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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]

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. Public Significance Statement: Our findings confirm the long-running notion that children are active participants in the parenting they receive. However, we find that child effects on positive parenting are also context-dependent, such that child effects on positive parenting are especially pronounced in underresourced neighborhood contexts. [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]

Emerging literature links neighborhood disadvantage to altered neural function in regions supporting socioemotional and threat processing. Few studies, however, have examined the proximal mechanisms through which neighborhood disadvantage is associated with neural functioning. In a sample of 7- to 19-year-old twins recruited from disadvantaged neighborhoods (354 families, 708 twins; 54.5% boys; 78.5% White, 13.0% Black, 8.5% other racial/ethnic group membership), we found that exposure to community violence was related to increased amygdala reactivity during socioemotional processing and may be one mechanism linking neighborhood disadvantage to amygdala functioning. Importantly, parenting behavior appeared to modulate these effects, such that high parental nurturance buffered the effect of exposure to community violence on amygdala reactivity. These findings elucidate the potential impact of exposure to community violence on brain function and highlight the role parents can play in protecting youth from the neural effects of exposure to adversity. Public Significance Statement: Although prior studies have primarily focused on family-level adversities, developmental researchers are now paying increased attention to the effect of neighborhood-level adversity on youth brain development. We find that increased exposure to community violence is related to heightened amygdala reactivity to threat and may be a mechanism explaining the link between neighborhood disadvantage and brain function in youth. Further, the study highlights that nurturing parenting can protect children from the risks posed by living in a disadvantaged and dangerous neighborhood. [ABSTRACT FROM AUTHOR]

The misconception that eating disorders are conditions of affluence has shaped research and public understanding for decades. Here, we highlight links between socioeconomic disadvantage and eating disorder risk. With prevailing stereotypes discredited, we argue that considering disadvantage as a key eating disorder risk factor will advance science and reduce disparities The misconception that eating disorders are conditions of affluence has shaped research and public understanding for decades. Here, we highlight links between socioeconomic disadvantage and eating disorder risk. With prevailing stereotypes discredited, we argue that considering disadvantage as a key eating disorder risk factor will advance science and reduce disparities. [ABSTRACT FROM AUTHOR]

Twin and adoption studies compare the similarities of people with differing degrees of relatedness to estimate genetic and environmental contributions to trait population variance. The analytic workhorse of these kinds of variancefocused designs is the intraclass correlation, which estimates similarity between pairs of individuals. Group means, by contrast, play no overt role in estimating genetic and environmental influences. Although this focus on variance has made very important contributions to understanding psychological characteristics, we contend that the exclusion of mean effects from behavioral genetic designs may have obscured key environmental influences and impeded full appreciation of the ubiquity and nature of gene–environment interplay in human outcomes. We provide empirical examples already in the literature and a theoretical framework for thinking through the incorporation of mean effects using largely forgotten, non-Mendelian theory regarding how genes influence human outcomes. We conclude that the field needs to develop models capable of fully incorporating mean effects into twin and adoption studies. [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]

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]

In the current study, we leveraged differences within twin pairs to examine whether harsh parenting is associated with children's antisocial behavior via environmental (vs. genetic) transmission. We examined two independent samples from the Michigan State University Twin Registry. Our primary sample contained 1,030 families (2,060 twin children; 49% female; 6–10 years old) oversampled for exposure to disadvantage. Our replication sample included 240 families (480 twin children; 50% female; 6–15 years old). Co-twin control analyses were conducted using a specification-curve framework, an exhaustive modeling approach in which all reasonable analytic specifications of the data are interrogated. Results revealed that, regardless of zygosity, the twin experiencing harsher parenting exhibited more antisocial behavior. These effects were robust across multiple operationalizations and informant reports of both harsh parenting and antisocial behavior with only a few exceptions. Results indicate that the association between harsh parenting and children's antisocial behavior is, to a large degree, environmental in origin. [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]

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]

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]

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]

Familial resemblance in eating pathology is typically attributed to parents providing an environment that leads to the development of eating pathology. However, offspring raised by biological parents receive both their environment and genes from their parents, raising the possibility that genetic influences, environmental influences, and/or gene-environment interplay may account for familial resemblance. Past studies have not explored the possibility of parents' genes influencing the environment they provide (i.e., passive gene-environment correlations or "passive rGE"). If present, passive rGE is most likely to "hide" in estimates of shared environmental influence in classical twin models. The current study used a nuclear twin family design to explore the possibility of passive rGE during pre- and early puberty when past studies have demonstrated the importance of shared environmental influence. Additionally, the present study explored whether sibling-specific (i.e., influences specific to the twin generation) or family-specific (i.e., "cultural" influences within the home) environmental influences account for shared environmental influences found in past studies. Participants included preearly pubertal same-sex female twins and their biological parents (N = 547 families) from the Minnesota Twin Family Study and the Michigan State University Twin Registry. Disordered eating was assessed with self-report measures in the twins and parents. Pubertal status was determined using an established cut-off on a self-report measure. Passive rGE was not indicated in this study of pre- and early pubertal twins. Instead, sibling-specific shared environmental and nonshared environmental influences were most influential. Future research should work to identify the sibling-specific environmental influences that contribute to sibling similarity in disordered eating. (PsycINFO Database Record (c) 2019 APA, all rights reserved). [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]

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]

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]

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]

Sex differences in the etiology of youth antisocial behavior are an intuitively appealing hypothesis given the consistently higher prevalence of antisocial behavior in boys versus girls. Although a few early studies supported this possibility, reporting stronger genetic influences in females and stronger environmental influences in males, subsequent meta-analyses found that antisocial behavior was equally heritable in males and females. Critically however, none of the meta-analyses evaluated whether sex differences in etiology might be enhanced in particular subpopulations or contexts. The current study sought to do just this. We examined 1,030 child twin pairs from the Michigan State University Twin Registry, half of whom were oversampled for neighborhood disadvantage, thereby allowing us to meaningfully evaluate whether sex differences in etiology were enhanced in disadvantaged contexts. We also directly evaluated the possibility of sex differences in the etiology of teacher- versus maternal-informant reports of antisocial behavior, evaluating each informant-report for possible sex differences. Results were not consistent with differential effects of sex on etiology in disadvantaged versus advantaged contexts, but did suggest moderation by informant-report. Namely, genetic influences were stronger in girls, and environmental influences were stronger in boys, when antisocial behavior was assessed using teacher informant-reports, but not when assessed using maternal informant-reports. Critically, these findings were confirmed when we reanalyzed meta-analytic data from Burt (2009a) separately by informant. Such findings suggest that, at least in school contexts, the etiology of antisocial behavior does indeed vary across sex. Implications are discussed. (PsycINFO Database Record [ABSTRACT FROM AUTHOR]

Genetic influences on disordered eating (DE) increase across age and puberty in girls, an effect that is at least partially due to ovarian hormone activation. However, development shifts in genetic effects have not been detected in boys; genetic influences have been found to be relatively constant from prepuberty to adulthood, suggesting that gonadal hormones may be less important. One caveat is that studies have examined males ages 10 or older. Genetic effects on DE may emerge earlier in boys, such as during adrenarche, when androgens begin to increase but the physical changes of puberty are not yet observable. The current study investigated this hypothesis in 1,212 male twins (ages 6-28) from the Michigan State University Twin Registry. Results supported a potential role of adrenarche, as genetic influences on DE increased during middle childhood, prior to the external physical changes of puberty. Specifically, genetic influences on DE were negligible (0%) in twins during pre- to early adrenarche, but increased incrementally across advancing adrenarche (17% to 44%) and into early puberty (57%). Genetic effects then remained stable into midpuberty and postpuberty (58%), suggesting that nearly all of the genetic effects on DE become prominent during adrenarche in males. Findings suggest that genetic effects on DE emerge sooner in boys than the midpubertal activation that is consistently found in girls. These data highlight a potentially important role for adrenarche in the genetic diathesis for DE in males and a need to examine younger ages in studies of developmental effects. (PsycINFO Database Record [ABSTRACT FROM AUTHOR]

Negative parenting is shaped by the genetically influenced characteristics of children (via evocative rGE) and by parental antisocial behavior; however, it is unclear how these factors jointly impact parenting. This study examined the effects of birth parent and adoptive parent antisocial behavior on negative parenting. Participants included 546 families within a prospective adoption study. Adoptive parent antisocial behavior emerged as a small but significant predictor of negative parenting at 18 months and of change in parenting from 18 to 27 months. Birth parent antisocial behavior predicted change in adoptive father's (but not mother's) parenting over time. These findings highlight the role of parent characteristics and suggest that evocative rGE effects on parenting may be small in magnitude in early childhood. [ABSTRACT FROM AUTHOR]

Eating disorders are conceptualized as categorical rather than dimensional in the current major diagnostic system (Diagnostic and Statistical Manual of Mental Disorders; 5th ed.; American Psychiatric Association, 2013) and in many previous studies. However, previous research has not critically evaluated this assumption or tested hybrid models (e.g., modeling latent variables with both dimensional and categorical features). Accordingly, the current study directly compared categorical, dimensional, and hybrid models for eating pathology in a large, population-based sample. Participants included 3,032 female and male twins (ages 9-30 years) from the Michigan State University Twin Registry. The Minnesota Eating Behaviors Survey was used to assess disordered eating symptoms including body dissatisfaction, weight preoccupation, binge eating, and compensatory behaviors. Results showed that dimensional models best fit the data in the overall sample as well as across subgroups divided by sex and pubertal status (e.g., prepubertal vs. postpubertal). It is interesting to note that the results favored more categorical models when using a case-control subset of our sample with participants who either endorsed substantial eating pathology or no/little eating pathology. Overall, findings provide support for a dimensional conceptualization of eating pathology and underscore the importance of using community samples to capture the full range of severity of eating pathology when investigating questions about taxonomy. (PsycINFO Database Record [ABSTRACT FROM AUTHOR]

Previous studies suggest strong associations between exposure to weight-conscious peer groups and increased levels of disordered eating. This association has been attributed to socialization effects (i.e., membership leads to disordered eating); however, selection effects (i.e., selecting into peer groups based on genetic and/or environmental predispositions toward disordered eating) could contribute to or even account for these associations. The current study was the first to use a co-twin control design to disentangle these types of selection factors from socialization effects. Participants included 610 female twins (ages 8-14) drawn from the Michigan State University Twin Registry. To comprehensively examine a range of eating pathology, several disordered eating attitudes and behaviors (e.g., body dissatisfaction, binge eating) were examined via self-report questionnaires. Questionnaires also were used to assess peer group emphasis on body weight and shape. Replicating previous results, significant individual-level associations were found between membership in weight-conscious peer groups and disordered eating. However, co-twin control analyses indicated that these associations were largely due to genetic and/or shared environmental selection factors rather than pure socialization effects. Importantly, results remained unchanged when controlling for pubertal status, suggesting that effects do not vary across developmental stage. Overall, these findings question whether associations between weight-conscious peer groups and disordered eating are due entirely to socialization processes. Future studies are needed to identify the specific genetic and/or shared environmental factors that may drive selection into weight-conscious peer groups. [ABSTRACT FROM AUTHOR]

Gene-environment interactions (G × E) are thought to constitute a core mechanism through which genes influence youth conduct problems. Although biometric G × E studies have yielded provocative leads, two interrelated issues have yet to be meaningfully considered. First, most work has been focused on the diathesis-stress model of G × E, in which genetic risk is amplified following exposure to an environmental pathogen. Although this form of G × E appears to be important, other possible instantiations of G × E exist. For example, in bioecological G × E, deleterious environments amplify environmental influences on the outcome. Second, conduct problems change dramatically from childhood to adolescence in that high levels of physical aggression give way to high levels of nonaggressive delinquency. As such, researchers must consider development to understand G × E. I consider both of these issues in relation to one another to encourage additional research on the development of G × E. [ABSTRACT FROM AUTHOR]

We are pleased to present this special issue of JCPP, which brings together a collection of cutting‐edge empirical studies that focuses on developmental trajectories and pathways associated with ADHD, conduct problems and other externalizing behaviors. JCPP has had a long‐standing focus on theoretically strong prospective longitudinal studies that elucidate behavioral change and outcomes over time, including in the areas of ADHD and externalizing disorders (Kuja‐Halkola, Lichtenstein, D'Onofrio & Larsson, 2015; Sonuga‐Barke & Halperin, 2010). Keeping with that tradition, all of the papers in this special issue employ a prospective longitudinal design and a focus on changes that unfold over development. [ABSTRACT FROM AUTHOR]

Conduct problems (CP) are actions that violate societal norms and/or the personal/property rights of others, and include behaviors such as vandalism, theft, bullying, and assault. Roughly 8%–10% of children engage in the more severe childhood‐onset form of CP, while another 25% initiate clinically‐significant levels of CP during adolescence. As deftly observed in Rivenbark et al. ( ), however, the high prevalence of CP belies its severity: Youth with CP are at increased risk for a number of deleterious individual outcomes, including academic delay/dropout, low professional achievement, psychopathology, addiction, and family instability. [ABSTRACT FROM AUTHOR]

Aggression (e.g., assaulting others, bullying, oppositionality; AGG) and non-aggressive rule-breaking (e.g., lying, stealing, vandalism; RB) appear to constitute meaningfully distinct dimensions of antisocial behavior. Despite these differences, it is equally clear that AGG and RB are moderately-to-strongly intercorrelated with one another. To date, however, we have little insight into the sampling and methodologic characteristics that might moderate the association between AGG and RB. The current study sought to evaluate several such moderators (i.e., age, sex, informant, and society) in a sample of 27,861 parent–adolescent dyads from 25 societies. AGG and RB were assessed with the well-known Child Behavior Checklist and Youth Self-Report (Achenbach & Rescorla, 2001). Results revealed small effects of informant and adolescent sex, such that the association between AGG and RB was stronger for parents’ reports than for adolescents’ self-reports, and for boys than for girls. The association also varied by society. Unexpectedly, the specific operationalization of ‘aggression’ emerged as a particularly strong moderator, such that the association was stronger for a general measure of AGG than for a more focused measure of physical aggression per se. Such findings inform our understanding of similarities and differences between aggressive and non-aggressive antisocial problems. [ABSTRACT FROM AUTHOR]

ABSTRACT Objective Negative urgency (NU; tendency to act impulsively when experiencing negative emotions) is a risk factor for binge eating, although few studies have examined interviewer-assessed objective binge episodes (OBEs). Moreover, research has not investigated how NU relates to the core components of OBEs: loss of control (LOC) eating and objective overeating (OO). Understanding the relationship between NU and these core components will enhance etiologic models of eating disorder development. Thus, the current study examined the associations between NU, OBEs, and the components of OBEs by comparing levels of NU in women with OBEs, LOC eating only, and OO only to women with no pathological eating. Method Participants were 612 women who endorsed lifetime OBEs (5.4%), LOC eating outside of OBEs (5.7%), OO only (2.8%), or none of these eating episodes (85.9%). Results Women with OBEs, LOC only, and OO only had significantly higher levels of NU than women without these episodes, suggesting that NU is associated with both the LOC and OO components of OBEs. Discussion NU relates to the spectrum of pathology present in women with OBEs. Future research should examine the mechanisms underlying these associations, including impaired behavioral/psychological control and/or increased reward sensitivity in response to negative affect. © 2015 Wiley Periodicals, Inc.© 2015 Wiley Periodicals, Inc (Int J Eat Disord 2015; 48:527-531). [ABSTRACT FROM AUTHOR]

Background Conduct Disorder ( CD) is among the most highly represented diagnostic problems in child and adolescent mental health treatment settings. There is a great deal of heterogeneity within the CD category, with potentially important implications for case conceptualization and treatment. The current review sought to detail forms of heterogeneity within CD, including callous-unemotional traits, comorbid Attention-Deficit Hyperactivity Disorder ( ADHD), aggressive and nonaggressive antisocial behavior, and age of onset. Methods The current review summarizes research on etiological factors, correlates, and trajectories associated with distinguishable dimensions of CD, and considers how this heterogeneity should be incorporated into the assessment and treatment of CD. Results Callous-unemotional traits have been associated with a more severe and persistent form of CD, as have comorbid ADHD and child-onset CD. Aggressive antisocial behavior is a stable behavioral dimension that emerges in early childhood and is associated with high levels of neuroticism. Nonaggressive antisocial behavior demonstrates specific associations with impulsivity, is most frequent during adolescence, and evidences more moderate levels of stability. Conclusions Conduct disorder is a highly heterogeneous disorder. Although the clinical implications of this heterogeneity are discussed, future research is clearly needed to shore up our understanding of the clinical ramifications of the sub-dimensions within CD. [ABSTRACT FROM AUTHOR]

The editor muses about studies that might complement and enhance current etiologic studies of psychopathology, many of which focus on monotonically increasing maladaptative outcomes in response to increasing levels of risk/vulnerability. More meaningful and consistent considerations of the resilience counterfactual (e.g., Why are some youth with a given neural deficit unaffected? Why are some youth exposed to a given adversity unaffected?) should strengthen our causal inferences. We might also more frequently test for U-shaped associations with outcome (e.g., Does level of psychopathology predict deleterious outcomes in a dose-response fashion, or is the association curvilinear whereby moderate predict good outcomes?). In line with the latter, we might also more frequently consider the adaptive value of the disorder in evolutionary terms (e.g., Why is this disorder still part of the human repertoire? What might be its adaptive value for the species?). [ABSTRACT FROM AUTHOR]

The studies included in this special issue on gene-peer interplay in child and adolescent outcomes can uniformly be described as cutting edge and methodologically sophisticated. When viewed together, they all but conclusively document the presence and importance of gene-peer interplay in child and adolescent outcomes. Nevertheless, more work on the topic is needed, both because the inherent complexity of peer studies means we know less on this topic than on many others, but also because available research is limited by the descriptive nature of the findings. The current commentary offers suggestions for future work that would begin to remedy these limitations. [ABSTRACT FROM AUTHOR]

Decades of research have indicated the foundational importance of parenting to offspring outcomes during childhood and beyond. Unearthing the specific origins of parenting is therefore a critically important research objective. Extant research on this topic has suggested that parenting behaviors are multidetermined (Belsky, 1984) and are associated with a wide range of contextual and familial characteristics (e.g., ethnicity, community, family financial stress), as well as characteristics of the parents (e.g., personality) and their children (e.g., temperament). Behavioral genetic studies have further indicated that parenting behaviors are in fact heritable—that is, individual differences in parenting are at least partially a function of genetic differences between persons. Critically, however, the estimates of these genetic influences have varied dramatically across studies. It is also unclear how factors such as parent gender, child age, and methodological considerations may impact genetic influences on parenting behavior. In the current set of meta-analyses, we sought to quantitatively synthesize twin and adoption studies (n = 56) examining the etiology of parenting behavior, with the goal of more definitively cataloguing genetic and environmental effects on parenting. Results reveal significant effects of parental genetic makeup on parental behavior, but also highlight the genetic makeup of the child as a particularly prominent source of genetic transmission (via evocative gene-environment correlation). Environmental contributions to parenting also emerged as important, including both shared and nonshared environmental effects. Theoretical implications of these findings are discussed. [ABSTRACT FROM AUTHOR]

Personality traits are known to be associated with a host of important life outcomes, including interpersonal dysfunction. The interpersonal circumplex offers a comprehensive system for articulating the kinds of interpersonal problems associated with personality traits. In the current study, traits as measured by the Multidimensional Personality Questionnaire in a sample of 124 young women were correlated with interpersonal dysfunction as measured by the Inventory of Interpersonal Problems–Circumplex. Results suggest that Multidimensional Personality Questionnaire traits vary in their associations with interpersonal distress and in their coverage of specific kinds of interpersonal difficulties among women undergoing the transition to adulthood. [ABSTRACT FROM PUBLISHER]

The primary aim of the Michigan State University Twin Registry (MSUTR) is on understanding developmental changes in genetic, environmental, and neurobiological influences on internalizing and externalizing disorders, with antisocial behavior and disordered eating representing our particular areas of interest. The MSUTR has two broad components: a large-scale, population-based registry of child, adolescent, and adult twins and their families (current N ~20,000) and a series of more focused and in-depth studies drawn from the registry (current N ~4,000). Participants in the population-based registry complete a family health and demographic questionnaire via mail. Families are then recruited for one or more of the intensive, in-person studies from the population-based registry based on their answers to relevant items in the registry questionnaire. These in-person assessments target a variety of biological, genetic, and environmental phenotypes, including multi-informant measures of psychiatric and behavioral phenotypes, census and neighborhood informant reports of twin neighborhood characteristics, buccal swab and salivary DNA samples, assays of adolescent and adult steroid hormone levels, and/or videotaped interactions of child twin families. This article provides an overview of the MSUTR and describes current and future research directions. [ABSTRACT FROM AUTHOR]

Rates of twinning have risen dramatically over the last 30 years, from 1 in 53 births in 1980 to 1 in 30 births in 2009 (Martin et al. (January 2012). Three decades of twin births in the United States, 1980–2009. Atlanta, GA: Centers for Disease Control and Prevention, National Center for Health Statistics). This increase is largely attributable to increases in the use of fertility treatments (i.e., ovulation induction and in vitro fertilization) combined with delays in parenthood. Although this increase means that more twins are available for recruitment into twin studies, it also has potential consequences for the heritability estimates obtained in these studies. This study sought to evaluate this possibility, making use of the ongoing Michigan Twins Project (N = 7,261 families with twins aged 3–17 years), an arm of the Michigan State University Twin Registry. Results revealed that, on average, twins conceived via fertility treatments had lower rates of behavior problems than those conceived naturally, although these behavioral differences could be explained largely by demographic and socio-economic differences across the two types of twin families. Twin similarity did not meaningfully differ across fertility treatment status. We thus conclude that estimates of genetic and environmental influences obtained from twin studies over the last 10–15 years are more or less unaffected by the inclusion of twins conceived via fertility treatments in their samples. [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]

Abstract: Extant research has highlighted meaningful distinctions in the correlates, developmental trajectories, and etiologies of physically aggressive (AGG) as compared to non-aggressive rule-breaking (RB) antisocial behavior. AGG is a highly heritable behavioral dimension that emerges in early childhood and exhibits specific ties to negative emotionality and executive dysfunction. Although the frequency of aggressive behaviors decreases after early childhood, those who are most aggressive early in life typically continue to aggress at relatively high rates across the lifespan. By contrast, RB demonstrates specific associations with impulsivity, is most frequent during adolescence, and evidences more moderate levels of stability and stronger environmental influences as compared to AGG. These etiological and developmental differences link up quite well to Moffitt''s (1993) developmental taxonomy of antisocial behavior, providing a clear theoretical basis for examining differences between AGG and RB. Perhaps more importantly, however, the link between AGG/RB and Moffitt''s taxonomy allows us to conceptualize her categorical taxonomy in dimensional terms, an important development given the recent emphasis on dimensional conceptualizations of psychopathology. Available evidence further indicates that neither AGG nor RB is redundant with callous–unemotional traits. The current review thus underscores the clear advantages of differentiating between AGG and RB when studying antisocial behavior. [Copyright &y& Elsevier]

Objective: Research suggests that shared genetic factors underlie relationships between eating disorder and depression diagnoses, but no studies to date have examined these associations using dimensional symptom measures. This study examined whether genetic associations observed between eating disorder and depression diagnoses extend to continuous measures of these phenotypes. Method: The sample consisted of 292 young adult female twins from the Michigan State University Twin Registry. Disordered eating was measured using the Minnesota Eating Behavior Survey. Depressive symptoms were assessed using the Beck Depression Inventory. Results: Univariate twin models indicated that genetic factors accounted for 55% to 60% of the variance in disordered eating and depressive symptoms, with the remaining variance accounted for by nonshared environmental effects. Bivariate models indicated that genetic factors primarily accounted for associations between disordered eating and depressive symptoms ( r a = .70). Discussion: Phenotypic associations between disordered eating and depressive symptoms appear to be due to common genetic factors. © 2010 by Wiley Periodicals, Inc. (Int J Eat Disord 2010) [ABSTRACT FROM AUTHOR]

A recent meta-analysis revealed moderate shared environmental influences (C) on most forms of child and adolescent psychopathology (), including antisocial behavior. Critically, however, the research analyzed in this meta-analysis relied largely on specific informant-reports (and particularly parent and child reports), each of which is subject to various sources of rater bias. Observer-ratings of children's behaviors avoid many of these biases, and are thus well suited to verify the presence of C. Given this, we sought to buttress the evidence supporting C in two key ways. First, we sought to confirm that C contributes to observer-ratings in a sample of adoptive siblings, as similarity between adoptive siblings constitutes a 'direct' estimate of C. Second, we sought to confirm that these shared environmental influences persist across informants (i.e., the effects are not specific to the rater or the context in question). The current study examined the etiology of observer-ratings of acting-out behaviors, as well as sources of etiological overlap across observer-ratings, adolescent self-report and maternal-report in sample of over 600 biological and adoptive sibling pairs from the Sibling Interaction and Behavior Study (SIBS). Results revealed moderate and significant shared environmental influences on observer-ratings (31%), as well as on the other informant-reports (20-23%). Moreover, a portion of these effects overlapped across measures (C correlations ranged from .32 to .34). Such findings argue against passive gene-environment correlations (rGE) and rater bias as primary explanations for earlier findings of C on antisocial behavior, and in this way, offer a critical extension of prior work indicating that the role of shared environmental influences on child and adolescent antisocial behavior was dismissed too soon. [ABSTRACT FROM AUTHOR]

Dietary restraint is a prospective risk factor for the development of binge eating and bulimia nervosa. Although many women engage in dietary restraint, relatively few develop binge eating. Dietary restraint may increase susceptibility for binge eating only in individuals who are at genetic risk. Specifically, dietary restraint may be a behavioral exposure factor that activates genetic predispositions for binge eating. We investigated this possibility in 1,678 young adolescent and adult same-sex female twins from the Minnesota Twin Family Study and the Michigan State University Twin Registry. Twin moderation models were used to examine whether levels of dietary restraint moderate genetic and environmental influences on binge eating. Results indicated that genetic and nonshared environmental factors for binge eating increased at higher levels of dietary restraint. These effects were present after controlling for age, body mass index, and genetic and environmental overlap among dietary restraint and binge eating. Results suggest that dietary restraint may be most important for individuals at genetic risk for binge eating and that the combination of these factors could enhance individual differences in risk for binge eating. [ABSTRACT FROM AUTHOR]

A handful of prior adoption studies have confirmed that the cross-sectional relationship between child conduct problems and parent-child conflict at least partially originates in the shared environment. However, as the direction of causation between parenting and delinquency remains unclear, this relationship could be better explained by the adolescent's propensity to elicit conflictive parenting, a phenomenon referred to as an evocative gene-environment correlation. In the current study, the authors thus examined the prospective relationship between conduct problems and parent-child conflict in a sample of adoptive families. Participants included 672 adolescents in 405 adoptive families assessed at 2 time points roughly 4 years apart. Results indicated that parent-child conflict predicts the development of conduct problems, whereas conduct problems do not predict increases in parent-child conflict. Such findings suggest that evocative gene-environment correlations are highly unlikely to be an explanation of prior shared environmental effects during adolescence. Moreover, because the adolescents in this study do not share genes with their adoptive parents, the association between conduct problems and parent-child conflict is indicative of shared environmental mediation in particular. Implications of the findings are discussed. [ABSTRACT FROM AUTHOR]

Objective: Previous research has shown important developmental shifts in genetic and environmental influences for disordered eating. However, little research has examined age differences for weight/shape concerns, two key components of eating disorders. The goal of this study was to investigate these age differences in preadolescent, adolescent, young adult, and mid-adult twins. Method: Participants included 2,618 female twins (ages of 10-41 years) from three large twin registries. Shape and weight concerns were assessed with the Eating Disorders Examination Questionnaire. Results: Genetic influences were modest in preadolescent twins, but significant from early-adolescence through middle adulthood. Shared environmental factors showed the opposite pattern, with the largest shared environmental contributions occurring in the youngest age group. Nonshared environmental effects remained relatively constant across age. Discussion: Findings highlight the importance of age differences in genetic and environmental influences. Possible mechanisms include gene x environment interactions and biological changes associated with key developmental stages. [ABSTRACT FROM AUTHOR]

Abstract: There is growing recognition that substantively important distinctions exist across physically aggressive, rule-breaking, and socially aggressive forms of antisocial behavior. Even so, one limitation to accumulating additional scientific insights into the correlates and origins of these three varieties of antisocial behavior has been the lack of an efficient self-report assessment in the public domain. The Subtypes of the Antisocial Behavior Questionnaire (STAB) was developed to address this need. Although there is already a good deal of psychometric support for the STAB, prior research has yet to examine its “ecological” validity. In other words, it remains unclear whether the STAB scales would predict the frequency of acting-out behaviors in daily life. The current study sought to examine this question via an electronic diary study, in which participants reported on their momentary behaviors on multiple occasions in their natural environments. Analyses revealed that each STAB scale uniquely predicted only the momentary acting-out behaviors characteristic of that scale. Such findings provide further support for the STAB as a promising self-report measure of physically aggressive, rule-breaking, and socially aggressive forms of antisocial behavior. [Copyright &y& Elsevier]

It has recently been argued that shared environmental influences are moderate, identifiable, and persistent sources of individual differences in most forms of child and adolescent psychopathology, including antisocial behavior. Unfortunately, prior studies examining the stability of shared environmental influences over time were limited by possible passive gene-environment correlations, shared informants effects, and/or common experiences of trauma. The current study sought to address each of these limitations. We examined adolescent self-reported antisocial behavior in a 3.5 year longitudinal sample of 610 biological and adoptive sibling pairs from the Sibling Interaction and Behavior Study (SIBS). Results revealed that 74–81% of shared environmental influences present at time 1 were also present at time 2, whereas most non-shared environmental influences (88–89%) were specific to a particular assessment period. Such results provide an important constructive replication of prior research, strongly suggesting that shared environmental contributions to antisocial behavior are systematic in nature. [ABSTRACT FROM AUTHOR]

There are two common approaches to sub-typing the well-documented heterogeneity within antisocial behavior: age-of-onset (i.e., child-onset versus adolescent-onset; see Moffitt, 1993) and behavioral (i.e., physical aggression versus nonaggressive rule-breaking). These approaches appear to be intimately connected, such that aggression is particularly characteristic of child-onset antisocial behavior whereas rule-breaking is largely specific to adolescent-onset antisocial behavior (see Moffitt, 2003). Even so, it remains unclear which approach, if either, substantively drives these different manifestations of antisocial behavior. We examined this question in a sample of 1,726 adults in treatment for alcoholism, evaluating the two approaches in regards to their prediction of anger and alcohol dependency. Although age-of-onset predicted both outcomes when analyzed alone, these associations fully dissipated once we controlled for aggression and rule-breaking. Such findings suggest that the behavioral sub-types may prove to be a stronger predictor of antisocial behavior outcomes than is age-of-onset. [ABSTRACT FROM AUTHOR]

Objective: Few studies have examined associations between externalizing behaviors and eating disorders in either sex. The current study investigated sex differences in associations between internalizing and externalizing symptoms and disordered eating. Method: A sample of 541 men and women completed self-reported measures of disordered eating (e.g., binge eating), internalizing symptoms (e.g., anxiety), and externalizing behaviors (e.g., delinquency). Hierarchical linear modeling was used to examine sex differences in associations between these symptoms and disordered eating. Results: Internalizing symptoms showed the strongest associations with disordered eating in both sexes. Hyperactivity and aggression were more strongly associated with disordered eating in men, whereas alcohol use was more strongly associated with disordered eating in women. Discussion: Results indicated several sex similarities in associations between internalizing symptoms and disordered eating, but some important sex differences among externalizing behaviors. Externalizing behaviors may play a significant role in the development of disordered eating uniquely within men and women. © 2009 by Wiley Periodicals, Inc. Int J Eat Disord 2010 [ABSTRACT FROM AUTHOR]

Behavioral genetic investigations have consistently demonstrated large genetic influences for the core symptom dimensions of attention-deficit/hyperactivity disorder (ADHD), namely inattention (INATT) and hyperactivity (HYP). Yet little is known regarding potential similarities and differences in the type of genetic influence (i.e., additive vs. nonadditive) on INATTand HYP. As these symptom dimensions form the basis of the current Diagnostic and Statistical Manual of Mental Disorders subtype classification system, evidence of differential genetic influences would have important implications for research investigating causal mechanisms for ADHD. The current meta-analysis aimed to investigate the nature of etiological influences for INATT and HYP by comparing the type and magnitude of genetic and environmental influences each. A comprehensive literature search yielded 79 twin and adoption studies of INATT and/or HYP. Of these, 13 samples of INATT and 9 samples of HYP were retained for analysis. Results indicated that both dimensions were highly heritable (genetic factors accounted for 71% and 73% of the variance in INATT and HYP, respectively). However, the 2 dimensions were distinct as to the type of genetic influence. Dominant genetic effects were significantly larger for INATT than for HYP, whereas additive genetic effects were larger for HYP than for INATT. Estimates of unique environmental effects were small to moderate and shared environmental effects were negligible for both symptom dimensions. The pattern of results generally persisted across several moderating factors, including gender, age, informant, and measurement method. These findings highlight the need for future studies to disambiguate INATT and HYP when investigating the causal mechanisms, and particularly genetic influences, behind ADHD. [ABSTRACT FROM AUTHOR]

Objective: Unlike twin studies of general weight and shape concerns, studies examining the heritability of the undue influence of weight and shape concerns on self-evaluation have found little evidence for genetic effects. The present study sought to resolve these discrepancies by examining the heritability of both types of weight and shape concerns in a young adult twin sample. Method: Participants included 270 female twins from the Michigan State University Twin Registry. General weight and shape concerns were assessed with subscales from the Eating Disorder Examination Questionnaire (EDEQ). Similar to previous research, the undue influence of weight and shape on self-evaluation was assessed using averaged scores from two EDEQ items. Results: The heritability of all weight and shape measures was estimated at 49–66%. Discussion: General weight and shape concerns and the undue influence of these concerns on self-evaluation are influenced by genetic factors in young adult female twins. © 2009 by Wiley Periodicals, Inc. Int J Eat Disord 2010 [ABSTRACT FROM AUTHOR]

As usual, the research published in this issue of the Journal of Child Psychology and Psychiatry contains impressive state-of-the-science studies of child and adolescent psychopathology and related issues. Breeman and colleagues, for example, found that children born before 32 weeks gestation or with a very low birth weight (<1,500 g) were not only more frequently diagnosed with Attention-Deficit Hyperactivity Disorder (ADHD) during childhood, but continued to have an increased risk for attention problems up through early adulthood. [ABSTRACT FROM AUTHOR]