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.
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.
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.
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.
Emotional eating; genetic; environmental; menstrual cycle; ovarian hormones
Human height variation is determined by genetic and environmental factors, but it remains unclear whether their influences differ across birth-year cohorts. We conducted an individual-based pooled analysis of 40 twin cohorts including 143,390 complete twin pairs born 1886–1994. Although genetic variance showed a generally increasing trend across the birth-year cohorts, heritability estimates (0.69-0.84 in men and 0.53-0.78 in women) did not present any clear pattern of secular changes. Comparing geographic-cultural regions (Europe, North America and Australia, and East Asia), total height variance was greatest in North America and Australia and lowest in East Asia, but no clear pattern in the heritability estimates across the birth-year cohorts emerged. Our findings do not support the hypothesis that heritability of height is lower in populations with low living standards than in affluent populations, nor that heritability of height will increase within a population as living standards improve.
height; twins; heritability; birth cohorts; CODATwins project; Human
Previous studies suggest strong associations between exposure to weight
conscious peer groups and increased levels of disordered eating. This
association has been attributed to socialization effects (i.e., membership leads
to disordered eating); however, selection effects (i.e., selecting into peer
groups based on genetic and/or environmental predispositions toward disordered
eating) could contribute to or even account for these associations. The current
study was the first to use a co-twin control design to disentangle these types
of selection factors from socialization effects. Participants included 610
female twins (ages 8–14) drawn from the Michigan State University Twin
Registry. To comprehensively examine a range of eating pathology, several
disordered eating attitudes and behaviors (e.g., body dissatisfaction, binge
eating) were examined via self-report questionnaires. Questionnaires also were
used to assess peer group emphasis on body weight and shape. Replicating
previous results, significant individual-level associations were found between
membership in weight conscious peer groups and disordered eating. However,
co-twin control analyses indicated that these associations were largely due to
genetic and/or shared environmental selection factors rather than pure
socialization effects. Importantly, results remained unchanged when controlling
for pubertal status, suggesting that effects do not vary across developmental
stage. Overall, these findings question whether associations between weight
conscious peer groups and disordered eating are due entirely to socialization
processes. Future studies are needed to identify the specific genetic and/or
shared environmental factors that may drive selection into weight conscious peer
selection; socialization; co-twin control; disordered eating; weight conscious peer groups
Purging Disorder (PD) was recently included as an Otherwise Specified Feeding or Eating Disorder (OSFED) in the DSM-5; however, limited information is available on its prevalence, and its etiology is unknown.
Data from 1790 monozygotic and 1440 dizygotic European American female twins (age range = 18 – 29 years) from the Missouri Adolescent Female Twin Study were used to investigate prevalence and familial influences for PD. A structured clinical interview assessed lifetime DSM-IV criteria for eating disorders and PD. After adjustment for age, twin correlations and biometrical twin models were used to estimate familial (i.e., genetic plus shared environmental) influences on PD.
One hundred and twenty one (3.77%; 95% CI: 3.14, 4.49) women met criteria for lifetime PD. Twin correlations suggested that genetic, shared environmental, and nonshared environmental factors influenced liability to PD. Nonshared environmental factors accounted for 56% [35%, 79%] of the variance in PD. Although familial effects accounted for a significant proportion of variance (44% [21%, 65%]), it was not possible to disentangle the independent contributions of additive genetic effects (20% [0%, 65%]) and shared environmental effects (24% [0%, 57%]).
PD is a prevalent form of eating pathology. Familial factors are relevant to the development of PD but do not demonstrate the magnitude of heritable factors found for other eating disorders.
purging disorder; twins; genetics; women; eating disorders
Prenatal testosterone exposure may be protective against disordered eating. However, prior studies have produced mixed results. Developmental differences in prenatal testosterone's protective effects on disordered eating may explain these discrepancies. Indeed, studies have differed in the age of participants assessed, with data supporting prenatal testosterone effects on disordered eating in early adolescent and young adult samples but not in late adolescence. The present series of studies are the first to investigate age differences in prenatal testosterone's protective effects on disordered eating. Two indirect markers of higher prenatal testosterone were examined: 1) lower finger-length ratios [index (2D)/ring (4D) finger] (Study 1), and 2) lower disordered eating in females from opposite-sex twin pairs (who are thought to be exposed to higher prenatal testosterone from their male co-twin) relative to female controls (Study 2). Participants were twins from the Michigan State University Twin Registry (Study 1: n = 409; Study 2: n = 1,538) in early adolescence, late adolescence, or young adulthood. Disordered eating was assessed with well-validated questionnaires. Finger-length ratios were measured from hand scans, using electronic computer calipers. Findings were consistent across both studies. Higher prenatal testosterone (lower 2D:4D; females from opposite-sex twin pairs vs. controls) predicted lower disordered eating in early adolescence and young adulthood only. Prenatal testosterone-disordered eating associations were not observed during late adolescence. Results point to the possibility of developmental windows of expression for prenatal testosterone's protective effects on disordered eating and suggest that prior discrepant results may reflect age differences across samples.
disordered eating; eating disorder; sex difference; testosterone; hormones; 2D:4D
Previous research has shown that fluctuations in ovarian hormones (i.e., estradiol and progesterone) predict changes in binge eating and emotional eating across the menstrual cycle. However, the extent to which other eating disorder symptoms fluctuate across the menstrual cycle and are influenced by ovarian hormones remains largely unknown. The current study sought to examine whether levels of weight preoccupation vary across the menstrual cycle and whether changes in ovarian hormones and/or other factors (i.e., emotional eating, negative affect) account for menstrual-cycle fluctuations in this eating disorder phenotype.
For 45 consecutive days, 352 women ages 15–25 provided daily ratings of weight preoccupation, negative affect, and emotional eating. Daily saliva samples also were collected and assayed for estradiol and progesterone levels using enzyme-immunoassay techniques.
Weight preoccupation varied significantly across the menstrual cycle, with the highest levels in the pre-menstrual and menstrual phases. However, ovarian hormones did not account for within-person changes in weight preoccupation across the menstrual cycle. Instead, the most significant predictor of menstrual-cycle changes in weight preoccupation was changes in emotional eating.
Fluctuations in weight preoccupation across the menstrual cycle appear to be influenced primarily by emotional eating rather than ovarian hormones. Future research should continue to examine relationships among ovarian hormones, weight preoccupation, emotional eating, and other core eating disorder symptoms (e.g., body dissatisfaction, compensatory behaviors) in an effort to more fully understand the role of these biological and behavioral factors for the full spectrum of eating pathology.
Negative urgency (NU; tendency to act impulsively when experiencing negative emotions) is a risk factor for binge eating, although few studies have examined interviewer-assessed objective binge episodes (OBEs). Moreover, research has not investigated how NU relates to the core components of OBEs: loss of control (LOC) eating and objective overeating (OO). Understanding the relationship between NU and these core components will enhance etiologic models of eating disorder development. Thus, the current study examined associations between NU, OBEs, and the components of OBEs by comparing levels of NU in women with OBEs, LOC eating only, and OO only to women with no pathological eating.
Participants were 612 women who endorsed lifetime OBEs (5.4%), LOC eating outside of OBEs (5.7%), OO only (2.8%), or none of these eating episodes (85.9%).
Women with OBEs, LOC only, and OO only had significantly higher levels of NU than women without these episodes, suggesting that NU is associated with both the LOC and OO components of OBEs.
NU relates to the spectrum of pathology present in women with OBEs. Future research should examine the mechanisms underlying these associations, including impaired behavioral/psychological control and/or increased reward sensitivity in response to negative affect.
binge eating; loss of control eating; objective overeating; negative urgency
Height variation is known to be determined by both genetic and environmental factors, but a systematic description of how their influences differ by sex, age and global regions is lacking. We conducted an individual-based pooled analysis of 45 twin cohorts from 20 countries, including 180,520 paired measurements at ages 1–19 years. The proportion of height variation explained by shared environmental factors was greatest in early childhood, but these effects remained present until early adulthood. Accordingly, the relative genetic contribution increased with age and was greatest in adolescence (up to 0.83 in boys and 0.76 in girls). Comparing geographic-cultural regions (Europe, North-America and Australia, and East-Asia), genetic variance was greatest in North-America and Australia and lowest in East-Asia, but the relative proportion of genetic variation was roughly similar across these regions. Our findings provide further insights into height variation during childhood and adolescence in populations representing different ethnicities and exposed to different environments.
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.
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.
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.
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.
Thin-ideal; thin-ideal internalization; body image; twin study; behavior genetics; risk factors; developmental 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.
binge eating; ovarian hormones; estrogen; progesterone; emotional eating
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
A trend toward greater body size in dizygotic (DZ) than in monozygotic (MZ) twins has been suggested by some but not all studies, and this difference may also vary by age. We analyzed zygosity differences in mean values and variances of height and body mass index (BMI) among male and female twins from infancy to old age. Data were derived from an international database of 54 twin cohorts participating in the COllaborative project of Development of Anthropometrical measures in Twins (CODATwins), and included 842,951 height and BMI measurements from twins aged 1 to 102 years. The results showed that DZ twins were consistently taller than MZ twins, with differences of up to 2.0 cm in childhood and adolescence and up to 0.9 cm in adulthood. Similarly, a greater mean BMI of up to 0.3 kg/m2 in childhood and adolescence and up to 0.2 kg/m2 in adulthood was observed in DZ twins, although the pattern was less consistent. DZ twins presented up to 1.7% greater height and 1.9% greater BMI than MZ twins; these percentage differences were largest in middle and late childhood and decreased with age in both sexes. The variance of height was similar in MZ and DZ twins at most ages. In contrast, the variance of BMI was significantly higher in DZ than in MZ twins, particularly in childhood. In conclusion, DZ twins were generally taller and had greater BMI than MZ twins, but the differences decreased with age in both sexes.
twins; height; BMI; zygosity differences
A trend towards greater body size in dizygotic (DZ) than in monozygotic (MZ) twins has been suggested by some but not all studies, and this difference may also vary by age. We analyzed zygosity differences in means and variances of height and body mass index (BMI) among male and female twins from infancy to old age. Data were derived from an international database of 54 twin cohorts participating in the CODATwins project and included 842,951 height and BMI measurements from age 1 to 102 years. The results showed that DZ twins were consistently taller than MZ twins, with differences of up to 2.0 cm in childhood and adolescence and up to 0.9 cm in adulthood. Likewise, a greater mean BMI of up to 0.3 kg/m2 in childhood and adolescence and up to 0.2 kg/m2 in adulthood was observed in DZ twins, although the pattern was less consistent. DZ twins presented up to 1.7% greater height and 1.9% greater BMI than MZ twins; these percentage differences were largest in middle and late childhood and decreased with age in both sexes. The variance of height was similar in MZ and DZ twins at most ages. In contrast the variance of BMI was significantly higher in DZ than in MZ twins particularly in childhood. In conclusion, DZ twins were generally taller and had greater BMI than MZ twins, but the differences decreased with age in both sexes.
Advanced paternal age at birth has been linked to several psychiatric disorders in offspring (e.g., schizophrenia), and genetic mechanisms are thought to underlie these associations. This study is the first to investigate whether advanced paternal age at birth is associated with eating disorder risk using a twin study design capable of examining both phenotypic and genetic associations.
In a large, population-based sample of female twins ages 8–17 years in mid-puberty or beyond (N = 1,722), we investigated whether advanced paternal age was positively associated with disordered eating symptoms and an eating disorder history (i.e., anorexia nervosa, bulimia nervosa, or binge eating disorder) in offspring. Biometric twin models examined whether genetic and/or environmental factors underlie paternal age effects for disordered eating symptoms.
Advanced paternal age was positively associated with disordered eating symptoms and an eating disorder history, where the highest level of pathology was observed in offspring born to fathers ≥ 40 years old. Results were not accounted for by maternal age at birth, body mass index, socioeconomic status, fertility treatment, or parental psychiatric history. Twin models indicated decreased genetic, and increased environmental, effects on disordered eating with advanced paternal age.
Advanced paternal age increased risk for the full spectrum of eating pathology, independent of several important covariates. However, contrary to leading hypotheses, environmental rather than genetic factors accounted for paternal age-disordered eating associations. These data highlight the need to explore novel (potentially environmental) mechanisms underlying the effects of advanced paternal age on offspring eating disorder risk.
advanced paternal age; eating disorders; disordered eating; genetic; environmental; twin study
Non-shared environmental influences show only minimal stability over time prior to adulthood. The long assessment lags (typically 3-5 years) that characterize most longitudinal twin studies, however, make it difficult to interpret these results. To more rigorously evaluate non-shared environmental stability prior to adulthood, we fitted biometric correlated factors models to 1) seven consecutive days of self-reported negative and positive affect in 239 twin pairs aged 16-25 years and 2) seven consecutive minutes of observer rated warmth and control in 687 twin pairs aged 6-10 years. We then empirically examined patterns of etiologic stability over time using a mixed effects analog to the one-way ANOVA. Genetic and shared environmental correlations were found to be highly stable over both days and minutes. By contrast, non-shared environmental correlations decreased monotonically with increasing lag length, and moreover, were small-to moderate in magnitude when examining intervals longer than a few minutes. Such findings imply that the non-shared environment may be comprised primarily of transient and idiosyncratic effects prior to adulthood.
non-shared environment; stability; genetic
For over one hundred years, the genetics of human anthropometric traits has attracted scientific interest. In particular, height and body mass index (BMI, calculated as kg/m2) have been under intensive genetic research. However, it is still largely unknown whether and how heritability estimates vary between human populations. Opportunities to address this question have increased recently because of the establishment of many new twin cohorts and the increasing accumulation of data in established twin cohorts. We started a new research project to analyze systematically 1) the variation of heritability estimates of height, BMI and their trajectories over the life course between birth cohorts, ethnicities and countries, and 2) to study the effects of birth related factors, education and smoking on these anthropometric traits and whether these effects vary between twin cohorts. We identified 67 twin projects including both monozygotic and dizygotic twins using various sources. We asked for individual level data on height and weight including repeated measurements, birth related traits, background variables, education and smoking. By the end of 2014, 48 projects participated. Together, we have 893,458 height and weight measures (52% females) from 434,723 twin individuals, including 201,192 complete twin pairs (40% monozygotic, 40% same-sex dizygotic and 20% opposite-sex dizygotic) representing 22 countries. This project demonstrates that large-scale international twin studies are feasible and can promote the use of existing data for novel research purposes.
Emotional eating (EE) reflects an urge to eat in response to emotional rather than physical cues and is a risk factor for the development of binge eating. EE has been conceptualized as an attempt to regulate negative affect (NA), a posited maintenance factor for binge eating. However, no study has examined whether EE urges regulate affect. Further, no studies have examined longitudinal associations between EE urges and positive affect (PA).
We examined within-subject longitudinal associations between affect and EE urges in a community-based sample of female twins (mean age=17.8 years). Participants (N=239) completed ratings of affect and EE urges for 45 consecutive days.
Greater NA was concurrently associated with greater EE urges. Additionally, greater EE urges predicted worse NA for both concurrent and prospective (next-day) analyses. Finally, lower PA was associated with greater EE urges in concurrent analyses, but there were no prospective associations between changes in PA and EE urges.
EE urges do not appear to effectively regulate affect. EE urges in a community-based sample appears to have the same functional relationship with affect as binge eating in clinical samples, further supporting EE as a useful dimensional construct for examining processes related to binge eating.
There is a robust association between negative parenting and child antisocial behavior problems. However, the etiology of this association remains unclear. Extant literature has reported strikingly different conclusions across studies, with some highlighting genetic mediation and others highlighting environmental mediation. One possible reason for these discrepancies across studies may be the failure to differentiate between aggressive and non-aggressive (rule-breaking) dimensions of childhood antisocial behavior, given their notably different etiologies and developmental trajectories (Burt, 2012). The current study sought to examine the phenotypic and etiologic associations of maternal negativity with aggressive and rule-breaking antisocial behavior, respectively. Participants included 824 mothers and their twin children between the ages of 6 and 10. Our results highlighted clear etiologic distinctions in the associations of aggression and rule-breaking with maternal negativity. Aggression was associated with maternal negativity via both genetic and environmental factors, whereas the association between non-aggressive rule-breaking and maternal negativity was entirely environmental in origin. These findings provide additional support for the presence of meaningful distinctions between aggressive and non-aggressive forms of antisocial behavior, and highlight the complex relationship between parenting and child outcome.
negative parenting; antisocial behavior; aggression; rule-breaking; gene-environment correlation
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
Prior meta-analytic work has highlighted important etiological distinctions between aggressive (AGG) and non-aggressive rule-breaking (RB) dimensions of antisocial behavior. Among these is the finding that RB is influenced by the environment more than is AGG. Relatively little research, however, has sought to identify the specific environmental experiences that contribute to this effect.
The current study examined whether adults residing in the same neighborhood (N = 1,915 participants in 501 neighborhoods) were more similar in their AGG and RB than would be expected by chance. Analyses focused on simple multi-level models, with the participant as the lower-level unit and the neighborhood as the upper-level unit.
Results revealed little-to-no evidence of neighborhood-level variance in AGG. By contrast, 11+% of the variance in RB could be predicted from participant neighborhood, results that persisted even when considering the possibility of genetic relatedness across participants and neighborhood selection effects. Moreover, 17% of this neighborhood-level variance in RB was accounted for by neighborhood structural characteristics and social processes.
Findings bolster prior suggestions that broader contextual experiences, like the structural and social characteristics of one's neighborhood, contribute in a meaningful way to RB in particular. Our results also tentatively imply that this association may be environmental in origin. Future work should seek to develop additional, stronger designs capable of more clearly leveraging genetic un-relatedness to improve causal inferences regarding the environment.
antisocial behavior; aggression; rule-breaking; neighborhood; environment
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.