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.     

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

ABSTRACT— 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.     

Etiological Distinctions between Aggressive and Non-aggressive Antisocial Behavior: Results from a Nuclear Twin Family Model

A recent meta-analysis of 103 studies Burt (Clinical Psychology Review, 29:163-178, 2009a) highlighted the presence of etiological distinctions between aggressive (AGG) and non-aggressive rule-breaking (RB) dimensions of antisocial behavior, such that AGG was more heritable than was RB, whereas RB was more influenced by the shared environment. Unfortunately, behavioral genetic research on antisocial behavior to date (and thus, the research upon which the meta-analysis was based) has relied almost exclusively on the classical twin model. This reliance is problematic, as the strict assumptions that undergird this model (e.g., shared environmental and dominant genetic influences are not present simultaneously; there is no assortative mating) can have significant consequences on heritability estimates when they are violated. The nuclear twin family model, by contrast, allows researchers to relax and statistically evaluate many of the assumptions of the classical twin design by incorporating parental self-report data along with the more standard twin data. The goal of the current study was thus to evaluate whether prior findings of etiological distinctions between AGG and RB persisted when using the nuclear twin family model. We examined a sample of 312 child twin families from the Michigan State University Twin Registry. Results strongly supported prior findings of etiological distinctions between AGG and RB, such that broad genetic influences were observed to be particularly important to AGG whereas shared environmental influences contributed only to RB. Nevertheless, the current findings also implied that additive genetic influences on antisocial behavior may be overestimated when using the classical twin design.     

Etiological Contributions to the Covariation Between Children’s Perceptions of Inter-Parental Conflict and Child Behavioral Problems

Prior work has suggested that inter-parental conflict likely plays an etiological role in child behavior problems. However, family-level measurement of inter-parental conflict in most traditional child twin studies has made it difficult to tease apart the specific causal mechanisms underlying this association. The Children’s Perception of Inter-parental Conflict scale (CPIC) provides a child-specific measurement tool for examining these questions, as its subscales tap multiple dimensions of conflict assessed from the child’s (rather than the parent’s) perspective. The current study examined (1) the degree of genetic and environmental influence on each of the CPIC subscales, and (2) etiological contributions to the covariation between the CPIC scales and parental reports of child behavioral problems. The CPIC was completed by 1,200 child twins (aged 6–11 years) from the Michigan State University Twin Registry (MSUTR). Parents completed the Child Behavior Checklist (CBCL) to assess child internalizing and externalizing behavior problems. Multivariate models were examined to evaluate the relative contributions of genetic and environmental factors to both the CPIC scales and to their overlap with child behavioral outcomes. Modeling results indicated no significant moderation of sex or age. Significant environmental overlap emerged between the CPIC conflict properties scale and child internalizing and externalizing problems. By contrast, significant genetic correlations emerged between the CPIC self-blame scale and externalizing problems as well as between the CPIC threat scale and internalizing problems. Overall, findings suggest that the subscales of the CPIC are somewhat etiologically diverse and may provide a useful tool for future investigations of possible gene-environment interplay.     

Childhood anxiety associated with low BMI in women with Anorexia Nervosa

Objective

Extremely low body mass index (BMI) values are associated with increased risk for death and poor long-term prognosis in individuals with anorexia nervosa (AN). The present study explores childhood personality characteristics that could be associated with the ability to attain an extremely low BMI.

Methods

Participants were 326 women from the Genetics of Anorexia Nervosa (GAN) Study who completed the Structured Interview for Anorexia Nervosa and Bulimic Syndromes and whose mother completed the Child Behavioral Checklist and/or Revised Dimensions of Temperament Survey.

Results

Children who were described as having greater fear or anxiety by their mothers attained lower BMIs during AN (p < 0.02). Path analysis in the GAN and a validation sample, Price Foundation Anorexia Nervosa Trios Study, confirmed the relation between early childhood anxiety, caloric restriction, qualitative food item restriction, excessive exercise, and low BMI. Path analysis also confirmed a relation between childhood anxiety and caloric restriction, which mediated the relation between childhood anxiety and low BMI in the GAN sample only.

Conclusion

Fearful or anxious behavior as a child was associated with the attainment of low BMI in AN and childhood anxiety was associated with caloric restriction. Measures of anxiety and factors associated with anxiety-proneness in childhood may index children at risk for restrictive behaviors and extremely low BMIs in AN.     

Dietary restraint moderates genetic risk for binge eating

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 increase susceptibility for binge eating only 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 nonshared environmental factors for binge eating increased at higher levels of dietary restraint. 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 that the combination of these factors could enhance individual differences in risk for binge eating.     

Genetic relationships between personality and eating attitudes and behaviors

Genetic and environmental factors underlying relationships between personality traits and disordered eating were examined in 256 female adolescent twin pairs (166 monozygotic, 90 dizygotic). Eating behaviors were assessed with the Total Score, Body Dissatisfaction, Weight Preoccupation, Binge Eating, and Compensatory Behavior subscales from the Minnesota Eating Disorders Inventory (M-EDI; K. L. Klump, M. McGue, & W. G. Iacono, 2000). Personality characteristics were assessed with the Negative Emotionality, Positive Emotionality, and Constraint scales from the Multidimensional Personality Questionnaire (MPQ; A. Tellegen, 1982). Model-fitting analyses indicated that although genetic factors were more likely to contribute to MPQ and M-EDI phenotypic associations than environmental factors, shared genetic variance between the 2 phenotypes was limited. MPQ personality characteristics may represent only some of several genetic risk factors for eating pathology.