The current study explores the extent to which genetic and environmental factors influence liability to binge eating in the absence of compensatory behaviors (BE) in a population-based sample of twins.
Questionnaire data on 8,045 same-sex and opposite-sex twins, aged 18-31 years, from a Norwegian twin registry were used to assess BE during the last 6 months.
The best-fitting biometrical model suggested that the heritability of BE was 41% (95% confidence interval [CI]: 0.31-0.50). Individual environmental factors accounted for the rest of the variance (59%; 95% CI: 0.50-0.69). No significant sex differences were found, but the statistical power to detect such effects was low. Shared environmental influences on the liability to BE in males could not be ruled out.
The findings indicate significant additive genetic influences on BE, supporting the validity of the core features of binge eating disorder as a diagnostic category.
"Mothers with an eating disorder history, or current eating disorder symptoms, may also find it difficult to know when and how to feed their children, or doubt their judgement in this area
. As noted by others
[10,27,28], it is likely that these family environmental factors work in conjunction with genetic vulnerability to increase eating disorder risk. "
[Show abstract][Hide abstract] ABSTRACT: Previous studies have found associations between maternal and family factors and child eating disorder symptoms. However, it is not clear whether family factors predict eating disorder symptoms specifically, or relate to more general child psychopathology, of which eating disorder symptoms may be one component. This study aimed to identify maternal and family factors that may predict increases or decreases in child eating disorder symptoms over time, accounting for children's body mass index z-scores and levels of general psychological distress.
Participants were 221 mother-child dyads from the Childhood Growth and Development Study, a prospective cohort study in Western Australia. Participants were assessed at baseline, 1-year follow-up and 2-year follow-up using interview and self-report measures. Children had a mean age of 10 years at baseline and 46% were male. Linear mixed models and generalised estimating equations were used to identify predictors of children's eating disorder symptoms, with outcome variables including a global index of eating disorder psychopathology, levels of dietary restraint, levels of emotional eating, and the presence of loss of control ('binge') eating.
Children of mothers with a current or past eating disorder reported significantly higher levels of global eating disorder symptoms and emotional eating than other children, and mothers with a current or past eating disorder reported significantly more concern about their children's weight than other mothers. Maternal concern about child weight, rather than maternal eating disorder symptoms, was significant in predicting child eating disorder symptoms over time. Family exposure to stress and low maternal education were additional risk factors for eating disorder symptoms, whilst child-reported family satisfaction was a protective factor.
After adjusting for relevant confounding variables, maternal concern about child weight, children's level of family satisfaction, family exposure to stress, and maternal education are unique predictors of child eating disorder symptoms.
Journal of Eating Disorders 04/2014; 2(1):11. DOI:10.1186/2050-2974-2-11
"Yet, findings for bulimic behaviors are somewhat inconsistent with regard to the magnitude of these factors. With few exceptions (i.e., heritability 8–17%; see Wade et al. 2008), several studies indicated that the heritability of binge eating exceeds 40% (Bulik et al. 1998; Sullivan et al. 1998; Bulik et al. 2003; Reichborn-Kjennerud et al. 2004; Klump et al. 2002) and compensatory behavior ranges from 35 to 70%, depending on whether several compensatory behaviors are examined together (heritability = 50%) or specific types of behaviors are examined separately (e.g., laxative use only; heritability = 43%) are examined (Klump et al. 2000; Mazzeo et al. 2010; Sullivan et al. 1998). Nonetheless, in general, each of these studies indicated that these behaviors are heritable with the remaining variance due to nonshared environmental factors. "
[Show abstract][Hide abstract] ABSTRACT: Bulimic behaviors are frequently associated with alcohol use disorders. However, extant family and twin study findings have been inconsistent with regard to whether these behaviors share etiologic influences. A sample of 292 young adult, female twins was used to examine genetic and environmental factors underlying the association between binge eating and compensatory behaviors (e.g., vomiting)and alcohol use. Binge eating and compensatory behaviors were assessed using the Minnesota Eating Behavior Survey.Alcohol use was measured using the Alcohol Use Disorders Identification Test. Univariate models indicated that the heritability of binge eating, compensatory behaviors, and alcohol use was 41, 28, and 78%, respectively, with the remaining variance due to nonshared environmental effects.Bivariate models indicated that there was a moderate-to-large degree of overlap (genetic correlation = 0.31–0.61) in additive genetic factors between alcohol use and binge eating and compensatory behaviors, and no overlap in environmental effects. Findings suggest that these phenotypes co-aggregate in families and that similar genes or heritable traits may be contributing to their co-occurrence.
"Animal research of binge eating has largely focused on group comparisons where between-group effects (i.e., rats with versus without experimental manipulation) are examined rather than between-rat individual differences in response to experimental manipulations (Asarian and Geary, 2006; Yu et al., 2008). A between-groups approach is useful for identifying initial effects, but it does not map well onto binge eating risk as it is expressed in humans, where individuals vary in their propensity to engage in binge eating (Bulik et al., 1998; Klump et al., 2010; Klump et al., 2000; Reichborn-Kjennerud et al., 2004), despite similar exposure to environmental " risks " (e.g., access to highly palatable food). Indeed, while binge eating exists on a continuum (ranging from low to high) in women, some women are binge prone while others are binge resistant, despite relative similarity in access to food and other environmental circumstances. "
[Show abstract][Hide abstract] ABSTRACT: 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.
Hormones and Behavior 03/2011; 59(4):585-93. DOI:10.1016/j.yhbeh.2011.02.015 · 4.63 Impact Factor
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