Michigan State University Twin Registry Research Articles

Child effects on positive parenting vary with neighborhood opportunity.

Prior theoretical and empirical research has highlighted links between positive parenting and the socioeconomic characteristics of the family's neighborhood, but has yet to illuminate the etiologic origins of this association. One possibility is that the various predictors of parenting outlined by Belsky (1984; e.g., characteristics of the child, characteristics of the parent, and contextual influences) may matter more in some neighborhood contexts than in others. To examine this possibility, we conducted etiologic moderation analyses in a sample of 1,030 families of twins (average age 8 years; 51% male, 49% female; racial composition: 82% White, 10% Black, 1% Asian, 1% Indigenous, and 6% multiracial) from the Twin Study of Behavioral and Emotional Development in Children in the Michigan State University Twin Registry. Neighborhood and parenting were assessed using multiple informants and assessment strategies (neighborhood and family informants, administrative data, and videotaped parent-child interactions). Results pointed to strong evidence of etiologic moderation, such that child effects on positive mothering were prominent in neighborhoods with little opportunity and near zero in neighborhoods with ample opportunity. Such findings not only reframe the magnitude of child effects on the parenting they receive as context-dependent, but also indicate that mothers in impoverished neighborhoods may be more responsive to their children's characteristics than mothers in neighborhoods with ample opportunity. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Comorbidity Between Internalizing Symptoms and Disordered Eating Is Primarily Driven by Genetic Influences on Emotion Regulation in Adult Female Twins

Internalizing (e.g., anxiety, depression) and disordered eating (DE; e.g., binge eating, dietary restraint) are highly comorbid, but the mechanisms underlying their comorbidity remain unknown. This was the first twin study to examine whether their co-occurrence may be driven by genetic and/or environmental influences on emotion regulation (ER; ability to modulate duration/intensity of emotions). Analyses included 688 adult female twins from the Michigan State University Twin Registry. Cholesky decomposition twin models showed that comorbidity between dimensionally modeled internalizing and DE was due to overlapping genetic ( r = .55; 69.3% of shared variance) and nonshared environmental influences ( r = .26; 30.7% of shared variance). When ER was added into the model, all genetic influences shared between internalizing and DE were attributable to ER, suggesting genetic influences on ER are the primary driver of comorbidity between internalizing and DE. Shared genes may shape affective processing, interoceptive sensitivity, or other brain-based processes (e.g., cognitive control) implicated in ER.

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

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. 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. 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. 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. 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.

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

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. 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. Twins with gastrointestinal disease had significantly greater dimensional ED symptoms (β = 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. 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.

Bayesian linear mixed model with multiple random effects for family-based genetic studies

Motivation: Family-based study design is one of the popular designs used in genetic research, and the whole-genome sequencing data obtained from family-based studies offer many unique features for risk prediction studies. They can not only provide a more comprehensive view of many complex diseases, but also utilize information in the design to further improve the prediction accuracy. While promising, existing analytical methods often ignore the information embedded in the study design and overlook the predictive effects of rare variants, leading to a prediction model with sub-optimal performance.Results: We proposed a Bayesian linear mixed model for the prediction analysis of sequencing data obtained from family-based studies. Our method can not only capture predictive effects from both common and rare variants, but also easily accommodate various disease model assumptions. It uses information embedded in the study design to form surrogates, where the predictive effects from unmeasured/unknown genetic and environmental risk factors can be modelled. Through extensive simulation studies and the analysis of sequencing data obtained from the Michigan State University Twin Registry study, we have demonstrated that the proposed method outperforms commonly adopted techniques.Availability: R package is available at https://github.com/yhai943/FBLMM.

Estrogen moderation of genetic influences on eating disorder symptoms during gonadarche in girls: Specific effects on binge eating

The heritability of eating disorder (ED) symptoms increases dramatically across gonadarche in girls. Past studies suggest these developmental differences could be due to pubertal activation of estrogen, but findings have been limited to only one ED symptom (i.e., binge eating). The current study examined whether estrogen contributes to gonadarcheal differences in genetic influences on overall levels of ED symptoms as well as key cognitive symptoms (i.e., weight/shape concerns) that are present across all EDs and are early risk factors for eating pathology. Given that binge eating frequently co-occurs with all of these symptoms, analyses also examined whether estrogen effects exist for overall levels of ED symptoms and body weight/shape concerns after accounting for the known effects of estrogen on genetic risk for binge eating. Participants included 964 female twins (ages 8–16) from the Michigan State University Twin Registry. Overall levels of ED symptoms were assessed with the Minnesota Eating Behavior Survey (MEBS) total score. Weight/shape concerns were assessed with a latent factor modeled using subscales from the MEBS and the Eating Disorder Examination Questionnaire. Estradiol levels were assessed with saliva samples. Twin moderation models were used to examine whether genetic influences on overall levels of ED symptoms and weight/shape concerns differed significantly across estradiol levels. Although initial models suggested modest differences in genetic influences on overall levels of ED symptoms across estradiol levels, these effects were eliminated when binge eating was accounted for in the models. In addition, weight/shape concerns did not show significant moderation of genetic influences by estradiol in models with or without binge eating. Taken together, results are significant in suggesting that individual differences in estradiol levels during gonadarche have a unique and specific impact on genetic risk for binge eating, while other etiologic factors must contribute to increased heritability of cognitive ED symptoms during this key developmental period in girls.

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

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. 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. 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. 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. 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.

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

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. 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. 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. 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.

Disadvantage and disordered eating in boys: Examining phenotypic and genotype × environment associations across development.

Socioeconomic disadvantage may be a significant risk factor for disordered eating, particularly for individuals with underlying genetic risk. However, little to nothing is known about the impact of disadvantage on disordered eating in boys during the critical developmental risk period. Crucially, risk models developed for girls may not necessarily apply to boys, as boys show different developmental patterns of disordered eating risk (i.e., earlier activation of genetic influences during adrenarche, an early stage of puberty). This is the first study to examine phenotypic and Genotype × Environment (G × E) effects of disadvantage in boys. Analyses examined 3,484 male twins ages 8-17 (Mage = 12.27, SD = 2.96) from the Michigan State University Twin Registry. Disordered eating (e.g., body dissatisfaction, binge eating) was measured using the parent-report Michigan Twins Project Eating Disorder Survey. Neighborhood disadvantage was measured using a census-tract level Area Deprivation Index, and family socioeconomic status was determined from parental income and education. Adrenarche status was determined using multiple indicators, including age and Pubertal Development Scale scores. G × E models suggested that genetic influences on disordered eating were activated earlier for boys experiencing familial or neighborhood disadvantage, with substantial genetic influences in early adrenarche, when genetic influences were low in more advantaged boys. Phenotypically, both neighborhood and familial disadvantage were associated with greater disordered eating for boys in late adrenarche, which could indicate a lasting impact of earlier activation of genetic influences on later risk. Results highlight disadvantage as a novel risk factor for disordered eating in boys, particularly those with genetic vulnerabilities. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

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

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. 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. 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. 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. 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.

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

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. 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. 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. 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. 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.

The effects of the COVID-19 pandemic on disordered eating symptoms in women: A 49-day, daily study before and during the outbreak in the United States.

Longitudinal data are needed to examine effects of the COVID-19 pandemic on disordered eating. We capitalized on an ongoing, longitudinal study collecting daily data to examine changes in disordered eating symptoms in women across 49 days that spanned the time before and during the COVID-19 outbreak in the United States. Women from the Michigan State University Twin Registry (N = 402) completed daily questionnaires assessing a range of symptoms (e.g., binge eating, weight/shape concerns, liking/wanting of palatable food (PF) and whole foods, hunger). Dates of the first US COVID-19 case, first case in each participant's state, and onset of the initial stay-at-home orders (SHOs) were used to categorize women into those who completed all daily assessments prior to, during, or after these dates. We used mixed linear models and specification-curve analysis to examine between-person (i.e., differences between women assessed before vs during/after COVID-19) and within-person (i.e., changes in symptoms from days before to days after the dates) effects of the pandemic. Results showed significantly higher levels of binge-related pathology (e.g., odds of binge eating, liking/wanting of PF) in women who completed assessments during/after COVID-19 events, and significantly increased liking/wanting of PF in the days following the pandemic onset. By contrast, minimal between- or within-person differences were observed for other variables, including weight/shape concerns, compensatory behaviors, hunger, or liking/wanting whole foods. Overall, results suggest a specific effect of the pandemic on binge-related phenotypes in women. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Exploring the possibility of parents' broad internalizing phenotype acting through passive gene-environment correlations on daughters' disordered eating.

Twin studies demonstrate significant environmental influences and a lack of genetic effects on disordered eating before puberty in girls. However, genetic factors could act indirectly through passive gene-environment correlations (rGE; correlations between parents' genes and an environment shaped by those genes) that inflate environmental (but not genetic) estimates. The only study to explore passive rGE did not find significant effects, but the full range of parental phenotypes (e.g., internalizing symptoms) that could impact daughters' disordered eating was not examined. We addressed this gap by exploring whether parents' internalizing symptoms (e.g., anxiety, depressive symptoms) contribute to daughters' eating pathology through passive rGE. Participants were female twin pairs (aged 8-14 years; M = 10.44) in pre-early puberty and their biological parents (n = 279 families) from the Michigan State University Twin Registry. Nuclear twin family models explored passive rGE for parents' internalizing traits/symptoms and twins' overall eating disorder symptoms. No evidence for passive rGE was found. Instead, environmental factors that create similarities between co-twins (but not with their parents) and unique environmental factors were important. In pre-early puberty, genetic factors do not influence daughters' disordered eating, even indirectly through passive rGE. Future research should explore sibling-specific and unique environmental factors during this critical developmental period.

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

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. 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. 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. 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.

Pubertal Emergence of Testosterone Effects on Depressive Symptoms in Boys.

Puberty-driven increases in the secretion of testosterone may be a biological factor that protects males against the development of depression. Although all males produce testosterone, there are substantial between-person differences that could contribute to differential vulnerability to depression among pre-adolescent and adolescent boys, particularly after pubertal onset. Indeed, experimental animal and human data have shown that low testosterone increases risk for depressive-like symptoms in males, whereas higher levels of testosterone may be protective; however, prior studies have primarily investigated these effects in adulthood. This study investigated whether lower circulating levels of testosterone predict depressive symptoms in pre-adolescent and adolescent boys, and in particular, whether the testosterone-depression association becomes prominent with advancing pubertal maturation. Male twins (N = 213; ages 10-15 years) from the Michigan State University Twin Registry self-reported their depressive symptoms and pubertal status using the Children's Depression Inventory and the Pubertal Development Scale, respectively. Salivary testosterone was assayed using high-sensitivity enzyme immunoassays. Mixed Linear Models (MLMs), which could account for the non-independence of twin data, were used for analyses. As expected, lower testosterone concentrations were associated with higher depressive symptoms, and the magnitude of this effect increased with advancing pubertal status. In contrast, boys with higher levels of testosterone showed low levels of depressive symptomatology at all stages of pubertal maturation. Overall, these findings enhance understanding of within-sex variability in risk for depression in boys - average-to-high testosterone levels may underlie the general male resilience to depression after pubertal onset, whereas lower levels may increase vulnerability during/after puberty.

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

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. 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. 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. 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. 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.

Understanding the effects of neighborhood disadvantage on youth psychopathology.

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. 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. 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. 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.

Context matters: Neighborhood disadvantage is associated with increased disordered eating and earlier activation of genetic influences in girls.

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 (β = .07). Moreover, Genotype × 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. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

The effects of puberty on associations between mood/personality factors and disordered eating symptoms in girls.

Negative and positive urgency, anxiety, and depressive symptoms are significant factors of disordered eating (DE) symptoms in early adolescence through young adulthood. However, it is unclear how puberty-a critical developmental milestone that is associated with increased risk for DE symptoms-affects the relationship between these factors and DE symptoms, given that the role of pubertal status has rarely been considered in relation to these associations. Thus, the present study examined whether puberty moderates associations between mood/personality factors and DE in pre-adolescent and adolescent girls. Participants included 981 girls (aged 8-16 years) from the Michigan State University Twin Registry. Mood/personality factors, pubertal status, and DE were assessed with self-report questionnaires. Puberty significantly moderated associations between several factors (negative urgency, positive urgency, trait anxiety, depressive symptoms) and the cognitive symptoms of DE (e.g., shape/weight concerns, body dissatisfaction). Associations between mood/personality factors and cognitive DE were stronger in girls with more advanced pubertal status. By contrast, no significant moderation effects were detected for mood/personality-dysregulated eating (e.g., binge eating, emotional eating) associations. Findings identify pubertal development as an important moderator of mood/personality-DE symptom associations, especially for cognitive DE symptoms that are known to predict the later onset of clinical pathology.

Continuity and Change in the Genetic and Environmental Etiology of Youth Antisocial Behavior.

Trajectories of youth antisocial behavior (ASB) are characterized by both continuity and change. Twin studies have further indicated that genetic factors underlie continuity, while environmental exposures unique to each child in a given family underlie change. However, most behavioral genetic studies have examined continuity and change during relatively brief windows of development (e.g., during childhood but not into adolescence). It is unclear whether these findings would persist when ASB trajectories are examined across multiple stages of early development (i.e., from early childhood into emerging adulthood). Our study sought to fill this gap by examining participants assessed up to five times between the ages of 3 and 22years using an accelerated longitudinal design in the Michigan State University Twin Registry (MSUTR). We specifically examined the etiologies of stability and change via growth curve modeling and a series of univariate and bivariate twin analyses. While participants exhibited moderate-to-high rank-order stability, mean levels of ASB decreased linearly with age. Genetic and nonshared environmental influences that were present in early childhood also contributed to both stability and change across development, while shared environmental contributions were negligible. In addition, genetic and nonshared environmental influences that were not yet present at the initial assessment contributed to change over time. Although ASB tended to decrease in frequency with age, participants who engaged in high levels of ASB during childhood generally continued to do so throughout development. Moreover, the genetic and nonshared environmental contributions to ASB early in development also shaped the magnitude of the decrease with age.