadal hormone milieus develop BE; behavior genetic studies provide empirical support for gene-by-hormone interactions in individual susceptibility.
Summary
Methodologically rigorous approaches (e.g., daily assessments, behavior genetics, hormone manipulation) have been critical in uncovering the complex etiologic influences of gonadal hormones on BE in females. Future research is needed to identify the specific neural circuits, genetic variants, and transcriptional pathways involved in these processes.