Shared genetic influences between eating disorders and gastrointestinal disease in a large, population-based sample of adult women and men.

BACKGROUND: Some preliminary research suggests higher rates of gastrointestinal disease in individuals with eating disorders (EDs). However, research is limited, and it remains unknown what etiologic factors account for observed associations. This was the first study to examine how EDs and dimensional ED symptoms (e.g. body dissatisfaction, binge eating) are phenotypically and etiologically associated with gastrointestinal disease in a large, population-based twin sample. METHODS: Adult female (N = 2980) and male (N = 2903) twins from the Michigan State University Twin Registry reported whether they had a lifetime ED (anorexia nervosa, bulimia nervosa, or binge-eating disorder) and completed a measure of dimensional ED symptoms. We coded the presence/absence of lifetime gastrointestinal disease (e.g. inflammatory bowel disease) based on responses to questions regarding chronic illnesses and medications. We first examined whether twins with gastrointestinal disease had higher rates of EDs and ED symptoms, then used correlated factors twin models to investigate genetic and environmental contributions to the overlap between disorders. RESULTS: Twins with gastrointestinal disease had significantly greater dimensional ED symptoms (ß = 0.21, p < 0.001) and odds of a lifetime ED (OR 2.90, p = 0.001), regardless of sex. Shared genetic factors fully accounted for the overlap between disorders, with no significant sex differences in etiologic associations. CONCLUSIONS: Comorbidity between EDs and gastrointestinal disease may be explained by overlap in genetic influences, potentially including inflammatory genes implicated in both types of disorders. Screening for gastrointestinal disease in people with EDs, and EDs in those with gastrointestinal disease, is warranted.

Parental Nurturance Moderates the Etiology of Youth Resilience.

Parenting behaviors are among the most robust predictors of youth resilience to adversity. Critically, however, very few studies examining these effects have been genetically-informed, and none have considered parenting as an etiologic moderator of resilience. What's more, despite the multidimensionality of resilience, extant etiologic literature has largely focused on a single domain. The current study sought to fill these respective gaps in the literature by examining whether and how parental nurturance shapes the etiology of academic, social, and psychological resilience, respectively. We employed a unique sample of twins (N = 426 pairs; ages 6-11) exposed to moderate-to-severe levels of environmental adversity (i.e., family poverty, neighborhood poverty, community violence) from the Twin Study of Behavioral and Emotional Development in Children. As expected, parental nurturance was positively correlated with all forms of resilience. Extended univariate genotype-by-environment interaction models revealed that parental nurturance significantly moderated genetic influences on all three domains of resilience (academic resilience A1= -0.53, psychological resilience A1= -1.22, social resilience A1= -0.63; all p < .05), such that as parental nurturance increased, genetic influences on youth resilience decreased. Put another way, children experiencing high levels of parental nurturance were more resilient to disadvantage, regardless of their genetic predisposition towards resilience. In the absence of nurturing parenting, however, genetic influences played an outsized role in the origins of resilience. Such findings indicate that parental nurturance may serve as a malleable protective factor that increases youth resilience regardless of genetic influences.

Changes in affect longitudinally mediate associations between emotion regulation strategy use and disordered eating.

BACKGROUND: Trait-level emotion regulation (ER) difficulties are associated with eating disorders (EDs) transdiagnostically. However, little research has examined whether within-person fluctuations in ER longitudinally predict ED behaviors in daily life or the mechanisms of ER effects. Investigating daily ER could help us better understand why people experience ED behaviors at a given time. We examined whether day-to-day changes in adaptive (e.g., cognitive reappraisal) and maladaptive (e.g., rumination) ER longitudinally predicted core ED behaviors (binge eating, purging, dieting) and whether changes in affect mediated effects. METHOD: Female participants (N = 688) ages 15-30 from the Michigan State University Twin Registry reported their adaptive and maladaptive ER use, negative affect (NA), positive affect (PA), binge eating, purging, and dieting on 49 consecutive days. Using structural equation modeling, we examined whether within-person fluctuations in ER predicted same- and next-day ED behaviors and whether changes in affect mediated longitudinal ER effects. RESULTS: Greater maladaptive ER predicted increased likelihood of same-day binge eating and next-day binge eating and purging. The association between maladaptive ER and next-day binge eating and purging was mediated by increased next-day NA. In contrast, dieting was more closely related to changes in PA. Adaptive ER did not predict reduced likelihood of any ED behavior. CONCLUSIONS: Maladaptive ER may longitudinally increase risk for binge eating and purging by amplifying NA. Interventions focused on decreasing maladaptive ER and subsequent NA might help disrupt binge eating-purging cycles. Conversely, results add to evidence that PA fluctuations may play a unique role in maintaining restrictive behaviors. PUBLIC SIGNIFICANCE: Little is known about how daily changes in emotion regulation may impact disordered eating. We found that maladaptive emotion regulation (e.g., rumination) was associated with a higher likelihood of binge eating and purging on the next day because it predicted increased next-day negative affect. In contrast, dieting was more closely tied to fluctuations in positive affect. Targeting daily emotion regulation and affective processes may help disrupt cycles of disordered eating.

Disordered eating in transgender and gender non-conforming youth: A comparison to community-based and clinical samples.

OBJECTIVE: This study investigates eating pathology in transgender and gender non-conforming (TGNC) youth compared to a community-based sample and individuals with eating disorders (EDs). METHOD: Participants (ages 13-21 years) included TGNC youth from a paediatric gender clinic (N = 97), a demographically matched community-based sample of cisgender males (N = 97) and cisgender females (N = 97), and treatment-seeking patients with EDs (N = 112). The Eating Disorder Examination Questionnaire (EDE-Q) was used to assess ED cognitions and behaviours. RESULTS: Transgender and gender non-conforming participants reported significantly higher EDE-Q global scores compared to the cisgender samples, but significantly lower than the ED sample. Transgender and gender non-conforming individuals reported a higher likelihood of objective binge episodes (OBEs) than the cisgender groups, albeit lower than youth with EDs. A substantial proportion of TGNC participants scored in elevated ranges on the EDE-Q global score (35% ≥ score of 3, 17% ≥ score of 4), significantly higher than cisgender males (0% ≥ score of 3, 0% ≥ score of 4) and females (9% ≥ score of 3, 3% ≥ score of 4). CONCLUSIONS: Findings indicate that TGNC youth exhibit increased ED cognitions and OBEs compared to cisgender samples, highlighting the need for screening and addressing ED symptoms in this population.

Combined oral contraceptive use and risk for binge eating in women: Potential gene × hormone interactions.

Extant animal and human data suggest endogenous ovarian hormones increase risk for binge eating in females, possibly via gene × hormone interactions and hormonally induced increases in genetic influences. Approximately 85 % of women will take combined oral contraceptives (COCs) that mimic the riskiest hormonal milieu for binge eating (i.e., post-ovulation when both estrogen and progesterone are present). The purpose of this narrative review is to synthesize findings of binge eating risk in COC users. Few studies have been conducted, but results suggest that COCs may increase risk for binge eating and related phenotypes (e.g., craving for sweets), particularly in genetically vulnerable women. Larger, more systematic human and animal studies of COCs and binge eating are needed. The goal of this work should be to advance personalized medicine by identifying the extent of COC risk as well as the role of gene × hormone interactions in susceptibility.

Understanding the effects of neighborhood disadvantage on youth psychopathology.

BACKGROUND: In 1942, Shaw and McKay reported that disadvantaged neighborhoods predict youth psychopathology (Shaw & McKay, ). In the decades since, dozens of papers have confirmed and extended these early results, convincingly demonstrating that disadvantaged neighborhood contexts predict elevated rates of both internalizing and externalizing disorders across childhood and adolescence. It is unclear, however, how neighborhood disadvantage increases psychopathology. METHODS: Our study sought to fill this gap in the literature by examining the Area Deprivation Index (ADI), a composite measure of Census tract disadvantage, as an etiologic moderator of several common forms of psychopathology in two samples of school-aged twins from the Michigan State University Twin Registry (N = 4815 and 1030 twin pairs, respectively), the latter of which was enriched for neighborhood disadvantage. RESULTS: Across both samples, genetic influences on attention-deficit hyperactivity problems were accentuated in the presence of marked disadvantage, while nonshared environmental contributions to callous-unemotional traits increased with increasing disadvantage. However, neighborhood disadvantage had little moderating effect on the etiology of depression, anxiety, or somatic symptoms. CONCLUSIONS: Such findings suggest that, although neighborhood disadvantage does appear to serve as a general etiologic moderator of many (but not all) forms of psychopathology, this etiologic moderation is phenotype-specific.

Between- and within-person effects of stress on emotional eating in women: a longitudinal study over 49 days.

BACKGROUND: Stress is associated with binge eating and emotional eating (EE) cross-sectionally. However, few studies have examined stress longitudinally, limiting understanding of how within-person fluctuations in stress influence EE over time and whether stress is a risk factor or consequence of EE. Additionally, little is known regarding how the biological stress response relates to EE. METHODS: We used an intensive, longitudinal design to examine between-person and within-person effects of major life stress, daily stress, and cortisol on EE in a population-based sample of women (N = 477; ages 15-30; M = 21.8; s.d. = 3.0) from the Michigan State University Twin Registry. Participants reported past year major life stress, then provided daily ratings of EE and stress for 49 consecutive days. Hair cortisol concentration (HCC) was collected as a longitudinal biological stress measure. RESULTS: Women reported greater EE when they experienced greater mean stress across days (between-person effects) or greater stress relative to their own average on a given day (within-person effects). Daily stress was more strongly associated with EE than major life stress. However, the impact of daily stress on EE was amplified in women with greater past year major life stress. Finally, participants with lower HCC had increased EE. CONCLUSIONS: Findings confirm longitudinal associations between stress and EE in women, and highlight the importance of within-person shifts in stress in EE risk. Results also highlight HCC as a novel biological stress measure that is significantly associated with EE and may overcome limitations of prior physiological stress response indicators.

Determining menstrual cycle phase: An empirical examination of methodologies and recommendations for improvement in behavioral and brain sciences.

The recent decade has brought an exciting proliferation of behavioral, psychological and neuroscientific research involving the menstrual cycle. However, the reliability and validity of many popular methodologies for determining menstrual cycle phase lack empirical examination. These under-investigated methods include: (1) predicting menstrual cycle phase using self-report information only (e.g., "count" methods), (2) utilizing ovarian hormone ranges to determine menstrual cycle phase, and (3) using ovarian hormone changes from limited measurements (e.g., two time points) to determine menstrual cycle phase. In the current study, we examine the accuracy of these methods for menstrual cycle phase determination using 35-day within-person assessments of circulating ovarian hormones from 96 females across the menstrual cycle. Findings indicate that all three common methods are error-prone, resulting in phases being incorrectly determined for many participants, with Cohen's kappa estimates ranging from -0.13 to 0.53 indicating disagreement to only moderate agreement depending on the comparison. Such methodological challenges are surmountable through careful study design, more frequent hormone assays (when possible), and utilization of sophisticated statistical methods. With increased methodological rigor in behavioral, psychological and neuroscientific research, the field will be poised to detect biobehavioral correlates of ovarian hormone fluctuations for the betterment of the mental health and wellbeing of millions of females.

Binge Eating Risk During Midlife and the Menopausal Transition: Sensitivity to Ovarian Hormones as Potential Mechanisms of Risk.

PURPOSE OF REVIEW: Recent research suggests that binge eating may be more prevalent among women in midlife than previously believed. The menopausal transition, an important developmental stage during midlife, is characterized by substantial fluctuations and eventual decreases in ovarian hormones that may contribute to increased risk. This narrative review summarizes findings from studies of binge eating during midlife and menopause and discusses the potential role of ovarian hormones in binge eating risk. RECENT FINDINGS: Studies are few in number and findings are mixed, with only some studies showing increased binge eating during midlife and the menopausal transition. Sensitivity to ovarian hormones, potentially through gene x hormone interactions, may influence who experiences increased binge eating risk and could help explain mixed findings in the field. Future studies of hormone sensitivity and gene x hormone interactions are needed to further elucidate midlife and menopausal risk for binge eating in women.

Associations between household income and disordered eating differ across sex and racial identity in a population-based sample of adults.

BACKGROUND: Most research on socioeconomic status (SES) and eating disorders (EDs) has focused on young White women. Consequently, little is known regarding how SES may relate to EDs/disordered eating in older adults, men, or people with different racial identities. We examined whether associations between SES and EDs/disordered eating differed across age, sex, and racial identity in a large, population-based sample spanning early-to-later adulthood. METHODS: Analyses included 2797 women and 2781 men ages 18-65 (Mage = 37.41, SD = 7.38) from the population-based Michigan State University Twin Registry. We first examined associations between SES and dimensional ED symptoms, binge eating (BE), and self-reported ED diagnoses across age and sex in the full sample. We then examined the impact of racial identity on associations by conducting within- and between-group analyses among Black and White participants. RESULTS: In the full sample, lower SES was associated with significantly greater odds of BE and lifetime EDs in men, but not women, across adulthood. The association between lower SES and greater BE risk was stronger for Black men than for White men, though significant in both groups. Conversely, Black women showed a positive association between SES and dimensional ED symptoms that significantly differed from effects for Black men and White women. CONCLUSIONS: Associations between socioeconomic disadvantage and EDs/disordered eating may be particularly robust for men in adulthood, especially men with a marginalized racial identity. Oppositely, Black women may encounter social pressures and minority stress in higher SES environments that could contribute to somewhat heightened ED risk. PUBLIC SIGNIFICANCE: Little is known regarding how associations between socioeconomic status (SES) and eating disorders (EDs) may differ across age/sex or racial identity. We found lower SES was associated with greater odds of a lifetime ED or binge eating in men only, with a particularly strong association between lower SES and binge eating for Black men. Results highlight the importance of examining how SES-ED associations may differ across other aspects of identity.

A cotwin control study of associations between financial hardship and binge eating phenotypes during COVID-19.

BACKGROUND: COVID-19 was associated with significant financial hardship and increased binge eating (BE). However, it is largely unknown whether financial stressors contributed to BE during the pandemic. We used a longitudinal, cotwin control design that controls for genetic/environmental confounds by comparing twins in the same family to examine whether financial hardship during COVID-19 was associated with BE. METHODS: Female twins (N = 158; Mage  = 22.13) from the Michigan State University Twin Registry rated financial stressors (e.g., inability to afford necessities) daily for 49 consecutive days during COVID-19. We first examined whether financial hardship was associated with BE phenotypes across the full sample. We then examined whether cotwins who differed on financial hardship also differed in BE. RESULTS: Participants who experienced greater mean financial hardship across the study had significantly greater dimensional BE symptoms, and participants who experienced greater financial hardship on a given day reported significantly more emotional eating that day. These results were replicated in cotwin control analyses. Twins who experienced more financial hardship than their cotwin across the study reported greater dimensional BE symptoms than their cotwin, and participants who experienced more financial hardship than their cotwin on a given day reported greater emotional eating that day. Results were identical when restricting analyses to monozygotic twins, suggesting associations were not due to genetic confounds. CONCLUSIONS: Results suggest that BE-related symptoms may be elevated in women who experienced financial hardship during COVID-19 independent of potential genetic/environmental confounds. However, additional research in larger samples is needed. PUBLIC SIGNIFICANCE: Little is known regarding how financial difficulties during the COVID-19 pandemic may have contributed to increased binge eating (BE). We found preliminary evidence that financial hardship during COVID-19 may be associated with greater rates of BE-related symptoms even when comparing twins from the same family. While additional research is needed, results suggest that people who experienced financial hardship during COVID-19 may be at increased risk for BE.

Identifying the 'active ingredients' of socioeconomic disadvantage for youth outcomes in middle childhood.

BACKGROUND: Youth experiencing socioeconomic deprivation may be exposed to disadvantage in multiple contexts (e.g., neighborhood, family, and school). To date, however, we know little about the underlying structure of socioeconomic disadvantage, including whether the 'active ingredients' driving its robust effects are specific to one context (e.g., neighborhood) or whether the various contexts increment one another as predictors of youth outcomes. METHODS: The present study addressed this gap by examining the underlying structure of socioeconomic disadvantage across neighborhoods, families, and schools, as well as whether the various forms of disadvantage jointly predicted youth psychopathology and cognitive performance. Participants were 1,030 school-aged twin pairs from a subsample of the Michigan State University Twin Registry enriched for neighborhood disadvantage. RESULTS: Two correlated factors underlay the indicators of disadvantage. Proximal disadvantage comprised familial indicators, whereas contextual disadvantage represented deprivation in the broader school and neighborhood contexts. Results from exhaustive modeling analyses indicated that proximal and contextual disadvantage incremented one another as predictors of childhood externalizing problems, disordered eating, and reading difficulties, but not internalizing symptoms. CONCLUSIONS: Disadvantage within the family and disadvantage in the broader context, respectively, appear to represent distinct constructs with additive influence, carrying unique implications for multiple behavioral outcomes during middle childhood.

Parent Mental Health Before and During the COVID-19 Pandemic.

Although extant cross-sectional data suggest that parents have experienced numerous challenges (e.g., homeschooling, caregiver burden) and mental health consequences during the COVID-19 pandemic, longitudinal data are needed to confirm mental health changes relative to pre-pandemic levels and identify which specific pandemic-related changes most highly predict mental health during the pandemic. In two longitudinal subsamples (N = 299 and N = 175), we assessed change in anxiety, depression, and stress before and during the pandemic and whether the accumulation of pandemic-related changes predicted observed mental health changes. On average, parents reported increased depression and anxiety, but no significant changes in reported stress. Moreover, increased interpersonal conflict, difficulty managing work and caregiving responsibilities, and increased economic challenges were the types of pandemic-related changes that most strongly predicted worse mental health, highlighting that juggling caregiving responsibilities and economic concerns, along with the pandemic's impact on interpersonal family relationships are key predictors of worsening parental mental illness symptoms.

Risk for midlife psychosis in women: critical gaps and opportunities in exploring perimenopause and ovarian hormones as mechanisms of risk.

Women show a heightened risk for psychosis in midlife that is not observed in men. The menopausal transition (i.e. perimenopause) and accompanying changes in ovarian hormones are theorized to account for this midlife increase in risk. This narrative review aims to empirically examine these theories by reviewing studies of midlife and perimenopausal psychosis risk in women and potential ovarian hormone mechanisms of effects. Clinical and pre-clinical studies examining the effects of midlife age, menopausal stage, and ovarian hormones across adulthood on psychosis risk were identified. Synthesis of this body of work revealed that the peak ages of midlife psychosis risk in women overlap with the age range of key menopausal stages (especially the perimenopausal transition), although studies directly assessing menopausal stage are lacking. Studies examining ovarian hormone effects have almost exclusively focused on earlier developmental stages and events (e.g. pregnancy, the menstrual cycle) and show increases in psychotic symptoms in women and female rats during periods of lower estradiol levels. Estrogen treatment also tends to enhance the effects of neuroleptics in females across species at various reproductive phases. Initial data are promising in suggesting a role for menopausal stage and ovarian hormones in psychosis risk. However, critical gaps in our knowledge base remain, as there is a tendency to rely on indirect and proxy measures of menopausal status and hormones. Opportunities for future research are discussed with the goal of increasing research in this critical area of women's health.

Editorial: The critical need to assess pubertal development in studies of child and adolescent psychopathology.

Nearly all developmental studies of youth psychopathology assess the effects of age on risk factor-youth outcomes, yet very few examine the effects of pubertal development on developmental trajectories. Growing evidence underscores the importance of both stages of puberty (adrenarche and gonadarche) in risk for psychopathology and the need to consider these developmental stages as predictors and moderators of mental health outcomes and trajectories. The purpose of this Editorial is to provide examples of this evidence and highlight gaps in our literature base as well as opportunities for future research.

Parenting moderates the etiology of callous-unemotional traits in middle childhood.

BACKGROUND: Callous-unemotional (CU) traits are associated with chronic and escalating trajectories of antisocial behavior. Extant etiologic studies suggest that heritability estimates for CU traits vary substantially, while also pointing to an environmental association between parenting and CU traits. METHODS: We used twin modeling to estimate additive genetic (A), shared environmental (C), and nonshared environmental (E) influences on CU traits, measured with the Inventory of Callous-Unemotional Traits (ICU) and its subscales. Our sample included 600 twin pairs (age 6-11, 230 monozygotic) from neighborhoods with above-average levels of family poverty, a risk factor for antisocial behavior. We examined the extent to which correlations between parenting, measured via parent and child report on the Parental Environment Questionnaire, and CU traits reflected genetic versus environmental factors. Then, we tested whether parenting moderated the heritability of CU traits. RESULTS: In the context of lower-income neighborhoods, CU traits were moderately to highly heritable (A = 54%) with similar moderate-to-high nonshared environmental influences (E = 46%). Bivariate models revealed that associations between CU traits and warm parenting were genetic (rA = .22) and environmental (rE = .19) in origin, whereas associations between CU traits and harsh parenting were largely genetic in origin (rA = .70). The heritability of CU traits decreased with increasing parental warmth and decreasing harshness. CONCLUSIONS: Callous-unemotional traits are both genetic and environmental in origin during middle childhood, but genetic influences are moderated by parenting quality. Parenting may be an important target for interventions, particularly among youth with greater genetic risk.

Multivariate partial linear varying coefficients model for gene-environment interactions with multiple longitudinal traits.

Correlated phenotypes often share common genetic determinants. Thus, a multi-trait analysis can potentially increase association power and help in understanding pleiotropic effect. When multiple traits are jointly measured over time, the correlation information between multivariate longitudinal responses can help to gain power in association analysis, and the longitudinal traits can provide insights on the dynamic gene effect over time. In this work, we propose a multivariate partially linear varying coefficients model to identify genetic variants with their effects potentially modified by environmental factors. We derive a testing framework to jointly test the association of genetic factors and illustrated with a bivariate phenotypic trait, while taking the time varying genetic effects into account. We extend the quadratic inference functions to deal with the longitudinal correlations and used penalized splines for the approximation of nonparametric coefficient functions. Theoretical results such as consistency and asymptotic normality of the estimates are established. The performance of the testing procedure is evaluated through Monte Carlo simulation studies. The utility of the method is demonstrated with a real data set from the Twin Study of Hormones and Behavior across the menstrual cycle project, in which single nucleotide polymorphisms associated with emotional eating behavior are identified.

An investigation of associations between parenting and binge eating across pubertal development in pre-adolescent and adolescent female participants.

OBJECTIVE: Puberty is a period of increased risk for the development of binge eating in female adolescents. Although developmental changes in autonomy-seeking behaviors and body weight and shape may influence both parenting styles and binge eating during puberty, studies have yet to examine how parenting practices may be differentially associated with youth outcomes depending on developmental stage. The current study examines whether interactions between puberty and parenting are associated with higher levels of binge-eating symptoms during/after puberty in female youth. METHODS: Analyses used cross-sectional data from a previous study of disordered eating and puberty in 999 female youth (ages 8-16) and their parents from the Michigan State University Twin Registry. Youth self-reported binge eating, pubertal development, and perceived parental care and overprotection. Both parents and youth reported on parent-child conflict. Mixed linear models were used to examine whether pubertal development moderates the strength of associations between parenting (parent-child conflict, parental care, and parental overprotection) and offspring binge eating. RESULTS: Although higher levels of parental overprotection and conflict, and lower levels of parental care were all significantly associated with binge eating, none of the associations were significantly moderated by pubertal development or age. DISCUSSION: The quality of the parent-child relationship is significantly associated with binge eating in female youth regardless of developmental stage, highlighting the need for targeting harmful parenting strategies during adolescent eating disorder intervention. PUBLIC SIGNIFICANCE: This is the first study to examine whether parenting/binge-eating associations in female participants differ across pubertal development. In a large population-based sample, we found lower parental care, higher parent-child conflict, and higher parental overprotection were all associated with higher levels of binge eating. Notably, associations did not differ across pubertal stage or age, suggesting that parenting is significantly associated with binge eating, regardless of developmental stage.

A daily diary study of emotion regulation as a moderator of negative affect-binge eating associations.

BACKGROUND: While negative affect (NA) typically increases risk for binge eating, the ultimate impact of NA may depend on a person's ability to regulate their emotions. In this daily, longitudinal study, we examined whether emotion regulation (ER) modified the strength of NA-dysregulated eating associations. METHODS: Women (N = 311) from the Michigan State University Twin Registry first reported dimensional binge eating symptoms and broad ER difficulties (e.g., limited emotional awareness, difficulty controlling emotional impulses). Participants then rated use of adaptive (cognitive reappraisal, social sharing, situation modification, and acceptance) and maladaptive (rumination, expressive suppression, and self-criticism) ER strategies, emotional eating (EE), objective binge eating (OBE), and NA once daily for 49 consecutive days. RESULTS: There were several main effects of ER on binge-eating pathology in both between-person (i.e., comparing women who differed on average) and within-person (i.e., examining fluctuations in variables day-to-day) analyses. Between-person, greater broad ER difficulties, greater maladaptive strategy use, and lower adaptive strategy use were all associated with greater binge-eating pathology. Within-person, greater maladaptive strategy use was associated with greater odds of OBE on that day and on the following day. However, neither broad ER difficulties nor use of specific strategies moderated associations between NA and dysregulated eating in between- or within-person analyses. CONCLUSIONS: While ER is independently associated with risk for dysregulated eating, it may not fully mitigate the impact of NA. Additional strategies (e.g., decreasing environmental stressors and increasing social support) may be needed to minimize NA and its impact on dysregulated eating. PUBLIC SIGNIFICANCE: Negative affect (NA; e.g., sadness, guilt) increases dysregulated eating risk. Because NA is sometimes unavoidable, we examined whether emotion regulation (ER; i.e., how a person responds to their emotions) might impact whether NA leads to dysregulated eating. Although more effective ER was associated with less dysregulated eating overall, ER did not impact the association between NA and dysregulated eating. Other approaches may therefore be needed to mitigate NA-dysregulated eating associations.

The role of parenting in the intergenerational transmission of executive functioning: A genetically informed approach.

Deficits in executive functioning both run in families and serve as a transdiagnostic risk factor for psychopathology. The present study employed twin modeling to examine parenting as an environmental pathway underlying the intergenerational transmission of executive functioning in an at-risk community sample of children and adolescents (N = 354 pairs, 167 monozygotic). Using structural equation modeling of multi-informant reports of parenting and a multi-method measure of child executive functioning, we found that better parent executive functioning related to less harsh, warmer parenting, which in turn related to better child executive functioning. Second, we assessed the etiology of executive functioning via the nuclear twin family model, finding large non-shared environmental effects (E = .69) and low-to-moderate heritability (A = .22). We did not find evidence of shared environmental effects or passive genotype-environment correlation. Third, a bivariate twin model revealed significant shared environmental overlap between both warm and harsh parenting and child executive functioning (which may indicate either passive genotype-environment correlation or environmental mediation), and non-shared environmental overlap between only harsh parenting and child executive functioning (indicating an effect of harsh parenting separable from genetic confounds). In summary, genetics contribute to the intergenerational transmission of executive functioning, with environmental mechanisms, including harsh parenting, also making unique contributions.