Objective Recent data show significant phenotypic and genetic associations between ovarian hormones and binge eating in adulthood. Theories of hormonal risk focus on puberty and the possibility that hormone activation induces changes in genetic effects that then lead to differential risk for binge eating in post-puberty and adulthood. Although this theory is difficult to test in humans, an indirect test is to examine whether genetic influences on binge eating increase during the pubertal period in girls. Prior work has shown pubertal increases in genetic influences on overall disordered eating symptoms, but no study to date has examined binge eating. The present study was the first to examine these increases for binge eating. Methods Participants included 1,568 female twins (ages 8–25 years) from the Michigan State University Twin Registry. Binge eating and pubertal development were assessed with self-report questionnaires. Results Twin moderation models showed significant linear increases in genetic effects from pre-puberty (5%) to post-puberty (42%), even after controlling for the effects of age and body mass index. Discussion Results provide critical support for increased genetic influences on binge eating during puberty. Additional studies are needed to identify hormonal mechanisms and fully test contemporary models of ovarian hormone risk.

Background 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. Methods 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. Results 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. 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.

The rise in opioid-related harms is an issue of increasing public health importance in Canada. This analysis used data from the Hospital Morbidity Database and the National Ambulatory Care Reporting System to determine the number of opioid poisoning hospitalizations and emergency department visits in Canada. Opioid poisoning hospitalizations have increased over the past 10 years, reaching 15.6 per 100 000 population in 2016/17. Emergency department visits due to opioid poisoning have also increased in Alberta and Ontario, the two provinces that collect emergency department data at the level of detail required for this analysis. These findings highlight the importance of pan- Canadian surveillance of opioid-related harms, as well as the need for evidence-based policies to help reduce these harms.

Emerging evidence suggests socioeconomic disadvantage may increase risk for eating disorders (EDs). However, there are very few studies on the association between disadvantage and EDs, and all have focused on individual-level risk factors (e.g., family income). Neighborhood disadvantage (i.e., elevated poverty and reduced resources in one's neighborhood) is associated with increased risk for anxiety/depression and poor physical health. To date, no studies have examined phenotypic associations between neighborhood disadvantage and disordered eating, or how any form of disadvantage may interact with genetic individual differences in risk for EDs. We examined phenotypic and etiologic associations between neighborhood disadvantage and disordered eating in 2,922 girls ages 8-17 from same-sex twin pairs recruited through the Michigan State University Twin Registry. Parents rated the twins on nine items assessing core disordered eating symptoms (e.g., weight preoccupation, binge eating), and neighborhood disadvantage was calculated from 17 indicators of contextual disadvantage (e.g., median home value, neighborhood unemployment). Puberty was measured using the Pubertal Development Scale to examine whether associations were consistent across development. At a phenotypic level, greater neighborhood disadvantage was associated with significantly greater disordered eating symptoms in girls at all stages of puberty (b = .07). Moreover, Genotype 3 Environment models showed that girls living in more disadvantaged neighborhoods exhibited stronger and earlier (i.e., during pre/ early puberty) activation of genetic influences on disordered eating. Results highlight the critical importance of considering contextual disadvantage in research on etiology and risk for disordered eating, and the need for increased screening and treatment for EDs in disadvantaged youth. General Scientific SummaryThis was the first study to examine the association between neighborhood disadvantage and disordered eating in girls. We found that neighborhood disadvantage was associated with significantly greater disordered eating symptoms across all stages of puberty in girls, and that girls living in disadvantaged neighborhoods exhibited stronger and earlier (i.e., during pre/early puberty) activation of genetic influences on disordered eating. Results indicate that neighborhood disadvantage is a critical contextual factor with implications for etiology and risk for disordered eating in girls.

Objective 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. Method 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. Results Twin modeling suggested significant additive genetic and nonshared environmental influences on thin-ideal internalization. Shared environmental influences were small and non-significant. Discussion 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.