S. A. Burt

Preliminary evidence that estradiol moderates genetic influences on disordered eating attitudes and behaviors during puberty

BACKGROUND 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. METHOD 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 (MEBS). Afternoon saliva samples were assayed for estradiol levels. Moderation of genetic effects was examined by comparing twin correlations in low versus high estradiol groups. RESULTS 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. CONCLUSIONS 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.

The Michigan State University Twin Registry (MSUTR): Genetic, Environmental and Neurobiological Influences on Behavior Across Development

The primary aim of the Michigan State University Twin Registry (MSUTR) is to examine developmental differences in genetic, environmental, and neurobiological influences on internalizing and externalizing symptoms, with disordered eating and antisocial behavior representing particular areas of interest. Twin participants span several developmental stages (i.e., childhood, adolescence, and young adulthood). Assessments include comprehensive, multi-informant measures of psychiatric and behavioral phenotypes, buccal swab and salivary DNA samples, assays of adolescent and adult steroid hormone levels (e.g., estradiol, progesterone, testosterone, cortisol), and videotaped parent-child interactions of child and adolescent twin families. To date, we have collected data on over 1000 twins, with additional data collections underway. This article provides an overview of the newly developed MSUTR and describes current and future research directions.

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.

Delinquent peer affiliation as an etiological moderator of childhood delinquency

BACKGROUND Prior research has indicated that affiliation with delinquent peers activates genetic influences on delinquency during adolescence. However, because other studies have indicated that the socializing effects of delinquent peers vary dramatically across childhood and adolescence, it is unclear whether delinquent peer affiliation (DPA) also moderates genetic influences on delinquency during childhood. Method The current study sought to evaluate whether and how DPA moderated the etiology of delinquency in a sample of 726 child twins from the Michigan State University Twin Registry (MSUTR). RESULTS The results robustly supported etiological moderation of childhood delinquency by DPA. However, this effect was observed for shared environmental, rather than genetic, influences. Shared environmental influences on delinquency were found to be several-fold larger in those with higher levels of DPA as compared to those with lower levels. This pattern of results persisted even when controlling for the overlap between delinquency and DPA. CONCLUSIONS Our findings bolster prior work in suggesting that, during childhood, the association between DPA and delinquency is largely (although not solely) attributable to the effects of socialization as compared to selection. They also suggest that the process of etiological moderation is not specific to genetic influences. Latent environmental influences are also amenable to moderation by measured environmental factors.

Do etiological influences on aggression overlap with those on rule breaking? A meta-analysis.

BACKGROUND Although aggressive (AGG) and non-aggressive rule-breaking (RB) dimensions of antisocial behavior have been shown to be differentially heritable, available studies have disagreed on the extent to which the genetic and environmental factors influencing AGG also influence RB. The current meta-analysis sought to clarify the extent of etiological overlap between AGG and RB. Method Thirteen twin/sibling studies examining the covariation between AGG and RB were collected, of which 11 (with 12 independent samples) were ultimately included in the analyses (n=12923 twin/sibling pairs). Genetic and environmental correlations between AGG and RB served as study effect sizes. When squared, these correlations directly index the proportion of genetic and environmental overlap. Data were analyzed using mixed effect models. RESULTS Analyses revealed that genetic influences on AGG were largely, but not entirely, distinct from those on RB: only 38.4% of the genetic influences on AGG overlapped with those on RB. Similarly, only 10.2% of the non-shared environmental influences on AGG overlapped with those on RB. Although the conclusion that etiological influences on AGG are partially distinct from those on RB persisted across several potential moderators, the age of the sample and the informant used were found to moderate the extent of overlap. CONCLUSIONS The findings underscore the presence of meaningful etiological distinctions between AGG and RB, and imply that future conceptualizations of antisocial behavior should be organized (at least in part) around the dimensions of AGG and RB.

Genetic and environmental influences on sleep problems: a study of preadolescent and adolescent twins.

BACKGROUND/AIM The aim of this study was to examine the extent to which additive genetic, shared environmental and non-shared environmental factors contribute to adolescent and preadolescent sleep problems. METHODS The sample consisted of a cohort of 270 monozygotic and 246 dizygotic twins from a university-based twin registry. RESULTS Results demonstrated that genetic and environmental influences each appear to be important to adolescent sleep problems. CONCLUSIONS While the magnitude of genetic influence on sleep problems was consistent with findings from the adult literature, it was smaller than in studies with younger children, suggesting genetic effects may be less influential in adolescence and adulthood.

Sleep Problems and Temperament in Adolescents

The aim of this study was to determine the association between temperament and sleep in adolescents. Participants included 516 adolescents and their mothers drawn from the community. Findings indicated that as with younger children, sleep and dimensions of temperament (sociability, impulsivity and negative affect) are related in adolescents.

Prosocial peer affiliation suppresses genetic influences on non-aggressive antisocial behaviors during childhood

BACKGROUND Available research has suggested that affiliation with prosocial peers reduces child and adolescent antisocial behavior. However, the etiologic mechanisms driving this association remain unclear. The current study sought to evaluate whether this association takes the form of a gene-environment interaction (G × E) in which prosocial peer affiliation acts to reduce the consequences of genetic risk for non-aggressive antisocial behavior during childhood. METHOD Our sample consisted of 500 twin pairs aged 6-10 years from the Michigan State University Twin Registry (MSUTR). RESULTS The results robustly support moderation by prosocial peer affiliation. Genetic influences on non-aggressive antisocial behavior were observed to be several times larger in those with lower levels of prosocial peer affiliation than in those with higher levels of prosocial peer affiliation. This pattern of results persisted even after controlling for gene-environment correlations and deviant peer affiliation, and when restricting our analyses to those twins who shared all or nearly all of their friends. CONCLUSIONS Such findings not only suggest that prosocial peer affiliation moderates genetic influences on non-aggressive antisocial behaviors during childhood but also provide support for the theoretical notion that protective environmental experiences may exert their influence by promoting resilience to genetic risk.

Advanced paternal age at birth: phenotypic and etiologic associations with eating pathology in offspring

BACKGROUND 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. METHOD In a large, population-based sample of female twins aged 8-17 years in mid-puberty or beyond (n = 1722), we investigated whether advanced paternal age was positively associated with disordered eating symptoms and an eating disorder history [i.e. anorexia nervosa (AN), bulimia nervosa (BN) or binge eating disorder (BED)] in offspring. Biometric twin models examined whether genetic and/or environmental factors underlie paternal age effects for disordered eating symptoms. RESULTS 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. The results were not accounted for by maternal age at birth, body mass index (BMI), socio-economic status (SES), fertility treatment or parental psychiatric history. Twin models indicated decreased genetic, and increased environmental, effects on disordered eating with advanced paternal age. CONCLUSIONS 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.

Changes in genetic risk for emotional eating across the menstrual cycle: a longitudinal study

BACKGROUND Previous studies have shown 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. METHOD Participants were 230 female twin pairs (460 twins) from the Michigan State University Twin Registry 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. RESULTS Findings revealed important shifts in genetic and environmental influences, where estimates of genetic influences were two times higher in post- as compared with 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. CONCLUSIONS 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.