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Background Past studies indicate daily increases in estrogen across the menstrual cycle protect against binge-eating (BE) phenotypes (e.g. emotional eating), whereas increases in progesterone enhance risk. Two previous studies from our laboratory suggest these associations could be due to differential genomic effects of estrogen and progesterone. However, these prior studies were unable to directly model effects of daily changes in hormones on etiologic risk, instead relying on menstrual cycle phase or mean hormone levels. The current study used newly modified twin models to examine, for the first time, the effects of daily changes in estradiol and progesterone on genetic/environmental influences on emotional eating in our archival twin sample assessed across 45 consecutive days. Methods Participants included 468 female twins from the Michigan State University Twin Registry. Daily emotional eating was assessed with the Dutch Eating Behavior Questionnaire, and daily saliva samples were assayed for ovarian hormone levels. Modified genotype × environment interaction models examined daily changes in genetic/environmental effects across hormone levels. Results Findings revealed differential effects of daily changes in hormones on etiologic risk, with increasing genetic influences across progesterone levels, and increasing shared environmental influences at the highest estradiol levels. Results were consistent across primary analyses examining all study days and sensitivity analyses within menstrual cycle phases. Conclusions Findings are significant in being the first to identify changes in etiologic risk for BE symptoms across daily hormone levels and highlighting novel mechanisms (e.g. hormone threshold effects, regulation of conserved genes) that may contribute to the etiology of BE. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

One long-standing analytic approach in adoption studies is to examine correlations between features of adoptive homes and outcomes of adopted children (hereafter termed 'measured environment correlations') to illuminate environmental influences on those associations. Although results from such studies have almost uniformly suggested modest environmental influences on adopted children's academic achievement, other work has indicated that adopted children's achievement is routinely higher than that of their reared-apart family members, often substantially so. We sought to understand this discrepancy. We examined academic achievement and literacy-promotive features of the home in 424 yoked adoptive/biological families participating in the Early Growth and Development Study (EGDS; i.e., adopted children, adoptive mothers, birth mothers, and biological siblings of the adopted children remaining in the birth homes) using an exhaustive modeling approach. Results indicated that, as anticipated, adopted children scored up to a full standard deviation higher on standardized achievement tests relative to their birth mothers and reared-apart biological siblings. Moreover, these achievement differences were associated with differences in the literacy-promotive features of the adoptive and birth family homes, despite minimal measured environment correlations within adoptive families. A subsequent simulation study highlighted noise in measured environmental variables as an explanation for the decreased utility of measured environment correlations. We conclude that the field's heavy focus on measured environment correlations within adoptive families may have obscured detection of specific environmental effects on youth outcomes, and that future adoption studies should supplement their measured environment analyses with mean differences between reared-apart relatives. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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 (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. 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. [ABSTRACT FROM AUTHOR]

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. Highlights: Transgender and gender non‐conforming (TGNC) youth endorsed significantly higher levels of eating disorder (ED) cognitions and behaviours compared to the cisgender samples, but lower levels than youth with EDs.TGNC youth were more likely to report objective binge episodes (OBEs) than the cisgender male and female groups, although their likelihood was lower than that of youth with EDs.A significant proportion of TGNC participants scored in elevated ranges on the Eating Disorder Examination Questionnaire (EDE‐Q) Global score, significantly higher than the cisgender male and female groups, which emphasises the need for screening and addressing ED symptoms in TGNC youth. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

A growing literature links socioeconomic disadvantage and adversity to brain function, including disruptions in reward processing. Less research has examined exposure to community violence (ECV) as a specific adversity related to differences in reward-related brain activation, despite the prevalence of community violence exposure for those living in disadvantaged contexts. The current study tested whether ECV was associated with reward-related ventral striatum (VS) activation after accounting for familial factors associated with differences in reward-related activation (e.g. parenting and family income). Moreover, we tested whether ECV is a mechanism linking socioeconomic disadvantage to reward-related activation in the VS. We utilized data from 444 adolescent twins sampled from birth records and residing in neighborhoods with above-average levels of poverty. ECV was associated with greater reward-related VS activation, and the association remained after accounting for family-level markers of disadvantage. We identified an indirect pathway in which socioeconomic disadvantage predicted greater reward-related activation via greater ECV, over and above family-level adversity. These findings highlight the unique impact of community violence exposure on reward processing and provide a mechanism through which socioeconomic disadvantage may shape brain function. [ABSTRACT FROM AUTHOR]

Despite early‐life disadvantage (ELD) in humans being a highly heterogenous construct, it consistently predicts negative neurobehavioral outcomes. The numerous environmental contributors and neural mechanisms underlying ELD remain unclear, though. We used a laboratory rat model to evaluate the effects of limited resources and/or heavy metal exposure on mothers and their adult male and female offspring. Dams and litters were chronically exposed to restricted (1‐cm deep) or ample (4‐cm deep) home cage bedding postpartum, with or without lead acetate (0.1%) in their drinking water from insemination through 1‐week postweaning. Restricted‐bedding mothers showed more pup‐directed behaviors and behavioral fragmentation, while lead‐exposed mothers showed more nestbuilding. Restricted bedding‐raised male offspring showed higher anxiety and aggression. Either restricted bedding or lead exposure impaired goal‐directed performance in a reinforcer devaluation task in females, whereas restricted bedding alone disrupted it in males. Lead exposure, but not limited bedding, also reduced sucrose reward sensitivity in a progressive ratio task in females. D1 and D2 receptor mRNA in the medial prefrontal cortex and nucleus accumbens (NAc) were each affected by the early‐life treatments and differently between the sexes. Most notably, adult males (but not females) exposed to both early‐life treatments had greatly increased D1 receptor mRNA in the NAc core. These results illuminate neural mechanisms through which ELD threatens neurobehavioral development and highlight forebrain dopamine as a factor. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Background: In 1942, Shaw and McKay reported that disadvantaged neighborhoods predict youth psychopathology (Shaw & McKay, 1942). 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. [ABSTRACT FROM AUTHOR]

Objective: Our goal was to illuminate associations between specific characteristics of under‐resourced neighborhoods (i.e., socioeconomic deprivation, danger) and specific aspects of parenting (e.g., parental praise, parental nurturance, harsh parenting, and parental control). Background: Prior work has highlighted associations between level of neighborhood disadvantage and the parenting of its residents. However, this work has yet to clarify the specific characteristics of the neighborhood or the types of parenting involved. Method: Exhaustive modeling analyses were conducted in a sample of 1030 families of twins (average age 8 years; 51% male, 49% female; the racial composition was 82% White, 10% Black, 1% Asian, 1% Indigenous, 6% multiracial) from the Twin Study of Behavioral and Emotional Development in Children. Neighborhood and parenting were assessed using multiple informants and assessment strategies (neighborhood informants, family informants, administrative data, and videotaped parent–child interactions). Results: Neighborhood socioeconomic deprivation (i.e., limited institutional and economic structural resources) demonstrated small but consistent negative associations with positive parenting behaviors and maternal control, but not with negative parenting behaviors. Neighborhood danger (i.e., recorded crime, fear of crime, exposure to community violence), by contrast, demonstrated weaker associations with parenting that dissipated once we controlled for overlap with socioeconomic deprivation. Conclusion: Danger and socioeconomic deprivation do not function as interchangeable characteristics of under‐resourced neighborhoods, at least in terms of their association with positive parenting. Future studies should identify the specific mechanisms through which neighborhood socioeconomic deprivation is associated with less nurturing parenting. [ABSTRACT FROM AUTHOR]

Background: Psychopathic traits involve interpersonal manipulation, callous affect, erratic lifestyle, and antisocial behavior. Though adult psychopathic traits emerge from both genetic and environmental risk, no studies have examined etiologic associations between adult psychopathic traits and experiences of parenting in childhood, or the extent to which parenting practices may impact the heritability of adult psychopathic traits using a genetically-informed design. Methods: In total, 1842 adult twins from the community reported their current psychopathic traits and experiences of negative parenting during childhood. We fit bivariate genetic models to the data, decomposing the variance within, and the covariance between, psychopathic traits and perceived negative parenting into their genetic and environmental components. We then fit a genotype × environment interaction model to evaluate whether negative parenting moderated the etiology of psychopathic traits. Results: Psychopathic traits were moderately heritable with substantial non-shared environmental influences. There were significant associations between perceived negative parenting and three of four psychopathy facets (interpersonal manipulation, erratic lifestyle, antisocial tendencies, but not callous affect). These associations were attributable to a common non-shared environmental pathway and not to overlapping genetic effects. Additionally, we found that primarily shared environmental influences were stronger on psychopathic traits for individuals with a history of greater negative parenting. Conclusions: Utilizing a genetically-informed design, we found that both genetic and non-shared environmental factors contribute to the emergence of psychopathic traits. Moreover, perceptions of negative parenting emerged as a clear environmental influence on the development of interpersonal, lifestyle, and antisocial features of psychopathy. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Although it is well known that parental depression is transmitted within families across generations, the etiology of this transmission remains unclear. Our goal was to develop a novel study design capable of explicitly examining the etiologic sources of intergenerational transmission. We specifically leveraged naturally-occurring variations in genetic relatedness between parents and their adolescent children in the 720 families participating in the Nonshared Environment in Adolescent Development (NEAD) study, 58.5% of which included a rearing stepparent (nearly always a stepfather). Results pointed squarely to the environmental transmission of psychopathology between fathers and children. Paternal depression was associated with adolescent depression and adolescent behavior problems (i.e., antisocial behavior, headstrong behavior, and attention problems) regardless of whether or not fathers and their children were genetically related. Moreover, these associations persisted to a subset of "blended" families in which the father was biologically related to one participating child but not to the other, and appeared to be mediated via father–child conflict. Such findings are not only fully consistent with the environmental transmission of psychopathology across generations, but also add to extant evidence that parent–child conflict is a robust and at least partially environmental predictor of adolescent psychopathology. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Background: The specific 'active ingredients' through which neighborhood disadvantage increases risk for child psychopathology remains unclear, in large part because research to date has nearly always focused on poverty to the exclusion of other neighborhood domains. The objective of this study was to evaluate whether currently assessed neighborhood built, social, or toxicant conditions were associated with child externalizing psychopathology outcomes separately, and in a combined model, using data from the Detroit-metro county area.Methods: We conducted principal components analyses for built, social, or toxicant conditions. Next, we fitted separate multiple regression models for each of the child externalizing psychopathology measures (oppositional defiant and conduct problems) as a function of built, social, or toxicant components.Results: We found that built features (more non-profits, churches, and alcohol outlets, and less agriculture and vacant properties) were associated with conduct problems, while toxicant conditions (high percent industrial, toxins released and number of pre-1978 structures) were associated with oppositional defiance problems. There was no significant association between greenspace or social conditions and child externalizing outcomes. When examined simultaneously, only the significant independent association between built conditions and conduct problems remained.Conclusions: Built, social, and toxicant neighborhood conditions are not interchangeable aspects of a given neighborhood. What's more, built features are uniquely associated with child externalizing outcomes independently of other neighborhood characteristics. Future research should consider how changes in the built conditions of the neighborhood (e.g., development, decay) serve to shape child externalizing behaviors, with a focus on identifying potentially actionable elements. [ABSTRACT FROM AUTHOR]

Adolescence is a period of increased risk-taking behavior, thought to be driven, in part, by heightened reward sensitivity. One challenge of studying reward processing in the field of developmental neuroscience is finding a task that activates reward circuitry, and is short, not too complex, and engaging for youth of a wide variety of ages and socioeconomic backgrounds. In the present study, we tested a brief child-friendly reward task for activating reward circuitry in two independent samples of youth ages 7–19 years old enriched for poverty (study 1: n = 464; study 2: n = 27). The reward task robustly activated the ventral striatum, with activation decreasing from early to mid-adolescence and increasing from mid- to late adolescence in response to reward. This response did not vary by gender, pubertal development, or income-to-needs ratio, making the task applicable for a wide variety of populations. Additionally, ventral striatum activation to the task did not differ between youth who did and did not expect to receive a prize at the end of the task, indicating that an outcome of points alone may be enough to engage reward circuitry. Thus, this reward task is effective for studying reward processing in youth from different socioeconomic backgrounds. [ABSTRACT FROM AUTHOR]

Conventional longitudinal behavioral genetic models estimate the relative contribution of genetic and environmental factors to stability and change of traits and behaviors. Longitudinal models rarely explain the processes that generate observed differences between genetically and socially related individuals. We propose that exchanges between individuals and their environments (i.e., phenotype–environment effects) can explain the emergence of observed differences over time. Phenotype–environment models, however, would require violation of the independence assumption of standard behavioral genetic models; that is, uncorrelated genetic and environmental factors. We review how specification of phenotype–environment effects contributes to understanding observed changes in genetic variability over time and longitudinal correlations among nonshared environmental factors. We then provide an example using 30 days of positive and negative affect scores from an all-female sample of twins. Results demonstrate that the phenotype–environment effects explain how heritability estimates fluctuate as well as how nonshared environmental factors persist over time. We discuss possible mechanisms underlying change in gene–environment correlation over time, the advantages and challenges of including gene–environment correlation in longitudinal twin models, and recommendations for future research. [ABSTRACT FROM AUTHOR]

Callous-unemotional (CU) traits (i.e., callousness, low empathy, shallow affect) have been conceptualized as a downward extension of the interpersonal and affective components of adult psychopathy and are associated with stable and severe antisocial behavior. Research suggests that CU traits are moderately heritable, but also influenced by environmental factors, particularly parenting. We examined associations among mother and father psychopathic traits, parenting practices, and offspring CU traits in a community sample of 550 adolescent twins (Mean age = 13.99 years; SD 2.37; 56.4% male), incorporating multiple informants (mothers, fathers, child). Parental interpersonal-affective psychopathic traits were associated with adolescent CU traits and negative parenting (increased harshness, reduced warmth). Moreover, increased parental harshness and reduced warmth partially explained associations between parental interpersonal-affective traits and adolescent CU traits. There was also a significant direct effect specifically between mother interpersonal-affective traits and adolescent CU traits. Finally, using a twin difference design, we confirmed that adolescent CU traits were significantly impacted by non-shared environmental parenting influences (increased harshness, reduced warmth). These results suggest that mother and father interpersonal-affective traits appear to impact parenting practices and serve as risk factors for adolescent CU traits. However, many of the findings did not replicate when using cross-informant reports and were only present within single informant models, highlighting a role for shared informant variance as well. The results suggest the importance of accounting for parent personality in the development of effective parenting interventions for CU traits. [ABSTRACT FROM AUTHOR]

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 22 years 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. [ABSTRACT FROM AUTHOR]

Objective: 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. Method: 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. Results: 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. Discussion: 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. [ABSTRACT FROM AUTHOR]

The present report describes the motivation for the Michigan Twin Neurogenetic Study (MTwiNS), which seeks to illuminate the underlying biological mechanisms through which familial and community factors support resilience (i.e., adaptive competence in the face of adversity) in youth exposed to neighborhood disadvantage. To accomplish these goals, we must first understand how resilience manifests in this cohort. The current study uncovers evidence of three domains of youth resilience: psychiatric health, social engagement, and scholastic success. Although all three domains were relatively stable across a one-to-two year period, some change was observed. Additionally, although resilience in one domain was quite common, resilience across all three domains was less common. Finally, we show substantial variability in resilience within and across families, with large co-twin discordances that can be leveraged in future analyses that examine promotive contexts that are environmental in origin. [ABSTRACT FROM AUTHOR]

Many behavior genetics models follow the same general structure. We describe this general structure and analytically derive simple criteria for its identification. In particular, we find that variance components can be uniquely estimated whenever the relatedness matrices that define the components are linearly independent (i.e., not confounded). Thus, we emphasize determining which variance components can be identified given a set of genetic and environmental relationships, rather than the estimation procedures. We validate the identification criteria with several well-known models, and further apply them to several less common models. The first model distinguishes child-rearing environment from extended family environment. The second model adds a gene-by-common-environment interaction term in sets of twins reared apart and together. The third model separates measured-genomic relatedness from the scanner site variation in a hypothetical functional magnetic resonance imaging study. The computationally easy analytic identification criteria allow researchers to quickly address model identification issues and define novel variance components, facilitating the development of new research questions. [ABSTRACT FROM AUTHOR]

Background: Knowing the extent to which genetic and environmental factors influence percent body fatness (%Fat) and physical activity (PA) would be beneficial, since both are tightly correlated with future health outcomes. Thus, the purpose was to evaluate sex differences in genetic and environmental influences on %Fat and physical activity behavior in male and female adolescent twins. Methods: Subjects were adolescent (age range 8.3 to 16.6 yr) twins. %Fat (n = 518 twins) was assessed by bioelectrical impedance analysis (BIA) and PA (n = 296 twins) was measured using 3-Day PA Recall. Each activity was converted to total MET-minutes. Univariate twin models were used to examine sex differences in genetic and environmental factors influencing %Fat and PA. Results: %Fat was influenced by genetic effects in both boys and girls (88% and 90%, respectively), with slightly higher heritability estimates for girls. PA was influenced solely by environmental effects for both sexes with higher shared environmental influences in boys (66%) and higher nonshared effects in girls (67%). Conclusions: When developing interventions to increase PA in adolescents, it is important to consider the environment in which it takes place as it is the primary contributor to PA levels. [ABSTRACT FROM AUTHOR]

Cyberaggression (CA), or the use of information communication technologies to inflict harm on others, is an emerging public health crisis. Unfortunately, our current ability to assess CA in a research context remains limited, curtailing efforts to address this important issue. We sought to fill this gap in the literature by developing an adapted "chat" version of the Taylor aggression paradigm (TAP) that would more closely resemble a social gaming format (hereafter referred to as the TAP-Chat). In the TAP-Chat, participants have a chat function available to communicate with their (fictitious) co-player. Following loss trials in a competitive reaction time task, they receive a "mean chat" from their co-player. Participant messages to their (fictitious) co-player are then coded for aggressive content by a team of trained research assistants, and via automated linguistic analysis software (Linguistic Inquiry and Word Count). The current study evaluated the predictive utility of the TAP-Chat task in independent discovery and replication samples (N = 843 and N  = 350, respectively). Participants' publicly available tweets served as an important external criterion variable, along with a handful of self-report questionnaires assessing CA and related constructs. Analyses suggest that, although it can be completed in ∼13 min, the TAP-Chat predicts CA on Twitter and, to a lesser extent, as reported on questionnaires. Although there are still several issues to address, it is our hope that the research community will benefit from this straightforward behavioral assessment of CA. [ABSTRACT FROM AUTHOR]

The current study evaluated associations among externalizing psychopathology, personality, and relationship quality in a sample of 794 couples. Personality and psychopathology were assessed using dimensional measures, and relationship attributes were assessed with both self-report and observer reports of videotaped interactions. Results were consistent with prior work (i.e., Humbad, Donnellan, Iacono, & Burt, 2010) such that greater externalizing psychopathology remained a significant predictor of lower relationship adjustment, while controlling for personality traits. Importantly, dimensional measures of externalizing psychopathology showed stronger associations with relationship adjustment when compared to symptom count measures used in Humbad et al. (2010). These results highlight the importance of replication and extension studies, the usefulness of dimensional measures of psychopathology, and the value of multiple methods of assessment to increase confidence in the robustness of associations between pathological attributes of personality and features of romantic relationships. [ABSTRACT FROM AUTHOR]

Background: Prior work has robustly suggested that social processes in the neighborhood (i.e. informal social control, social cohesion, norms) influence child conduct problems (CP) and related outcomes, but has yet to consider how these community-level influences interact with individual-level genetic risk for CP. The current study sought to do just this, evaluating neighborhood-level social processes as etiologic moderators of child CP for the first time. Methods: We made use of two nested samples of child and adolescent twins within the Michigan State University Twin Registry (MSUTR): 5649 families who participated in in the Michigan Twins Project (MTP) and 1013 families who participated in the Twin Study of Behavioral and Emotional Development (TBED-C). The neighborhood social processes of informal social control, social cohesion, and norms were assessed using neighborhood sampling techniques, in which residents of each twin family's neighborhood reported on the social processes in their neighborhood. Standard biometric GxE analyses evaluated the extent to which they moderated the etiology of CP. Results: The 'no moderation' model provided the best fit to the data in nearly all cases, arguing against neighborhood social processes as etiologic moderators of youth CP. Conclusions: The neighborhood social processes evaluated here do not appear to exert their effects on child CP via etiologic moderation. The documented links between neighborhood social processes and child CP are thus likely to reflect a different etiologic process. Possibilities include environmental main effects of neighborhood social processes on child CP, or genotype-environment correlations. [ABSTRACT FROM AUTHOR]

Background: Low emotion differentiation (the tendency to experience vague affective states rather than discrete emotions) is associated with psychopathology marked by emotion regulation deficits and impulsive/maladaptive behavior. However, research examining associations between emotion differentiation and dysregulated eating is nascent and has yet to incorporate measures of clinically significant binge eating. Different measures of emotion differentiation have also been used, impeding cross‐study comparisons. We therefore examined associations between several emotion differentiation measures and binge eating‐related phenotypes across a spectrum of severity. Methods: Women (N = 482) from the Michigan State University Twin Registry completed the Positive and Negative Affect Schedule (PANAS) daily for 45 consecutive days. Three measures of negative/positive emotion differentiation (NED/PED) were created using the intraclass correlation coefficient (ICC), average interitem correlation, and average daily variance between negative/positive emotion ratings on the PANAS. Associations between NED/PED measures and emotional eating (EE) and a history of binge eating episodes (BEs) were then examined, controlling for affect intensity and BMI. Results: Lower PED was associated with greater odds of BEs across the ICC and average interitem correlation measures, and more EE on the daily variance measure. Findings involving NED were less consistent; lower NED was associated with greater EE and greater odds of BEs using the daily variance measure only. Conclusion: Low PED is associated with clinically significant binge eating, and some aspects of NED may also be relevant for binge eating‐related phenotypes. Further research examining the constructs captured by different emotion differentiation measures and their relevance to binge eating is needed. [ABSTRACT FROM AUTHOR]

This document is a correction notice for an article titled "Continuity and Change in the Genetic and Environmental Etiology of Youth Antisocial Behavior" published in the journal Behavior Genetics. The correction addresses an error in the reporting of parameter estimates from a multilevel growth curve model. The corrected table of parameter estimates is provided, and it is stated that the conclusions of the original article remain unchanged. The correction is authored by Sarah L. Carroll, D. Angus Clark, Luke W. Hyde, Kelly L. Klump, and S. Alexandra Burt. [Extracted from the article]

Prior research has suggested that disadvantaged neighborhood contexts alter the etiology of youth antisocial behavior (ASB). Unfortunately, these studies have relied exclusively on governmental data collected in administratively-defined neighborhoods (e.g., Census tracts or block groups, zip codes), a less than optimal approach for studying neighborhood effects. It would thus be important to extend prior findings of GxE using neighborhood sampling techniques, in which disadvantage is assessed via resident informant-reports of the neighborhood. The current study sought to do just this, examining two independent twin samples from the Michigan State University Twin Registry. Neighborhood disadvantage was assessed via maternal and neighbor informant-reports, the latter of which were analyzed multiple ways (i.e., all neighbors within 1 km, nearest neighbor, and all neighbors within the County). Analyses revealed clear and consistent evidence of moderation by neighborhood disadvantage, regardless of informant or the specific operationalization of neighborhood. Shared environmental influences on ASB were observed to be several-fold larger in disadvantaged contexts, while genetic influences were proportionally more influential in advantaged neighborhoods. Such findings indicate that neighborhood disadvantage exerts rather profound effects on the origins of youth ASB. Efforts should now be made to identify the active ingredients of neighborhood disadvantage. [ABSTRACT FROM AUTHOR]

Background: Callous-unemotional (CU) traits are critical to developmental, diagnostic, and clinical models of antisocial behaviors (AB). However, assessments of CU traits within large-scale longitudinal and neurobiologically focused investigations remain remarkably sparse. We sought to develop a brief measure of CU traits using items from widely administered instruments that could be linked to neuroimaging, genetic, and environmental data within already existing datasets and future studies. Methods: Data came from a large and diverse sample (n = 4525) of youth (ages~9–11) taking part in the Adolescent Brain and Cognitive Development (ABCD) Study. Moderated nonlinear factor analysis was used to assess measurement invariance across sex, race, and age. We explored whether CU traits were distinct from other indicators of AB, investigated unique links with theoretically-relevant outcomes, and replicated findings in an independent sample. Results: The brief CU traits measure demonstrated strong psychometric properties and evidence of measurement invariance across sex, race, and age. On average, boys endorsed higher levels of CU traits than girls and CU traits were related to, yet distinguishable from other indicators of AB. The CU traits construct also exhibited expected associations with theoretically important outcomes. Study findings were also replicated across an independent sample of youth. Conclusions: In a large, multi-site study, a brief measure of CU traits can be measured distinctly from other dimensions of AB. This measure provides the scientific community with a method to assess CU traits in the ABCD sample, as well as in other studies that may benefit from a brief assessment of CU. [ABSTRACT FROM AUTHOR]

The current study examined how discrimination relates to adjustment outcomes in a sample of internationally, transracially adopted Korean Americans from the Minnesota Sibling Interaction and Behavior Study (N = 456 adoptees; Mage at T1 = 14.9, Mage at T2 = 18.3, Mage at T3 = 22.3). The moderating roles of ethnic socialization and preparation for bias by parents (i.e., ethnic-racial socialization) were also examined. Results indicated that discrimination predicted higher levels of depressive and externalizing symptoms in youth who reported less preparation for bias. In those experiencing more preparation for bias, associations were not significantly different from zero. Ethnic socialization did not moderate these associations. Such findings provide important information for adoptive parents regarding how to prepare their children to cope with discrimination. [ABSTRACT FROM AUTHOR]

The primary aim of the Michigan State University Twin Registry (MSUTR) is to examine developmental differences in genetic, environmental, neural, epigenetic, and neurobiological influences on psychopathology and resilience, particularly during childhood and adolescence. The MSUTR has two broad components: a large-scale, population-based registry of child, adolescent, and adult twins and their families (current N ~30,000) and a series of more focused and in-depth studies drawn from the registry (projected N ~7200). Participants in the population-based registry complete a family health and demographic questionnaire via mail. Families can then be recruited for one or more of the intensive, in-person studies from the population-based registry, using any one of several recruitment strategies (e.g., population-based, based on their answers to the registry questionnaire). These latter studies target a variety of biological, genetic, and environmental phenotypes, including multi-informant measures of psychiatric and behavioral phenotypes, functional and structural neuroimaging, comprehensive measures of the twin family environment (e.g., census and neighborhood informant reports of twin neighborhood characteristics, videotaped interactions of child twin families), buccal swab and salivary DNA samples, and/or assays of adolescent and adult steroid hormone levels. This article provides an overview of the MSUTR and describes current and future research directions. [ABSTRACT FROM AUTHOR]

Available twin-family data on sex differences in antisocial behavior (ASB) simultaneously suggest that ASB is far more prevalent in males than in females, and that its etiology (i.e. the effects of genes, environments, hormones, culture) does not differ across sex. This duality presents a conundrum: How do we make sense of mean sex differences in ASB if not via differences in genes, environments, hormones, and/or cultures? The current selective review and critique explores possible contributions to these seemingly incompatible sets of findings. We asked whether the presence of sex differences in behavior could be smaller than is typically assumed, or confined to a specific set of behaviors. We also asked whether there might be undetected differences in etiology across sex in twin-family studies. We found little evidence that bias or measurement invariance across sex account for phenotypic sex differences in ASB, but we did identify some key limitations to current twin-family approaches. These included the questionable ability of qualitative sex difference analyses to detect gender norms and prenatal exposure to testosterone, and concerns regarding specific analytic components of quantitative sex difference analyses. We conclude that the male preponderance in ASB is likely to reflect a true sex difference in observed behavior. It was less clear, however, that the genetic and environmental contributions to ASB are indeed identical across sex, as argued by prior twin-family studies. It is our hope that this review will inspire the development of new, genetically-informed methods for studying sex differences in etiology. [ABSTRACT FROM AUTHOR]

Although there is growing recognition that disadvantaged contexts attenuate genetic influences on youth misbehavior, it is not yet clear how this dampening occurs. The current study made use of a "geographic contagion" model to isolate specific contexts contributing to this effect, with a focus on nonaggressive rule-breaking behaviors (RB) in the families' neighbors. Our sample included 847 families residing in or near modestly-to-severely disadvantaged neighborhoods who participated in the Michigan State University Twin Registry. Neighborhood sampling techniques were used to recruit neighbors residing within 5km of a given family (the mean number of neighbors assessed per family was 13.09; range, 1–47). Analyses revealed clear evidence of genotype–environment interactions by neighbor RB, such that sibling-level shared environmental influences on child RB increased with increasing neighbor self-reports of their own RB, whereas genetic influences decreased. Moreover, this moderation appeared to be driven by geographic proximity to neighbors. Sensitivity analyses further indicated that this effect was specifically accounted for by higher levels of neighbor joblessness, rather than elements of neighbor RB that would contribute to neighborhood blight or crime. Such findings provocatively suggest that future genotype–environment interactions studies should integrate the dynamic networks of social contagion theory. [ABSTRACT FROM AUTHOR]

There is a strong relationship between sleep and behavioral problems. These findings are often interpreted via environmental explanations, such that poor sleep directly exacerbates or causes symptoms of aggression and behavior problems. However, there are other possible explanations, such that the genes predicting poor sleep also predict aggression or rule-breaking. The current study sought to elucidate the origin of this relationship. The sample was composed of 1030 twin pairs (426 monozygotic and 604 dizygotic). The sample was 51.3% male with a mean age of 8.06 years (range 6-11.96; SD = 1.45). Aggression, rule-breaking and sleep were assessed through the Child Behavior Checklist (CBCL). We fitted bivariate Cholesky genetic models to the data, decomposing the variance within, and the covariance among, aggression, rule-breaking, and sleep functioning into their genetic and environmental components. Genetic correlations between all sleep variables and aggression were significant and moderate to large in magnitude, but mostly small and non-significant between sleep and rule-breaking. We did not find evidence of a causal or environmental relationship between the majority of sleep variables and aggression, but rather clear evidence of genetic pleiotropy. However, the pattern of associations between rule-breaking and sleep measures was less consistent. Aggression and rule-breaking appear to be differentially associated with sleep. [ABSTRACT FROM AUTHOR]

Behavioral genetic (BG) research has yielded many important discoveries about the origins of human behavior, but offers little insight into how we might improve outcomes. We posit that this gap in our knowledge base stems in part from the epidemiologic nature of BG research questions. Namely, BG studies focus on understanding etiology as it currently exists, rather than etiology in environments that could exist but do not as of yet (e.g., etiology following an intervention). Put another way, they focus exclusively on the etiology of "what is" rather than "what could be". The current paper discusses various aspects of this field-wide methodological reality, and offers a way to overcome it by demonstrating how behavioral geneticists can incorporate an experimental approach into their work. We outline an ongoing study that embeds a randomized intervention within a twin design, connecting "what is" and "what could be" for the first time. We then lay out a more general framework for a new field—experimental BGs—which has the potential to advance both scientific inquiry and related philosophical discussions. [ABSTRACT FROM AUTHOR]

Objective: Elevated ovarian hormone levels are associated with increased risk for binge eating (BE) and emotional eating (EE) during the midluteal phase of the menstrual cycle. However, past studies have not examined whether pronounced hormonal changes that precede the midluteal phase (i.e., the dramatic decrease in estradiol and increase in progesterone during/after ovulation) also influence midluteal increases in binge‐related symptoms. Past theories and studies of phenotypes strongly related to BE (e.g., depression) suggest that these pronounced hormonal changes may also contribute. This study examined this possibility in 375 female twins (aged 15–25 years) from the Michigan State University Twin Registry. Methods: Daily ratings of EE (assessed with the Dutch Eating Behavior Questionnaire) and daily saliva samples of estradiol and progesterone were collected for 45 consecutive days. Results: No significant associations were found between pronounced changes in estradiol or progesterone across ovulation and changes in EE scores in the midluteal phase. Results remained unchanged after controlling for body mass index and negative affect and examining participants with clinical BE episodes or more extreme hormonal fluctuations. Discussion: In aggregate, the current findings and past data suggest that hormone levels are more significant predictors of EE than pronounced hormonal changes across the menstrual cycle. [ABSTRACT FROM AUTHOR]

Background: Social aggression is a form of antisocial behavior in which social relationships and social status are used to damage reputations and inflict emotional harm on others. Despite extensive research examining the prevalence and consequences of social aggression, only a few studies have examined its genetic–environmental etiology, with markedly inconsistent results. Method: We estimated the etiology of social aggression using the nuclear twin family (NTF) model. Maternal-report, paternal-report, and teacher-report data were collected for twin social aggression (N = 1030 pairs). We also examined the data using the classical twin (CT) model to evaluate whether its strict assumptions may have biased previous heritability estimates. Results: The best-fitting NTF model for all informants was the ASFE model, indicating that additive genetic, sibling environmental, familial environmental, and non-shared environmental influences significantly contribute to the etiology of social aggression in middle childhood. However, the best-fitting CT model varied across informants, ranging from AE and ACE to CE. Specific heritability estimates for both NTF and CT models also varied across informants such that teacher reports indicated greater genetic influences and father reports indicated greater shared environmental influences. Conclusions: Although the specific NTF parameter estimates varied across informants, social aggression generally emerged as largely additive genetic (A = 0.15–0.77) and sibling environmental (S = 0.42–0.72) in origin. Such findings not only highlight an important role for individual genetic risk in the etiology of social aggression, but also raise important questions regarding the role of the environment. [ABSTRACT FROM AUTHOR]

Objective: Emotional eating has been linked to ovarian hormone functioning, but no studies to‐date have considered the role of brain function. This knowledge gap may stem from methodological challenges: Data are heterogeneous, violating assumptions of homogeneity made by between‐subjects analyses. The primary aim of this paper is to describe an innovative within‐subjects analysis that models heterogeneity and has potential for filling knowledge gaps in eating disorder research. We illustrate its utility in an application to pilot neuroimaging, hormone, and emotional eating data across the menstrual cycle. Method: Group iterative multiple model estimation (GIMME) is a person‐specific network approach for estimating sample‐, subgroup‐, and individual‐level connections between brain regions. To illustrate its potential for eating disorder research, we apply it to pilot data from 10 female twins (N = 5 pairs) discordant for emotional eating and/or anxiety, who provided two resting state fMRI scans and hormone assays. We then demonstrate how the multimodal data can be linked in multilevel models. Results: GIMME generated person‐specific neural networks that contained connections common across the sample, shared between co‐twins, and unique to individuals. Illustrative analyses revealed positive relations between hormones and default mode connectivity strength for control twins, but no relations for their co‐twins who engage in emotional eating or who had anxiety. Discussion: This paper showcases the value of person‐specific neuroimaging network analysis and its multimodal associations in the study of heterogeneous biopsychosocial phenomena, such as eating behavior. [ABSTRACT FROM AUTHOR]

We examined the nomological network surrounding digital aggression (DA), in regards to other forms of aggression/antisocial behavior and individual difference variables commonly associated with other forms of aggression/antisocial behavior. Two large samples of university students (N = 713 and 633, respectively) completed a series of questionnaires and in some cases, an additional experience sampling study. Results revealed that, in emerging adulthood, DA appears to have a unique demographic profile relative to the other forms of aggression and antisocial behavior. Results further suggested that, when examined simultaneously, only social aggression and non‐aggressive rule‐breaking evidenced independent associations with DA. These associations persisted even in the absence of social media use. Unique associations with most individual difference variables dissipated once we controlled for social aggression and rule‐breaking, although DA was independently associated with extraversion and alcohol use problems. Such findings begin to embed DA in its broader nomological network and suggest clear functional links with both social aggression and non‐aggressive rule‐breaking. [ABSTRACT FROM AUTHOR]

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 postpuberty 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 (aged 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 prepuberty (5%) to postpuberty (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. [ABSTRACT FROM AUTHOR]