Behavioral genetic research has concluded that the more important environmental influences result in differences between siblings (referred to as nonshared; e2), whereas environmental influences that create similarities between siblings (referred to as shared; c2) are indistinguishable from zero. However, there is mounting evidence that during childhood and adolescence, c2 may make important contributions to most forms of psychopathology. The aim of the meta-analysis was to empirically confirm this hypothesis. The author examined twin and adoption studies (n=490) of internalizing and externalizing psychopathology prior to adulthood. Analyses revealed that c2 accounted for 10%-19% of the variance within conduct disorder, oppositional defiant disorder, anxiety, depression, and broad internalizing and externalizing disorders, regardless of their operationalization. When age, informant, and sex effects were considered, c2 generally ranged from 10%-30% of the variance. Importantly, c2 estimates did not vary across twin and adoption studies, suggesting that these estimates reflect actual environmental influences common to siblings. The only exception was attention-deficit/hyperactivity disorder, which appeared to be largely genetic (and particularly nonadditive genetic) in origin. Conceptual, methodological, and clinical implications of these findings are discussed.

The present study attempted to determine the direction and etiology of the robust relationship between childhood externalizing (EXT) symptoms and parent-child conflict using a genetically informative longitudinal model and data from the ongoing Minnesota Twin Family Study. Participants consisted of 1,506 same-sex twins assessed at ages 11 and 14, and their parents. The relationship between EXT and parent-child conflict from ages 11 to 14 was examined within a biometrical cross-lagged design. The results revealed three primary findings: first, the stability of conflict and externalizing over time is largely, although not solely, a result of genetic factors. Second, there appears to be a bidirectional relationship between conflict and EXT over time, such that both conflict and EXT at 11 independently predict the other 3 years later. Finally, the results are consistent with the notion that parent-child conflict partially results from parental responses to their child's heritable externalizing behavior, while simultaneously contributing to child externalizing via environmental mechanisms. These results suggest a "downward spiral" of interplay between parent-child conflict and EXT, and offer confirmation of a (partially) environmentally mediated effect of parenting on child behavior.Recent research (e.g., Rothbaum & Weisz, 1994;Waschbusch, 2002) has converged in suggesting a robust association, both concurrent and longitudinal, between conflictive/negative parent-child relationships and child and adolescent externalizing disorders, namely attentiondeficit/hyperactivity disorder (ADHD), conduct disorder (CD), and oppositional defiant disorder (ODD). A "parent effects model," in which a conflictual/negative parenting style causes and/or exacerbates child externalizing behavior, has traditionally been cited as responsible for this association (Collins, Maccoby, Steinberg, Hetherington, & Bornstein, 2000;Maccoby, 2000). Supporting this interpretation is the large body of experimental treatment research that has found that improving parents' discipline strategies leads to a reduction in children's externalizing problems (Dishion, Andrews, Kavanagh, & Soberman, 1996;Dishion & Kavanagh, 2000;Forgatch & DeGarmo, 1999;Patterson, 1974;Patterson, Dishion, & Chamberlain, 1993). Furthermore, numerous correlational studies (Campbell, Pierce, Moore, Marakovitz, & Newby, 1996;Gardner, Sonuga-Barke, Sayal, 1999;Loukas, Fitzgerald, Zucker, & von Eye, 2001;Wasserman, Miller, Pinner, & Jaramillo, 1996) have also found evidence of significant effects of poor parenting/negative parent-child relationships on later child externalizing, even when controlling for earlier externalizing.However, some researchers have argued that the association between parent-child conflict and externalizing is not solely parent driven, but may also be instigated by the child, such that the Address correspondence and reprint requests to: Alex Burt, Department of Psychology, Michigan State University, Psychology Building, East Lansing, MI, 48824; E-mail:...

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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 INATT and 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.

Studies suggest that within-person changes in estrogen and progesterone predict changes in binge eating across the menstrual cycle. However, samples have been extremely small (maximum N = 9), and analyses have not examined the interactive effects of hormones that are critical for changes in food intake in animals. The aims of the current study were to examine ovarian hormone interactions in the prediction of within-subject changes in emotional eating in the largest sample of women to date (N = 196). Participants provided daily ratings of emotional eating and saliva samples for hormone measurement for 45 consecutive days. Results confirmed that changes in ovarian hormones predict changes in emotional eating across the menstrual cycle, with a significant estradiol x progesterone interaction. Emotional eating scores were highest during the mid-luteal phase, when progesterone peaks and estradiol demonstrates a secondary peak. Findings extend previous work by highlighting significant interactions between estrogen and progesterone that explain mid-luteal increases in emotional eating. Future work should explore mechanisms (e.g., gene-hormone interactions) that contribute to both within- and between-subject differences in emotional eating.

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.

Parent-child conflict appears to act as a common vulnerability that increases risk for multiple childhood disorders. Furthermore, this association is mediated via common genetic and environmental factors. These findings support the idea that the comorbidity among these disorders partially reflects core psychopathological processes in the family environment that link putatively separate psychiatric disorders.