The most prevalent forms of eating disorders are those characterized by binge eating (i.e., the consumption of a large amount of food, in a short period of time, with a loss of control over eating), including bulimia nervosa (BN), binge eating disorder (BED), and other specified feeding and eating disorders (OSFEDs) (American Psychiatric Association, 2013). These binge-related eating disorders (hereto referred to as BE syndromes or BE-S) are associated with some of the highest mortality rates of all psychiatric disorders (American Psychiatric Association, 2013, Arcelus et al., 2011, Crow et al., 2009, Crow et al., 2014) and often have chronic courses characterized by substantial psychiatric and medical morbidity (American Psychiatric Association, 2013, Keel and Brown, 2010, Kessler et al., 2013). Their decidedly bleak psychosocial outcomes (e.g., Keel et al., 2000) further attest to their public health significance and the urgent need to understand their development.

Given this clinical significance, experts have called for transdiagnostic studies that increase understanding of the full array of BE-S (Sysko and Walsh, 2011; Walsh and Sysko, 2009). Thus, in this narrative review, we focus on binge eating as the core maladaptive behavior that is common to all BE-S. This approach directly addresses recent initiatives (e.g., the NIMH’s Research Domain Criteria; Sanislow et al., 2010) that focus on transdiagnostic dimensions of observable behavior contributing to mental disorders. This focus on observable behaviors (rather than the complex constellation of behavior, cognition, and affect) provides a more powerful approach for identifying etiological processes that form the core of full syndromes (Sanislow et al., 2010) and it allows for translational research in non-human species. In addition to its significance for understanding BE-S, binge eating is an important target for women’s health research because it disproportionally affects females1 relative to males (2:1 up to 6:1) (Klump et al., 2017) and contributes to significant psychiatric comorbidity, medical complications, and risk for weight gain (American Psychiatric Association, 2013, Mitchell and Crow, 2010, Wassenaar et al., 2019).

Critically, this research is also needed to inform public health policy. Animal and human data show endogenous ovarian hormones (i.e., estrogen and progesterone) substantially increase risk for binge eating potentially via hormonally induced increases in genetic risk (Asarian and Geary, 2013, Harden et al., 2014, Klump et al., 2017). Approximately 85 % of women will take contraceptives (Bensyl et al., 2002; Chadwick et al., 2012, Hall and Trussell, 2012, Mosher and Jones, 2010) that mimic the riskiest hormonal milieus for binge eating (i.e., combined oral contraceptives (COCs) containing both synthetic estrogens (ethinyl estradiol) and progestins). Although the effects of the synthetic COC hormones within the central nervous system (CNS) are less studied, initial evidence suggests that they have regulatory effects (Singh and Su, 2013, Spona et al., 1980; Tofoletto et al., 2014) that are similar to, or in some cases more deleterious (e.g., decrease neuroprotection – see Singh and Su, 2013), than those of estrogen and progesterone. Unfortunately, these COCs are some of the most commonly used hormonal contraceptives (Bensyl et al., 2002; Mosher and Jones, 2010), and women typically begin taking these medications during the highest period of risk for BE-S (i.e., late adolescence/early adulthood) (American Psychiatric Association, 2013).

Given the above, the goal of this narrative review is to describe and synthesize studies examining the impact of COCs on risk for binge eating. We begin by reviewing evidence that endogenous estrogen and progesterone are associated with increased risk for binge eating in women. We then discuss the ways in which COCs may mimic and enhance this risk and review the (scant) data that are available thus far. We end by discussing potential mechanisms of effects, including individual differences in genetic risk that may explain why some, but not all, women develop binge eating in the presence of risky endogenous and exogenous hormone levels. We also outline directions for future research with an emphasis on large-scale, longitudinal, and translational studies in humans and animals that can substantially move the field forward in this important area of women’s health research.

Importantly, our goal in writing this review is NOT to dissuade women from using COCs. Our goal is to highlight potential adverse consequences of one type of hormonal contraceptive (COCs) for one type of woman (e.g., those with genetic risk) and spearhead personalized medicine approaches to this critical area of women’s health.