Ovarian hormones are associated with binge eating in women, however findings are limited by the lack of experimental control inherent in human studies. Animal research that manipulates ovarian hormone status and examines individual differences in extreme binge eating proneness are needed to model clinical phenotypes in humans and to confirm causal effects. The purpose of this study was to examine the effects of adult ovariectomy on overall binge eating risk and extreme binge eating phenotypes using the binge eating resistant (BER)/ binge eating prone (BEP) rat model. We predicted that palatable food consumption would significantly increase after ovariectomy in all rats because ovarian hormones generally suppress food intake. If differences in responsiveness to ovarian hormones underlie BER/BEP phenotypes, then differences in binge eating between BER and BEP rats would be eliminated or diminished after ovariectomy. Changes in palatable food (PF) intake were compared in BER and BEP rats before and after ovariectomy in two samples of adult females. Findings were highly similar in the two samples. PF intake increased significantly following ovariectomy in all rats. However, BEP rats consistently consumed larger amounts of PF than BER rats, both before and after ovariectomy. The consistency of findings across two samples of rats provides strong support for activational effects of ovarian hormones on binge eating. However, the immunity of extreme binge eating phenotypes to ovarian hormone ablation suggests that other, earlier mechanisms (e.g., organizational hormone effects or hormone-independent effects) determine the expression of binge eating phenotypes.

Puberty is a critical risk period for binge eating and eating disorders characterized by binge eating. Previous research focused almost entirely on psychosocial risk factors during puberty to the relative exclusion of biological influences. The current study addressed this gap by examining the emergence of binge eating during puberty in a rat model. We predicted that there would be minimal differences in binge eating proneness during pre-early puberty, but significant differences would emerge during puberty. Two independent samples of female Sprague-Dawley rats (n = 30 and n = 36) were followed longitudinally across pre-early puberty, mid-late puberty, and adulthood. Binge eating proneness was defined using the binge eating resistant (BER)/binge eating prone (BEP) model of binge eating that identifies BER and BEP rats in adulthood. Across two samples of rats, binge eating proneness emerged during puberty. Mixed linear models showed little difference in palatable food intake between BER and BEP rats during pre-early puberty, but significant group differences emerged during mid-late puberty and adulthood. Group differences could not be accounted for by changes in non-palatable food intake or body weight. Similar to patterns in humans, individual differences in binge eating emerge during puberty in female rats. Findings provide strong confirming evidence for the importance of biological risk factors in developmental trajectories of binge eating risk across adolescence.

Twin studies indicate significant genetic, but little shared environmental, influences on eating disorders. However, critics argue that study limitations constrain the conclusions that can be drawn. Adoption studies avoid many of these limitations, but to date, no adoption studies of eating pathology have been conducted. The current study was the first adoption study to examine genetic/ environmental effects for disordered eating. Participants included 123 adopted and 56 biological female sibling pairs. Disordered eating (i.e., overall eating pathology, body dissatisfaction, weight preoccupation, binge eating) was assessed using the Minnesota Eating Behaviors Survey. Biometric model-fitting indicated significant genetic influences (59-82%) on all forms of disordered eating, with nonshared environmental factors accounting for the remaining variance. Shared environmental factors did not contribute significantly to any disordered eating symptom. Our findings bolster those from twin studies and provide critical evidence of significant genetic effects on disordered eating symptoms.Keywords eating disorders; anorexia nervosa; bulimia nervosa; genetic; adoption study Twin studies suggest moderate-to-high heritability (i.e., ~50-85%) of anorexia nervosa (AN;Klump, Miller, Keel, McGue, & Iacono, 2001;Kortegaard, Hoerder, Joergensen, Gillberg, & Kyvik;Mazzeo, et al., 2009;Wade, Bulik, Neale, & Kendler, 2000) bulimia nervosa (BN;Baker, Mazzeo, & Kendler, 2007;Bulik, Sullivan, Wade, & Kendler, 2000;Kendler, et al.,1991;Kendler, et al., 1995; and disordered eating symptoms (e.g., weight preoccupation, body dissatisfaction, binge eating, the use of compensatory behaviors; Keski-Rahkonen, et al., 2005;Klump, McGue, & Iacono, 2002;Reichborn-Kjennerud et al., 2003;Rutherford, McGuffin, Katz, & Murray, 1993;Silberg & Bulik, 2005; Spanos, Burt, & Klump, submitted;Wade, Martin, et al., 2000;Wade et al., 1999) during adolescence and adulthood. Indeed, over 30 such twin studies have been conducted, and all but two (focusing on cognitive criteria for AN and BN; see Reichborn-Kjennerud et al., 2004 and Tiggeman, 1998) 1999) have noted that heritability estimates vary across twin studies and even within the same twin study (see Kendler, et al., 1991;Kendler, et al., 1995), making it difficult to determine the actual contribution of genetic factors. Others point out that the 95% confidence intervals for genetic effects have sometimes included 0, suggesting a lack of statistically significant effects (Levine & Smolak, 2006). The validity (or invalidity) of the Equal Environments Assumption is also frequently cited as a stumbling block to establishing the presence of genetic influences (Fairburn et al., 1999;Levine & Smolak, 2006). Despite evidence to the contrary Bulik et al., 2000;Kendler, Neale, Kessler, Heath & Eaves, 1993;Klump, Holly, Iacono, McGue, & Willson, 2000;, increased physical and/or environmental similarity of MZ relative to DZ twins has been theorized to artificially inflate MZ twin concordance and heritabili...

Objective Mean-levels of thin-ideal internalization increase during adolescence and pubertal development, but it is unknown whether these phenotypic changes correspond to developmental changes in etiological (i.e., genetic and environmental) risk. Given the limited knowledge on risk for thin-ideal internalization, research is needed to guide the identification of specific types of risk factors during critical developmental periods. The present twin study examined genetic and environmental influences on thin-ideal internalization across adolescent and pubertal development. Method Participants were 1,064 female twins (ages 8–25 years) from the Michigan State University Twin Registry. Thin-ideal internalization and pubertal development were assessed using self-report questionnaires. Twin moderation models were used to examine if age and/or pubertal development moderate genetic and environmental influences on thin-ideal internalization. Results Phenotypic analyses indicated significant increases in thin-ideal internalization across age and pubertal development. Twin models suggested no significant differences in etiologic effects across development. Nonshared environmental influences were most important in the etiology of thin-ideal internalization, with genetic, shared environmental, and nonshared environmental accounting for approximately 8%, 15%, and 72%, respectively, of the total variance. Discussion Despite mean-level increases in thin-ideal internalization across development, the relative influence of genetic versus environmental risk did not differ significantly across age or pubertal groups. The majority of variance in thin-ideal internalization was accounted for by environmental factors, suggesting that mean-level increases in thin-ideal internalization may reflect increases in the magnitude/strength of environmental risk across this period. Replication is needed, particularly with longitudinal designs that assess thin-ideal internalization across key developmental phases.

Objective Current research on the etiology of thin-ideal internalization focuses on psychosocial influences (e.g., media exposure). The possibility that genetic influences also account for variance in thin-ideal internalization has never been directly examined. This study used a twin design to estimate genetic effects on thin-ideal internalization and examine if environmental influences are primarily shared or nonshared in origin. Method Participants were 343 post-pubertal female twins (ages 12–22; M=17.61) from the Michigan State University Twin Registry. Thin-ideal internalization was assessed using the Sociocultural Attitudes toward Appearance Questionniare-3. Results Twin modeling suggested significant additive genetic and nonshared environmental influences on thin-ideal internalization. Shared environmental influences were small and non-significant. Discussion Although prior research focused on psychosocial factors, genetic influences on thin-ideal internalization were significant and moderate in magnitude. Research is needed to investigate possible interplay between genetic and nonshared environmental factors in the development of thin-ideal internalization.