Findings provide support for sex differences in rodent models of binge eating and highlight the promise of the BER/BEP model for understanding neurobiological mechanisms underlying sex differences in risk.

Changes in ovarian hormones predict changes in emotional eating across the menstrual cycle. However, prior studies have not examined whether the nature of associations varies across dysregulated eating severity. The current study determined whether the strength and/or nature of hormone/dysregulated eating associations differ based on the presence of clinically diagnosed binge episodes (BEs). Participants included 28 women with BEs and 417 women without BEs who provided salivary hormone samples, ratings of emotional eating, and BE frequency for 45 days. Results revealed stronger associations between dysregulated eating and ovarian hormones in women with BEs as compared to women without BEs. The nature of associations also differed, as progesterone moderated the effects of lower estradiol levels on dysregulated eating in women with BEs only. Although hormone/dysregulated eating associations are present across the spectrum of pathology, the nature of associations may vary in ways that have implications for etiological models and treatment.

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Background Previous studies show significant within-person changes in binge eating and emotional eating across the menstrual cycle, with substantial increases in both phenotypes during post-ovulation. Increases in both estradiol and progesterone levels appear to account for these changes in phenotypic risk, possibly via increases in genetic effects. However, to date, no study has examined changes in genetic risk for binge phenotypes (or any other phenotype) across the menstrual cycle. The goal of the present study was to examine within-person changes in genetic risk for emotional eating scores across the menstrual cycle. Methods Participants were 230 female twin pairs (460 twins) from the Michigan State University Twin Registry (MSUTR) who completed daily measures of emotional eating for 45 consecutive days. Menstrual cycle phase was coded based on dates of menstrual bleeding and daily ovarian hormone levels. Results Findings revealed important shifts in genetic and environmental influences, where estimates of genetic influences were two times higher in post- as compared to pre-ovulation. Surprisingly, pre-ovulation was marked by a predominance of environmental influences, including shared environmental effects which have not been previously detected for binge eating phenotypes in adulthood. Conclusions Our study was the first to examine within-person shifts in genetic and environmental influences on a behavioral phenotype across the menstrual cycle. Results highlight a potentially critical role for these shifts in risk for emotional eating across the menstrual cycle and underscore the need for additional, large-scale studies to identify the genetic and environmental factors contributing to menstrual cycle effects.

Objective: Little is known about biological factors that contribute to purging after normal amounts of food-the central feature of purging disorder (PD). This study comes from a series of nested studies examining ingestive behaviors in bulimic syndromes and specifically evaluated the satiety peptide YY (PYY) and the hunger peptide ghrelin in women with PD (n 5 25), bulimia nervosapurging (BNp) (n 5 26), and controls (n 5 26). Based on distinct subjective responses to a fixed meal in PD (Keel, Wolfe, Liddle, DeYoung, & Jimerson, 2007), we tested whether postprandial PYY response was significantly greater and ghrelin levels significantly lower in women with PD compared to controls and women with BNp.Method: Participants completed structured clinical interviews, self-report questionnaires, and laboratory assessments of gut peptide and subjective responses to a fixed meal.Results: Women with PD demonstrated a significantly greater postprandial PYY response compared to women with BNp and controls, who did not differ significantly. PD women also endorsed significantly greater gastrointestinal distress, and PYY predicted gastrointestinal intestinal distress.Ghrelin levels were significantly greater in PD and BNp compared to controls, but did not differ significantly between eating disorders. Women with BNp endorsed significantly greater postprandial hunger, and ghrelin predicted hunger.Discussion: PD is associated with a unique disturbance in PYY response. Findings contribute to growing evidence of physiological distinctions between PD and BNp. Future research should examine whether these distinctions account for differences in clinical presentation as this could inform the development of specific interventions for patients with PD.bulimia nervosa, classification, gut peptides, physiology, purging disorder 1 | I N TR ODU C TI ON Purging disorder (PD) was added to the DSM-5 within Other Specified Feeding and Eating Disorder to account for a substantial number of women who fail to meet criteria for bulimia nervosa (BN) because they purge following normal amounts of food (Allen, Byrne, Oddy, & Crosby, 2013; Field et al., 2012;Stice, Marti, & Rohde, 2013;Swanson, Brown, Crosby, & Keel, 2014). Prevalence estimates indicate PD affects 0.5%-0.9% of adolescent girls currently (Allen et al., 2013; Field et al., 2012;Stice et al., 2013) and 1%-5% of women over their lifetimes (Keel & Striegel-Moore, 2009). PD has been characterized as a "partial eating disorder" (Stice, Marti, Shaw, & Jaconis, 2009), and the ICD workgroup proposed revisions that could absorb PD into a broader definition of BN (Uher & Rutter, 2012) given that many individuals with PD experience a loss of control (LOC) after eating normal amounts of food (Keel, Haedt, & Edler, 2005). However, recent findings suggest that PD may be more than a subthreshold variant of BN. In the only longer-term follow-up study to date, PD demonstrated greater diagnostic perseverance compared to purging anorexia nervosa (AN) and higher mortality compared to BN purging (BNp) ...