Research suggests that prenatal testosterone exposure may masculinize (i.e., lower) disordered eating (DE) attitudes and behaviors and influence the lower prevalence of eating disorders in males versus females. How or when these effects become prominent remains unknown, although puberty may be a critical developmental period. In animals, the masculinizing effects of early testosterone exposure become expressed during puberty when gonadal hormones activate sex-typical behaviors, including eating behaviors. This study examined whether the masculinizing effects of prenatal testosterone exposure on DE attitudes emerge during puberty in 394 twins from opposite-sex and same-sex pairs. Twin type (opposite sex vs. same sex) was used as a proxy for level of prenatal testosterone exposure because females from opposite-sex twin pairs are thought to be exposed to testosterone in utero from their male co-twin. Consistent with animal data, there were no differences in levels of DE attitudes between opposite-sex and same-sex twins during pre-early puberty. However, during mid-late puberty, females from opposite-sex twin pairs (i.e., females with a male co-twin) exhibited more masculinized (i.e., lower) DE attitudes than females from same-sex twin pairs (i.e., females with a female co-twin), independent of several “third variables” (e.g., body mass index [BMI], anxiety). Findings suggest that prenatal testosterone exposure may decrease DE attitudes and at least partially underlie sex differences in risk for DE attitudes after mid-puberty.
disordered eating; eating disorder; puberty; sex difference; testosterone
Puberty is one of the most frequently discussed risk periods for the development of eating disorders. Prevailing theories propose environmentally mediated sources of risk arising from the psychosocial effects (e.g., increased body dissatisfaction, decreased self-esteem) of pubertal development in girls. However, recent research highlights the potential role of ovarian hormones in phenotypic and genetic risk for eating disorders during puberty. The goal of this paper is to review data from human and animal studies in support of puberty as a critical risk period for eating disorders and evaluate the evidence for hormonal contributions. Data are consistent in suggesting that both pubertal status and pubertal timing significantly impact risk for most eating disorders in girls, such that advanced pubertal development and early pubertal timing are associated with increased rates of eating disorders and their symptoms in both cross-sectional and longitudinal research. Findings in boys have been much less consistent and suggest a smaller role for puberty in risk for eating disorders in boys. Twin and animal studies indicate that at least part of the female-specific risk is due to genetic factors associated with estrogen activation at puberty. In conclusion, data thus far support a role for puberty in risk for eating disorders and highlight the need for additional human and animal studies of hormonal and genetic risk for eating disorders during puberty.
puberty; eating disorders; anorexia nervosa; bulimia nervosa; ovarian hormones; estrogen; twin studies
Negative urgency (i.e., the tendency to engage in rash action in response to negative affect) has emerged as a critical personality trait contributing to individual differences in binge eating. However, studies investigating the extent to which genetic and/or environmental influences underlie the effects of negative urgency on binge eating are lacking. Moreover, it remains unclear whether negative urgency-binge eating associations are simply due to the well-established role of negative affect in the development/maintenance of binge eating. The current study addresses these gaps by examining phenotypic and etiologic associations between negative urgency, negative affect, and dysregulated eating (i.e., binge eating, emotional eating) in a sample of 222 same-sex female twin pairs from the Michigan State Twin Registry. Negative urgency was significantly associated with both dysregulated eating symptoms, even after controlling for the effects of negative affect. Genetic factors accounted for the majority (62–77%) of this phenotypic association, although a significant proportion of this genetic covariation was due to genetic influences in common with negative affect. Non-shared environmental factors accounted for a relatively smaller (23–38%) proportion of the association, but these non-shared environmental effects were independent of negative affect. Findings suggest that the presence of emotion-based rash action, combined with high levels of negative affect, may significantly increase genetic risk for dysregulated eating.
binge eating; emotional eating; impulsivity; negative urgency; negative affect; twin study
Associations between within-person changes in ovarian hormones and dysregulated eating (binge eating, emotional eating) have been observed across the menstrual cycle. However, studies have not examined moderators that may contribute to differential associations between individuals. We investigated body-weight regulation variables (body mass index (BMI), dietary restraint) that have theoretical relevance by virtue of their associations with both phenotypes.
Women (N = 196) provided emotional eating ratings and saliva samples for 45 days. BMI and restraint were assessed at three time-points and averaged.
Results showed significant estradiol × progesterone interactions in the prediction of within-subject changes in emotional eating. Neither BMI nor restraint moderated these relationships, although a trend-level dietary restraint × estradiol interaction was observed where estradiol’s effects were enhanced in high restraint scorers.
Findings confirm a role for hormones in changes in emotional eating and suggest that restraint might enhance hormone effects in severe groups.
Within-person changes in estradiol and progesterone predict changes in
binge eating tendencies across the menstrual cycle. However, all women have
menstrual-cycle fluctuations in hormones, but few experience binge eating.
Personality traits may be critical individual difference factors that influence
who will engage in emotional eating in the presence of a vulnerable hormonal
environment. Women (N=239) provided self-reports of emotional eating and saliva
samples for hormone measurement for 45 consecutive days. Negative urgency and
negative emotionality were measured once and were examined as moderators of
hormone-emotional eating associations. Consistent with prior research,
within-person changes in the interaction between estradiol and progesterone
predicted emotional eating. Neither negative urgency nor negative emotionality
interacted with changes in estradiol and progesterone to predict changes in
emotional eating. Additional factors, other than the two personality traits
examined, may account for individual differences in within-person associations
between hormones and emotional eating.
ovarian hormones; personality; negative urgency; eating disorders; emotional eating
Studies suggest that within-person changes in estrogen and progesterone predict changes in binge eating across the menstrual cycle. However, samples have been extremely small (maximum N = 9), and analyses have not examined the interactive effects of hormones that are critical for changes in food intake in animals. The aims of the current study were to examine ovarian hormone interactions in the prediction of within-subject changes in emotional eating in the largest sample of women to date (N = 196). Participants provided daily ratings of emotional eating and saliva samples for hormone measurement for 45 consecutive days. Results confirmed that changes in ovarian hormones predict changes in emotional eating across the menstrual cycle, with a significant estradiol x progesterone interaction. Emotional eating scores were highest during the mid-luteal phase, when progesterone peaks and estradiol demonstrates a secondary peak. Findings extend previous work by highlighting significant interactions between estrogen and progesterone that explain mid-luteal increases in emotional eating. Future work should explore mechanisms (e.g., gene-hormone interactions) that contribute to both within- and between-subject differences in emotional eating.
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.
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.
Twin modeling suggested significant additive genetic and nonshared environmental influences on thin-ideal internalization. Shared environmental influences were small and non-significant.
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.
Thin-ideal; internalization; body image; disordered eating; twin study; heritability; Tripartite Model
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 1,006 male and female twins from the Michigan State University Twin Registry.
Disordered eating was assessed with the Minnesota Eating Behaviors Survey. Pubertal development was assessed with the Pubertal Development Scale.
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.
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.
eating disorders; males; genetic; twins; puberty; sex differences
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.
binge eating; puberty; animal models; bulimia nervosa; eating disorders
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.
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.
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.
Differential associations between ovarian hormones and specific disordered eating symptoms point to distinct etiological processes within the broader construct of disordered eating.
estradiol; progesterone; ovarian hormones; menstrual cycle; eating disorders; disordered eating; drive for thinness; body dissatisfaction; dietary restraint
Anorexia nervosa (AN) is a complex and heritable eating disorder characterized by dangerously low body weight. Neither candidate gene studies nor an initial genome wide association study (GWAS) have yielded significant and replicated results. We performed a GWAS in 2,907 cases with AN from 14 countries (15 sites) and 14,860 ancestrally matched controls as part of the Genetic Consortium for AN (GCAN) and the Wellcome Trust Case Control Consortium 3 (WTCCC3). Individual association analyses were conducted in each stratum and meta-analyzed across all 15 discovery datasets. Seventy-six (72 independent) SNPs were taken forward for in silico (two datasets) or de novo (13 datasets) replication genotyping in 2,677 independent AN cases and 8,629 European ancestry controls along with 458 AN cases and 421 controls from Japan. The final global meta-analysis across discovery and replication datasets comprised 5,551 AN cases and 21,080 controls. AN subtype analyses (1,606 AN restricting; 1,445 AN binge-purge) were performed. No findings reached genome-wide significance. Two intronic variants were suggestively associated: rs9839776 (P=3.01×10-7) in SOX2OT and rs17030795 (P=5.84×10-6) in PPP3CA. Two additional signals were specific to Europeans: rs1523921 (P=5.76×10-6) between CUL3 and FAM124B and rs1886797 (P=8.05×10-6) near SPATA13. Comparing discovery to replication results, 76% of the effects were in the same direction, an observation highly unlikely to be due to chance (P=4×10-6), strongly suggesting that true findings exist but that our sample, the largest yet reported, was underpowered for their detection. The accrual of large genotyped AN case-control samples should be an immediate priority for the field.
anorexia nervosa; eating disorders; GWAS; genome-wide association study; body mass index; metabolic
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.
binge eating; bulimia nervosa; ovariectomy; animal models; ovarian hormones
We investigated gene-environment interactions (G×E) for associations between parental divorce and disordered eating (DE).
Participants were 1,810 female twins from the Michigan State University Twin Registry and the Minnesota Twin Family Study. The Minnesota Eating Behaviors Survey was used to assess DE. We tested for G×E by comparing the heritability of DE in twins from divorced versus intact families. It was hypothesized that divorce would moderate the heritability of DE, in that heritability would be higher in twins from divorced than twins from intact families.
As expected, the heritability of body dissatisfaction was significantly higher in twins from divorced than intact families. However, genetic influences were equal in twins from divorced and intact families for all other forms of DE.
Although divorce did not moderate heritability of most DE symptoms, future research should replicate G×Es for body dissatisfaction and identify factors underlying this unique relationship.
Disordered Eating; Parental Divorce; Gene-Environment Interaction; Eating Disorders; Twins
Dietary restraint is a prospective risk factor for the development of binge eating and bulimia nervosa. Although many women engage in dietary restraint, relatively few develop binge eating. Dietary restraint may only increase susceptibility for binge eating in individuals who are at genetic risk. Specifically, dietary restraint may be a behavioral “exposure” factor that activates genetic predispositions for binge eating. We investigated this possibility in 1,678 young adolescent and adult same-sex female twins from the Minnesota Twin Family Study and the Michigan State University Twin Registry. Twin moderation models were used to examine whether levels of dietary restraint moderate genetic and environmental influences on binge eating. Results indicated that genetic and non-shared environmental factors for binge eating increased at higher levels of dietary restraint. Importantly, these effects were present after controlling for age, body mass index, and genetic and environmental overlap among dietary restraint and binge eating. Results suggest that dietary restraint may be most important for individuals at genetic risk for binge eating, and the combination of these factors could enhance individual differences in risk for binge eating.
binge eating; dietary restraint; gene-environment interactions; twins
Puberty moderates genetic influences on disordered eating attitudes and behaviors, with little genetic influence before puberty but large (≥ 50%) genetic effects during and after puberty. To date, however, nothing is known about the mechanisms that underlie these effects. Estradiol is a particularly promising candidate, as estrogens become elevated at puberty and regulate gene transcription within neurotransmitter systems important for eating-related phenotypes. The aim of this pilot study was to examine whether estradiol levels moderate genetic influences on disordered eating during puberty.
Participants included 198 female twins (ages 10-15 years) from the Michigan State University Twin Registry. Disordered eating attitudes and behaviors were assessed with the total score, weight preoccupation, body dissatisfaction, and binge eating/compensatory behavior subscales of the Minnesota Eating Behavior Survey. Afternoon saliva samples were assayed for estradiol levels. Moderation of genetic effects was examined by comparing twin correlations in low versus high estradiol groups.
In the low estradiol group, monozygotic (MZ) and dizygotic (DZ) twin correlations for all MEBS scales were similar, suggesting little genetic influence. In the high estradiol group, the MZ twin correlation was more than double the DZ twin correlation, indicating the presence of genetic effects. Findings could not be accounted for by age, body mass index, or the physical changes of puberty.
Estradiol may be one important moderator of genetic effects on disordered eating during puberty. Larger twin studies are needed to replicate this pilot work and quantify the extent of genetic moderation.
Animal studies indicate gonadal hormones at puberty have an effect on the development of masculine and feminine traits. However, it is unknown whether similar processes occur in humans. We examined whether women with anorexia nervosa (AN), who often experience primary amenorrhea, exhibit attenuated feminization in their psychological characteristics in adulthood due to the decrease/absence of gonadal hormones at puberty. Women with AN were compared on a number of psychological characteristics using General Linear Models based on the presence/absence of primary amenorrhea. Although women with primary amenorrhea exhibited lower anxiety scores than those without primary amenorrhea, in general, results did not provide evidence of attenuated feminization in women with AN with primary amenorrhea. Future research should utilize novel techniques and direct hormone measurement to explore the effects of pubertal gonadal hormones on masculine and feminine traits.
Organizational effects; sex differences; amenorrhea; pubertal timing; anorexia nervosa
Few studies have examined nonshared environmental risk factors for disordered eating, and none have done so using a longitudinal design. The current project employed a longitudinal, monozygotic twin differences design to examine parent-child conflict as a nonshared environmental risk factor for disordered eating. Participants included 468 monozygotic female twins (234 pairs) from the Minnesota Twin Family Study, followed every three years from ages 11 to 17. Twin differences in disordered eating were assessed with the Total Score, Body Dissatisfaction, Weight Preoccupation and Binge Eating subscales of the Minnesota Eating Behavior Survey. Differences in parent-child conflict were assessed with the Parental Environment Questionnaire. Cross-lagged models were used to examine longitudinal associations among these variables, controlling for within-age associations. Only the longitudinal association between twin differences in disordered eating at age 14 and differences in parent-child conflict at age 17 was significant; twin differences in disordered eating predicted later differences in parent-child conflict rather than the reverse. Findings suggest differences in parent-child conflict between genetically identical twins may be a consequence of, rather than a risk factor for, differences in disordered eating.
Research examining changes in eating disorder symptoms across adolescence suggests an increase in disordered eating from early to late adolescence. However, relevant studies have largely been cross-sectional in nature and most have not examined the changes in the attitudinal symptoms of eating disorders (e.g., weight concerns). This longitudinal study aimed to address gaps in the available data by examining the developmental trajectories of disordered eating in females from preadolescence into young adulthood.
Participants were 745 same-sex female twins from the Minnesota Twin Family Study. Disordered eating was assessed using the Total Score, Body Dissatisfaction subscale, Weight Preoccupation subscale, and a combined Binge Eating and Compensatory Behavior subscale from the Minnesota Eating Behavior Survey assessed at the ages of 11, 14, 18, 21, and 25. Several latent growth models were fit to the data to identify the trajectory that most accurately captures the changes in disordered eating symptoms from 11 to 25 years.
The best-fitting models for overall levels of disordered eating, body dissatisfaction, and weight preoccupation showed an increase in from 11 through 25 years. In contrast, bulimic behaviors increased to age of 18 and then stabilized to age of 25.
The findings expanded upon extant research by investigating longitudinal, symptom specific, within-person changes and showing an increase in cognitive symptoms into young adulthood and the stability of disordered eating behaviors past late adolescence.
disordered eating; longitudinal; developmental; growth curve
Women with bulimia nervosa (BN) frequently have co-occurring alcohol use disorders (AUDs). Studies of shared genetic transmission of these disorders have been mixed. Personality heterogeneity among individuals with BN may explain discrepant findings. Cluster analysis has characterized women with BN in groups on the basis of personality profiles. One group, the Dysregulated cluster, characterized largely by behavioural disinhibition and emotional dysregulation may be more closely linked etiologically to AUDs. This study examined whether genetic associations between BN and AUDs are the strongest among the Dysregulated cluster. Symptoms of BN and AUDs were assessed in female twins at ages 17 and 25 years from the Minnesota Twin Family Study. Personality clusters were defined using the Multidimensional Personality Questionnaire. Twin moderation models suggested small-to-moderate common genetic transmission between BN and AUDs. However, shared genetic effects did not differ by personality cluster. Findings suggest that personality clusters are unlikely to account for inconsistent findings regarding their shared aetiology.
bulimia nervosa; alcohol use disorders; personality
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 Behaviors 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.
binge eating; serotonin; impulsivity; dietary restraint; gene-environment interactions
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 (Rowe et al., 2002). Discrepant results may be due to methodological differences. The MTFS studies divided twins at mid-puberty, while Rowe et al. (2002) divided twins based on menarche alone. We 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, we observed nominal genetic effects in pre-pubertal twins, but significant genetic effects in pubertal and young adult twins. Conversely, genetic effects were moderate and equal in all groups using the 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.
eating disorders; anorexia nervosa; bulimia nervosa; twins; genetic
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, as it masculinizes behavior in animals and humans via its permanent effects on the central nervous system.
We examined 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 versus OS) is considered a proxy measure of prenatal hormone exposure, as 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.
Participants included 304 SS female twins, 59 OS female twins, 54 OS male twins, and 165 SS male twins from the Michigan State University Twin Registry (MSUTR).
Main Outcome Measures
Overall levels of disordered eating were assessed with the Minnesota Eating Behavior Survey.
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 to an independent sample of undergraduate women (N = 69) who were raised with one or more brothers.
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, may also contribute to sex differences in DE prevalence.
eating disorder; disordered eating; sex difference; organizational effects; testosterone; twins
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.
anorexia nervosa; bulimia nervosa; genetic; gene
Prior studies exploring gene-environment interactions (GxE) in the development of youth conduct problems (CP) have focused almost exclusively on single risk experiences, despite research indicating that the presence of other risk factors and/or the absence of protective factors can accentuate the influence of a given risk factor on CP. The goal of the current study was to fill this gap in the literature, evaluating whether risky and protective aspects of parenting might combine to jointly moderate the etiology of CP.
The sample consisted of 500 child twin pairs from the Michigan State University Twin Registry (MSUTR). Child CP was assessed using multiple informant reports. Maternal warmth and directiveness were assessed via videotaped dyadic interactions between mothers and each of their twins.
Biometric GxE analyses revealed that directiveness and warmth did appear to jointly moderate the etiology of CP. In particular, shared environmental influences were accentuated by colder, less directive or “less engaged” mothering, while genetic influences were strongest when the child was experiencing warmer, more directive or “more authoritative” mothering.
Such findings serve to highlight the synergistic effects of risky and protective experiences on child outcomes. They also provide additional empirical support for the bioecological form of GxE which postulates that, in some cases, genetic influences may be most strongly expressed in the presence of low risk environments.
child conduct problems; maternal directiveness or control; maternal warmth; GxE
Previous research has established a link between weight-based teasing and binge eating, though the precise mechanisms that drive this relationship remain unknown. This study examined negative affect as a mediator of the relationship between weight-based teasing and binge eating. Participants included 265 adolescent female twins (aged 10–15 years). Self-report measures assessed binge eating, weight-based teasing, and negative affect. Mediation was tested within hierarchical linear models to control for the non-independence of the twin data. Significant positive associations were observed between binge eating, teasing, and negative affect. In the regression analyses, negative affect partially mediated associations between weight-based teasing and binge eating. Results suggest that increases in negative affect are one way in which weight-based teasing leads to binge eating in girls. Future studies should examine additional mediators and assess possible clinical applications of these findings.
Negative affect; binge eating; eating disorders; teasing; weight-based teasing; disordered eating