Kristen M. Culbert

Ovarian hormones and binge eating: exploring associations in community samples

BACKGROUND Significant associations between changes in ovarian hormones and binge eating are present across the menstrual cycle in women with bulimia nervosa. However, no study has examined these relationships in a non-clinical sample, despite the need for these data for designing risk-factor studies. METHOD In study 1, we modified several continuous measures of binge eating and identified those that were most sensitive to menstrual-cycle fluctuations in a non-clinical sample of 10 women who completed measures for 35 days. In study 2, we explored associations between ovarian hormones and binge-eating scores in nine women who completed these same measures for 65 days and provided daily saliva samples for assays of estradiol and progesterone concentrations. RESULTS In study 1, the Emotional Eating subscale of the Dutch Eating Behavior Questionnaire exhibited superior reliability and was most sensitive to predicted menstrual-cycle changes in binge eating (i.e. increased scores in the mid-luteal/premenstrual compared with follicular/ovulatory phases). In study 2, this scale showed predicted inverse associations with estradiol and positive associations with progesterone across the menstrual cycle that could not be accounted for by changes in negative affect. CONCLUSION Associations between ovarian hormones and binge eating are robust and present in clinical and non-clinical samples. Findings support the ability to examine the role of ovarian hormones as risk factors for binge eating in large-scale prospective studies and twin studies.

Prenatal hormone exposure and risk for eating disorders: a comparison of opposite-sex and same-sex twins.

CONTEXT Although the sex difference in eating disorder prevalence has typically been attributed to psychosocial factors, biological factors may also play a role. Prenatal testosterone exposure is a promising candidate, since it masculinizes behavior in animals and humans via its permanent effects on the central nervous system. OBJECTIVE To examine whether in utero testosterone exposure has masculinizing effects on disordered eating (DE) by comparing opposite-sex (OS) and same-sex (SS) twins. Twin type (SS vs OS) is considered a proxy measure of prenatal hormone exposure, since females from OS pairs are exposed to more testosterone in utero than females from SS pairs. A linear trend in mean levels of DE was predicted based on expected prenatal testosterone exposure, with SS female twins exhibiting the highest levels of DE followed by OS female twins, OS male twins, and SS male twins. DESIGN A twin study comparison of OS vs SS twins. SETTING Michigan State University Twin Registry. PARTICIPANTS Participants included 304 SS female twins, 59 OS female twins, 54 OS male twins, and 165 SS male twins. MAIN OUTCOME MEASURE Overall levels of DE were assessed with the Minnesota Eating Behavior Survey. RESULTS Confirming hypotheses, DE exhibited significant linear trends, with SS female twins exhibiting the highest levels of DE followed by OS female twins, OS male twins, and SS male twins. This linear trend could not be accounted for by levels of anxiety or socialization effects. Indeed, OS female twins exhibited lower levels of DE compared with an independent sample of undergraduate women (n = 69) who were raised with 1 or more brothers. CONCLUSIONS The masculinization of DE in OS female twins is unlikely to be due to socialization effects alone. Biological factors, such as the masculinization of the central nervous system by prenatal testosterone exposure, may also contribute to sex differences in DE prevalence.

Puberty and the genetic diathesis of disordered eating attitudes and behaviors.

Twin studies from the Minnesota Twin Family Study (MTFS) suggest negligible genetic effects on eating pathology before puberty but increased genetic effects during puberty. However, an independent study found no pubertal differences in genetic and environmental effects (R. Rowe, A. Pickles, E. Simonoff, C. M. Bulik, & J. L. Silberg, 2002). Discrepant results may be due to methodological differences. The MTFS studies divided twins at mid-puberty, whereas R. Rowe et al. (2002) divided twins based on menarche alone. In the present study, the authors aimed to reconcile discrepant findings by examining differences in etiologic effects for disordered eating attitudes and behaviors (i.e., levels of weight preoccupation, body dissatisfaction, binge eating, compensatory behaviors) using both classification methods in a new sample of 656 female twins. Using the MTFS method (i.e., K. L. Klump, M. McGue, & W. G. Iacono, 2003), the authors observed nominal genetic effects in prepubertal twins but significant genetic effects in pubertal and young adult twins. Conversely, genetic effects were moderate and equal in all groups using the R. Rowe et al. (2002) method. Findings highlight the potentially important role of puberty in the genetic diathesis of disordered eating attitudes and behaviors and the need to use early indicators of pubertal status in studies of developmental effects.

An association of early puberty with disordered eating and anxiety in a population of undergraduate women and men

Eating and anxiety disorders are more prevalent in females, increase during adolescence, and are associated with early pubertal development. This study examined whether timing of puberty onset is associated with disordered eating and anxiety in a large sample of postpubertal male and female undergraduate students. Self-report questionnaires assessed timing of puberty, disordered eating, anxiety, alcohol use, personality, and sensation seeking. Females scored significantly higher on measures of disordered eating (binge eating, dietary restraint, eating concerns, and weight and shape concerns) and anxiety (state and trait anxiety) than did males. In addition, early maturing women and men scored significantly higher on measures of disordered eating and anxiety than on time or late maturing women and men. Measures of alcohol use, sensation seeking, and personality characteristics differed in males and females but did not vary with pubertal timing. Findings suggest that early puberty is associated with disordered eating and anxiety, and this association may be due to an organizational effect of pubertal hormones. Despite important differences in body fat composition, both males and females experiencing early puberty had an increased incidence of disordered eating. The fact that early puberty was associated with increased eating and anxiety symptoms in both sexes suggests that puberty may influence these symptoms through both biological and psychosocial mechanisms.

The possible influence of impulsivity and dietary restraint on associations between serotonin genes and binge eating

Although serotonin (5-HT) genes are thought to be involved in the etiology of bulimia nervosa and binge eating, findings from molecular genetic studies are inconclusive. This may be due to limitations of past research, such as a failure to consider the influence of quantitative traits and gene-environment interactions. The current study investigated these issues by examining whether quantitative traits (i.e., impulsivity) and environmental exposure factors (i.e., dietary restraint) moderate 5-HT gene/binge eating associations in a sample of young women (N = 344). Binge eating was assessed using the Minnesota Eating Behavior Survey and the Dutch Eating Behavior Questionnaire (DEBQ). Impulsivity was assessed with the Barratt Impulsiveness Scale-Version 11. Dietary restraint was measured with a factor score derived from common restraint scales. Saliva samples were genotyped for the 5-HT2a receptor T102C polymorphism and 5-HT transporter promoter polymorphism. As expected, impulsivity and dietary restraint were associated with binge eating. Although the T allele of the 5-HT2a receptor gene and the s allele of the 5-HTT gene were associated with higher levels of impulsivity, there were no main effects of 5-HT genotypes on any binge eating measure, and interactions between genotypes, impulsivity, and dietary restraint were non-significant. In conclusion, we found no evidence to suggest that dietary restraint or impulsivity moderate associations between binge eating and these 5-HT genes. Future research should continue to explore interaction effects by examining larger samples, assessing dietary intake directly, and investigating other genes, traits, and environmental factors that may be related to binge eating and bulimia nervosa.

The Effects of Puberty on Genetic Risk for Disordered Eating: Evidence for a Sex Difference

BACKGROUND Differences in genetic influences on disordered eating are present across puberty in girls. Heritability is 0% before puberty, but over 50% during and after puberty. Emerging data suggest that these developmental differences may be due to pubertal increases in ovarian hormones. However, a critical piece of evidence is lacking, namely, knowledge of genetic influences on disordered eating across puberty in boys. Boys do not experience increases in ovarian hormones during puberty. Thus, if pubertal increases in genetic effects are present in boys, then factors in addition to ovarian hormones may drive increases in heritability in girls. The current study was the first to examine this possibility in a sample of 1006 male and female twins from the Michigan State University Twin Registry. METHOD Disordered eating was assessed with the Minnesota Eating Behavior Survey. Pubertal development was assessed with the Pubertal Development Scale. RESULTS No significant differences in genetic influences on disordered eating were observed in males across any developmental stage. Heritability was 51% in boys during pre-puberty, puberty and young adulthood. By contrast, in girls, genetic factors accounted for 0% of the variance in pre-puberty, but 51% of the variance during puberty and beyond. Sex differences in genetic effects were only significant during pre-puberty, as the best-fitting models constrained heritability to be equal across all males, pubertal females and young adult females. CONCLUSIONS The results highlight sex-specific effects of puberty on genetic risk for disordered eating and provide indirect evidence of a role for ovarian hormones and/or other female-specific factors.

Binge Eating Proneness Emerges During Puberty in Female Rats: A Longitudinal Study

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 nonpalatable food intake or body weight. Similar to patterns in humans, individual differences in binge eating emerge during puberty in female rats. These findings provide strong confirming evidence for the importance of biological risk factors in developmental trajectories of binge eating risk across adolescence.

Differential associations between ovarian hormones and disordered eating symptoms across the menstrual cycle in women

OBJECTIVE We examined changes in drive for thinness, body dissatisfaction, and dietary restraint across the menstrual cycle and associations between these symptoms and ovarian hormones in two independent samples of women (N = 10 and 8 women, respectively) drawn from the community. METHOD Daily self-report measures of disordered eating and negative affect were completed for 35-65 days. Daily saliva samples were assayed for estradiol and progesterone in Study 2 only. RESULTS Levels of body dissatisfaction and drive for thinness were highest during the mid-luteal/pre-menstrual phases in both studies and were negatively associated with estradiol, and positively associated with progesterone. By contrast, dietary restraint showed less variation across the menstrual cycle and weaker associations with ovarian hormones. DISCUSSION Differential associations between ovarian hormones and specific disordered eating symptoms point to distinct etiological processes within the broader construct of disordered eating.

Molecular Genetic Studies of Eating Disorders: Current Status and Future Directions

We review association studies that have examined the genetic basis of eating disorders. Overall, findings suggest that serotonin, brain-derived neurotrophic factor, and estrogen genes may be important for the development of the disorders. These neuronal systems influence behavioral and personality characteristics (e.g., anxiety, food intake) that are disrupted in eating disorders. Future studies would benefit from larger sample sizes and inclusion of behavioral and personality covariates in analyses. Consideration of the mechanisms of genetic effects and interactions between genes and environment is also needed to extend conceptualizations of the genetic basis of these disorders.

The Effects of Ovariectomy on Binge Eating Proneness in Adult Female Rats

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 is 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.