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Maternal smoking during pregnancy (SDP) has been linked to poorer offspring executive function across development, but SDP does not occur independent of other familial risk factors. As such, poor and inconsistent control for potential confounds, notably shared familial (i.e., genetic and environmental) confounds, preclude concluding causal effects of SDP on child outcomes. We examined the within-family association between SDP and one component of executive function, inhibitory control, in a sample of families (N = 173) specifically selected for sibling pairs discordant for exposure to SDP. Thus, the present study examines if the SDP-inhibitory control association withstands rigorous control for potential child and familial confounds. 79% of the variation in child inhibitory control was attributable to within-family differences and 21% was attributable to differences between families, indicating that the variability in inhibitory control was primarily a function of differences between siblings rather than differences across families. Further, the association between SDP and inhibitory control was fully attenuated when confounds were considered. These findings suggest that co-occurring vulnerabilities act as more salient risk factors for poorer child inhibitory control than SDP and may serve as effective targets of interventions seeking to improve children's inhibitory control in families with nicotine dependent mothers.

Background: Findings from family and twin-based studies of Attention Deficit/Hyperactivity Disorder (ADHD) have indicated that inattentive and combined subtypes cluster together among sibling pairs who both express ADHD symptoms. The current report examines the familial clustering of ADHD subtypes, defined according to latent class and DSM-IV criteria, in a general population sample of 2,848 Australian twins, 1,013 of their non-twin siblings and 4,036 female twins from Missouri, USA. Significant clustering of DSM-IV inattentive and combined subtypes, and significant clustering of the same latent classes among siblings was predicted. Method: Logistic regression was used to assess 1) the clustering of same and different subtype combinations among twin and twin-sibling pairs and 2) whether genetic influences contribute significantly to the observed patterns of subtype combinations among siblings. Results: With the exception of the DSM-IV hyperactive-impulsive subtype and the severe hyperactive-impulsive latent class, all other sibling DSM-IV and latent class ADHD subtypes consistently exhibited significant same-subtype clustering with MZ probands, DZ probands and their siblings in both samples. Furthermore, a significant genetic influence contributing to subtype concordance was detected for every DSM-IV subtype excluding hyperactive-impulsive, and for all eight latent classes. While some instances of significant different-subtype clustering among siblings was observed across both classification systems and samples, the particular subtype combinations involved were largely inconsistent across samples and no significant genetic influences contributing towards these discordant subtype combinations were detected. Conclusions: For both DSM-IV and latent class subtypes, the overall pattern of findings in both samples indicated significant familial clustering of same-subtype combinations and significant genetic influences contributing to these patterns of subtype concordance, despite important sample differences. These findings further extend previous work and are most consistent with the presence of multiple independent forms of ADHD.

Background The aims of this study were to (i) characterize racial differences in alcohol involvement and (ii) examine the risk conferred by specific trauma exposures and posttraumatic stress disorder (PTSD) for different stages of alcohol involvement in European American ( EA) and African American ( AA) women. Methods Data are from the Missouri Adolescent Female Twins Study ( N = 3,787, 14.6% AA; mean age at most recent interview = 24.5 [ SD 2.8]). Trauma exposures (e.g., sexual abuse [ SA], physical abuse [ PA], witnessing another person being killed or injured, experiencing an accident, and experiencing a disaster) were modeled as time-varying predictors of alcohol initiation, transition to first alcohol use disorder ( AUD) symptom, and transition to AUD diagnosis using Cox proportional hazards regression while taking into account other substance involvement, parental characteristics, and commonly co-occurring psychiatric disorders. Results In EA women only, SA was associated with alcohol initiation prior to the age of 14, PA predicted transition from initiation to first AUD symptom, and PA, witnessing injury or death, and SA predicted transition to AUD diagnosis. No association was discovered between trauma exposures or PTSD for any stage of alcohol involvement in AA women. Conclusions Results reveal trauma experiences as important contributors to all stages of alcohol involvement in EA women only, with different trauma types conferring risk for each stage of alcohol involvement. PTSD was not revealed as a significant predictor of AUD in EA or AA women, suggesting trauma, independent of PTSD, directly contributes to alcohol involvement. Findings highlight the importance of considering racial differences when developing etiologic models of the association of traumatic experiences with alcohol involvement. [ABSTRACT FROM AUTHOR]

Objective: Despite well-known adverse health effects of maternal smoking during pregnancy (MSP), it is still unclear if MSP varies geographically and if neighborhood socioeconomic deprivation (SED) plays an important role in MSP. This study aims to investigate small-area geographic variation in MSP and examine the association of SED with MSP. Methods: The Missouri Adolescent Female Twin Study (MOAFTS) is a cohort study of female like-sex twins born in Missouri to Missouri-resident parents during 1975–1985. Biological mothers completed a baseline interview in 1995–1998 and reported MSP with the twins. Residential address of the mother at birth was geocoded. We developed a census tract-level SED index using a common factor approach based on 21 area-level socioeconomic variables from the 1980 Census data. Multilevel logistic regressions estimated geographic heterogeneity (random effect) in MSP and the odds ratios (ORs, fixed effects) of neighborhood SED associated with MSP. Results: Of 1658 MOAFTS mothers, 35.2% reported any MSP and 21.9% reported MSP beyond the first trimester. Neighborhood SED was associated with any MSP (the highest vs. the lowest quartile: OR = 1.90, 95% confidence interval [CI] = 1.40–2.57, Ptrend<0.001) and MSP beyond the first trimester (OR = 1.98, 95% CI = 1.38–2.85, Ptrend = 0.002) in unadjusted analyses. After adjusting for individual covariates (demographics, socioeconomic conditions, alcohol use, and parents’ cohabitation), neighborhood SED was not associated with MSP, but geographic variation still persisted in MSP (variance = 0.41, P = 0.003) and in MSP beyond the first trimester (variance = 0.82, P<0.001). Conclusions: Neighborhood SED was associated with MSP in unadjusted analyses but this association could be explained by individual socioeconomic conditions. Nonetheless, significant geographic variation in MSP persisted and was not accounted for by differences in neighborhood SED. To develop effective interventions to reduce MSP, further studies are necessary to explore underlying reasons for its geographic variation. [ABSTRACT FROM AUTHOR]

The Missouri Mothers and Their Children Study (MO-MATCH) was specifically designed to critically investigate prenatal environmental influences on child attention problems and associated learning and cognitive deficits. The project began as a pilot study in 2004 and was formally launched in 2008. Participants in the study were initially identified via the Department of Vital Statistics birth record (BR) database. Interview and lab-based data were obtained from: (1) mothers of Missouri-born children (born 1998–2005), who smoked during one pregnancy but not during another pregnancy; (2) biological fathers when available; and (3) the children (i.e., full sibling pairs discordant for exposure to maternal smoking during pregnancy (SDP). This within-mother, between-pregnancy contrast provides the best possible methodological control for many stable maternal and familial confounding factors (e.g., heritable and socio-demographic characteristics of the mother that predict increased probability of SDP). It also controls for differences between mothers who do and do not smoke during pregnancy, and their partners, that might otherwise artifactually create, or alternatively mask, associations between SDP and child outcomes. Such a design will therefore provide opportunities to determine less biased effect sizes while also allowing us to investigate (on a preliminary basis) the possible contribution of paternal or other second-hand smoke exposure during the pre, peri, and postnatal periods to offspring outcome. This protocol has developed a cohort that can be followed longitudinally through periods typically associated with increased externalizing symptoms and substance used initiation. [ABSTRACT FROM PUBLISHER]

ABSTRACT Objective Purging disorder (PD) was recently included as an otherwise specified feeding or eating disorder (OSFED) in the DSM-5; however, limited information is available on its prevalence, and its etiology is unknown. Method Data from 1,790 monozygotic and 1,440 dizygotic European American female twins (age range = 18-29 years) from the Missouri Adolescent Female Twin Study were used to investigate prevalence and familial influences for PD. A structured clinical interview assessed lifetime DSM-IV criteria for eating disorders and PD. After adjustment for age, twin correlations and biometrical twin models were used to estimate familial (i.e., genetic plus shared environmental) influences on PD. Results One hundred and twenty one (3.77%; 95% CI: 3.14, 4.49) women met criteria for lifetime PD. Twin correlations suggested that genetic, shared environmental, and nonshared environmental factors influenced liability to PD. Nonshared environmental factors accounted for 56% [35%, 79%] of the variance in PD. Although familial effects accounted for a significant proportion of variance (44% [21%, 65%]), it was not possible to disentangle the independent contributions of additive genetic effects (20% [0%, 65%]) and shared environmental effects (24% [0%, 57%]). Discussion PD is a prevalent form of eating pathology. Familial factors are relevant to the development of PD but do not demonstrate the magnitude of heritable factors found for other eating disorders. © 2015 Wiley Periodicals, Inc. (Int J Eat Disord 2015; 48:601-606) [ABSTRACT FROM AUTHOR]

Background Bulimic behaviors (i.e., binge eating and compensatory behaviors) and substance use frequently co-occur. However, the etiology underlying this association is poorly understood. This study evaluated the association between bulimic behaviors and early substance use, controlling for genetic and shared environmental factors. Methods Participants were 3,540 young adult women from the Missouri Adolescent Female Twin Study. A telephone adaptation of the Semi-Structured Assessment for the Genetics of Alcoholism interview assessed DSM- IV bulimic behaviors, substance use, and other psychological characteristics. Lifetime bulimic behaviors were examined in twin pairs concordant and discordant for early substance use. Logistic regressions were adjusted for the nonindependence of twin data, zygosity, age, body mass index, early menarche (onset before age 12), and early sex (first consensual sexual intercourse before age 15). Results In the entire study population, women who reported early use of alcohol or nicotine were more likely to engage in bulimic behaviors after adjusting for covariates. In 53 pairs of monozygotic twins discordant for alcohol experimentation before age 15, the twin who reported early alcohol experimentation had 3.21 (95% confidence interval = 1.54 to 6.67) times higher odds of reporting bulimic behaviors than the cotwin who did not report early alcohol experimentation, even after adjustment for covariates. Conclusions Findings suggest that early alcohol experimentation may contribute to the development of bulimic behaviors via mechanisms extending beyond shared vulnerability, including individual-specific environmental experiences or causal pathways. [ABSTRACT FROM AUTHOR]

Aims (1) To compare affective changes over drinking and non-drinking days among frequent drinkers and (2) to evaluate whether drinkers' expectations influence affective changes and perceived pleasure and relief from drinking. Design Observational study involving ecological momentary assessments collected via electronic diaries during the course of 3 weeks. Setting Drinkers' usual settings in Columbia, MO, USA. Participants A total of 400 adult, frequent drinkers, aged 18-70 years. Measurements Ecological assessments included morning reports, pre-drinking random prompts, user-initiated first-drink reports and device-prompted follow-ups over drinking episodes. Participants rated positive (enthusiastic, excited, happy) and negative (distressed, sad) affect and perceived pleasure and relief from drinking in real time. A self-report questionnaire completed at baseline evaluated expectancies for enhanced sociability and tension reduction from drinking. Findings Relative to affective changes over non-drinking days, positive affect increased prior to drinking [95% confidence interval (CI) = 0.004, 0.023], and at first drink (95% CI = 0.238, 0.317), whereas negative affect decreased prior to drinking (95% CI = − 0.007, 0.000) and at first drink (95% CI = − 0.154, − 0.098). Sociability expectancies augmented increases in positive affect prior to drinking (95% CI = 0.009, 0.027) and at first drink (95% CI = 0.017, 0.169). Sociability expectancies also enhanced perceived pleasure from first drinks (95% CI = 0.046, 0.318). Tension-reduction expectancies attenuated decreases in negative affect at first drink (95% CI = − 0.133, − 0.029), but augmented perceived relief from first drinks (95% CI = 0.001, 0.304). Conclusions Although theoretical models tend to focus on negative affective outcomes of drinking, changes in positive affect prior to drinking and early in drinking episodes are important for maintaining drinking behavior. Frequent drinkers' expectations for enhanced sociability or tension reduction from drinking influence their affective experiences over drinking days and perceptions of pleasure and relief from drinking. [ABSTRACT FROM AUTHOR]

Background Measures of hangover are associated with current and future problematic alcohol use. At present, it is not known whether these associations reflect any direct influence of hangover events on near-term drinking behaviors. The current study aimed to determine whether hangover following a drinking episode influences time to next drink ( TTND) and, if so, to determine the direction of this effect and identify any moderating personal or contextual factors. Methods Community-recruited, frequent drinkers oversampled for current smoking ( N = 386) carried electronic diaries for 21 days, reporting on drinking behaviors and other experiences. Survival analysis was used to model data from 2,276 drinking episodes, including 463 episodes that were followed by self-reported hangover in morning diary entries. Results When tested as the sole predictor in a survival model, hangover was associated with increased TTND. The median survival time was approximately 6 hours longer after episodes with hangovers compared to those without. In a multivariate model, hangover was only significant in the presence of interaction effects involving craving at the end of the index drinking episode and the occurrence of financial stressors. Additional predictors of TTND in the final multivariate model included age, lifetime alcohol use disorder diagnosis, typical drinking frequency, day of the week, and morning reports of craving, negative affect, and stressors after the index episode. There was no association between morning reports of hangover and contemporaneous diary ratings of likelihood of drinking later the same day. Conclusions The findings suggest that hangover has, at best, a modest or inconsistent influence on the timing of subsequent alcohol use among frequent drinkers. [ABSTRACT FROM AUTHOR]

Aspects of disordered eating and personality traits, such as neuroticism, are correlated and individually heritable. We examined the phenotypic correlation between binge eating episodes and indices of personality (neuroticism, extraversion, openness to experience, agreeableness, conscientiousness, and control/impulsivity). For correlations ≥|0.20|, we estimated the extent to which genetic and environmental factors contributed to this correlation. Participants included 3,446 European American same-sex female twins from the Missouri Adolescent Female Twin Study (median age = 22 years). Binge eating episode was assessed via interview questions. Personality traits were assessed by self-report questionnaires. There was a significant moderate phenotypic correlation between binge eating episode and neuroticism (r = 0.33) as well as conscientiousness (r = -0.21), while other correlations were significant but smaller (r ranging from -0.14 to 0.14). Individual differences in binge eating episodes, neuroticism, and conscientiousness were attributed to additive genetic influences (38% [95% CI: 21–53%], 45% [95% CI: 38–52%], and 44% [95% CI: 0.33–0.55%] respectively), with the remaining variance attributed to individual-specific environmental influences. Covariance was attributable to genetic (neuroticism rg = 0.37; conscientiousness rg = -0.22) and individual-specific environmental (neuroticism re = 0.28; conscientiousness re = -0.19) influences. Personality traits may be an early indicator of genetic vulnerability to a variety of pathological behaviors, including binge eating episode. Furthermore, prior research documenting phenotypic correlations between eating disorder diagnoses and personality may have stemmed from etiological overlap between these personality traits and aspects of disordered eating, such as binge eating episode. [ABSTRACT FROM PUBLISHER]

Background Differences in age at initiation of alcohol use and rates of problem drinking between African Americans and European Americans are well documented, but the association between early and problem use-and distinctions by ethnic group in this association-have yet to be examined in a genetically informative framework. Methods Data were derived from a longitudinal study of female twins in Missouri. The sample was composed of 3,532 twins (13.6% African-American [AA], 86.4% European-American [EA]), who participated in the fourth wave of data collection and reported consumption of at least 1 alcoholic drink over the lifetime. Mean age at Wave 4 was 21.7 (range = 18 to 29) years. Twin modeling was conducted to estimate the relative contributions of additive genetic (A), shared environmental (C), and unique environmental (E) factors to variation in age at first drink and problem alcohol use and the cross-phenotype overlap in these influences. Results Early initiation of alcohol use predicted problem use in EA but not AA women. Separate AA and EA twin models produced substantially different estimates (but not statistically different models) of the relative contributions of A and C to problem alcohol use but similar genetic correlations between the phenotypes. Whereas 33% of the variance in the EA model of problem use was attributed to C, no evidence for C was found in the AA model. Heritability estimates for problem alcohol use were 41% in the AA model, 21% in the EA model. Evidence for A and C were found in both AA and EA models of age at first drink, but the A estimate was higher in the EA than AA model (44% vs. 26%). Conclusions Findings are suggestive of distinctions between AA versus EA women in the relative contribution of genetic and environmental influences on the development of problem drinking. [ABSTRACT FROM AUTHOR]

Aim To assess the extent to which the association between childhood sexual abuse ( CSA) and early use of alcohol, cigarettes and cannabis in adolescent girls is mediated by risk factors that tend to cluster in families where CSA occurs. Design An abridged version of the Semi- Structured Assessment for the Genetics of Alcoholism ( SSAGA) was administered by telephone. Participants A total of 3761 female twins aged 18-29 (14.6% African American, 85.4% European American). Measurements CSA experiences and history of substance use were queried in the SSAGA-based interviews. Findings After controlling for familial influences on early substance use by including co-twin early use status in models, separate Cox proportional hazards regression analyses predicting onset of alcohol, cigarette and cannabis use revealed a significant association with CSA. The effect was observed to age 19 years for cigarettes and to age 21 years for cannabis, but was limited to age 14 years or younger for alcohol, with the most pronounced risk before age 10 [hazard ratio ( HR) = 4.59; confidence interval ( CI): 1.96-10.74]. CSA-associated risk for initiation of cigarette and cannabis use was also highest in the youngest age range, but the decline with age was much more gradual and the hazard ratios significantly lower (HR: 1.70; CI: 1.13-2.56 for cigarettes and HR: 2.34, CI: 1.57-3.48 for cannabis). Conclusions Childhood sexual abuse history is a distinct risk factor for use of cigarettes and cannabis, and a very strong predictor of early age at first drink. [ABSTRACT FROM AUTHOR]

ABSTRACT Aims To investigate the relative contribution of genetic and environmental factors on smoking trajectory membership and to test whether individual smoking trajectories represent phenotypical thresholds of increasing genetic risk along a common genetic liability dimension. Design Prospective study of a birth cohort of female like-sex twin pairs. Setting Participants completed diagnostic interview surveys four times from adolescence (average age 16) to young adulthood (average age 25). Participants Female twins who had smoked ≥100 cigarettes life-time ( n = 1466 regular smokers). Measurements Number of cigarettes smoked per day during the heaviest period of smoking (two waves) or during the past 12 months (two waves). Findings A four-trajectory class solution provided the best fit to cigarette consumption data and was characterized by low ( n = 564, 38.47%), moderate ( n = 366, 24.97%) and high-level smokers ( n = 197, 13.44%), and smokers who increased their smoking from adolescence to young adulthood ( n = 339, 23.12%). The best genetic model fit was a three-category model that comprised the low, a combined increasing + moderate and high trajectories. This trajectory categorization was heritable (72.7%), with no evidence for significant contribution from shared environmental factors. Conclusions The way in which smoking patterns develop in adolescence has a high level of heritability. [ABSTRACT FROM AUTHOR]

ABSTRACT Aims To determine the prevalence of past 12-month DSM-5 alcohol use disorders (AUDs), to quantify and characterize individuals who remain stably unaffected or affected and those who 'switch' diagnostically between DSM-IV and DSM-5 classifications. Design Data from the nationally representative wave 2 of the National Epidemiological Survey of Alcohol and Related Conditions (NESARC) collected in 2004-05. Setting General population survey. Participants All surveyed participants ( n = 34 653, aged 21 years and older) and 29 993 individuals reporting life-time alcohol use across both waves of NESARC. Measurements DSM-IV and DSM-5 criteria were coded using proposed guidelines. Findings The prevalence of DSM-5 AUDs was 10.8% with the corresponding prevalence of DSM-IV abuse/dependence being 9.7%, implying a modest 11.3% increase. Those who switched diagnostically from affected to unaffected (19.6% of DSM-IV affected) were most likely to have endorsed hazardous use, due particularly to drinking and driving, while those who transitioned from unaffected to affected (3.3% of DSM-IV unaffected) were primarily DSM-IV diagnostic orphans reporting larger/longer and quit/cut-back. Dropping the legal criterion did not affect the prevalence significantly, while the addition of craving also had a relatively modest impact on prevalence. Conclusion The proposed DSM-5 revisions eliminate successfully individuals diagnosed previously with DSM-IV alcohol abuse due primarily to hazardous use alone and incorporate diagnostic orphans into the diagnostic realm. Definitions of craving and importantly, hazardous use require considerable attention as it is likely that they will contribute to variations in reports of increased prevalence of alcohol use disorders between DSM-IV to DSM-5. [ABSTRACT FROM AUTHOR]

Excessive alcohol consumption contributes to significant morbidity and mortality. Heritable influences contribute to 50% of the variation in alcohol consumption, suggesting the important role of genes. We used data on a previously defined alcohol consumption factor score in a sample of 827 young women to investigate association with 1,014 single-nucleotide polymorphisms in genes related to addiction. Data were drawn from the Missouri Adolescent Female Twin Study (MOAFTS) with replication in the college drinking sample (CDS). Genotypic and phenotypic data were available on 827 MOAFTS and 100 CDS women of European-American ancestry. Data on 1,014 single-nucleotide polymorphisms (SNPs) across 130 genes related to addiction were utilized. Association was conducted in QTDT, which allows for identity-by-descent information to account accurately for twin status in the analysis. The total association variance components model was used, with specification of variance components for relatedness in MOAFTS. The top signals included clusters of SNPs in tryptophan hydroxylase 2 ( TPH2) (e.g., rs1386496, p = 0.0003) and dopa decarboxylase ( DDC) (e.g., rs3779084, p = 0.0008), genes that encode proteins responsible for serotonin synthesis. Additional polymorphisms in ADH1B, ADH1C, ADH7, and ADH1A1 were also associated at p < 0.05. The false discovery rate for the top signal ( p = 0.0003) was 0.15, suggesting nominal significance only. Replication was limited and noted for 2 SNPs in ADH1C. While no results survive the burden of multiple testing, nominal findings in TPH2 and DDC suggest the potential role of the serotonin synthesis pathway in alcohol consumption. [ABSTRACT FROM AUTHOR]

Alcohol and tobacco use often co-occur. Human and animal studies indicate that nicotine increases alcohol's rewarding effects and the motivation to consume it. The aims of this study were to examine whether the factorial architecture of self-reported motivations to consume alcohol differed between regular and nonregular cigarette smokers while taking into account the lifetime history of alcohol dependence and psychopathology, and to estimate the genetic and environmental influences on the motivations. Using data on 2,189 monozygotic and dizygotic female twins, we examined the factorial structure (item thresholds and factor loadings, means, and variances) of the items from the Drinking Motives Questionnaire (DMQ) in regular and nonregular smokers. Post hoc tests examined the association between the latent drinking motives factors and alcohol dependence in both groups. Twin models were fitted to the latent drinking motives factors, testing for variations in the magnitude of additive genetic, shared, and nonshared environmental influences between the groups. The 4 DMQ factors (social, conformity, coping, and enhancement) were recovered in both groups, and their measurement structure was consistent across the groups. Regular smokers reported higher levels of coping, enhancement, and social motives while nonregular smokers reported higher conformity motives. Alcohol dependence was associated with higher scores on all motives in both groups; however, in a regression analysis that included all of the motives as predictor variables, only coping was significantly related to alcohol dependence. While twin models revealed evidence for substantially greater genetic influences on enhancement ( h = 0.40), coping ( h = 0.35) and social ( h = 0.37) drinking motives in regular compared to nonregular smokers, the power to statistically distinguish the 2 groups was low. While the measurement structure of the drinking motive factors appears to be similar across regular and nonregular smokers, regular smokers report more motivation to drink for internal affect-related reasons and to obtain social reward. Of all the motives, coping was the most robust predictor of alcohol dependence in both the regular and the nonregular smokers. Further, genetic influences might play a larger role in drinking motives among regular smokers, which provides tentative evidence for latent genetic × smoking status interactions. [ABSTRACT FROM AUTHOR]

Background: The development of alcohol dependence (AD) involves transitions through multiple stages of drinking behaviors and is shaped by both heritable and environmental influences. We attempted to capture this dynamic process by characterizing genetic and environmental contributions to the rate at which women progressed through 3 significant transitions along the pathway to AD: nonuse to initiation, initiation to onset of first alcohol-related problem, and first problem to onset of AD. Methods: The sample consisted of 3,546 female twins from the Missouri Adolescent Female Twin Study. Participants ranged in age from 18 to 29 years. Retrospective reports of alcohol use histories were collected by telephone diagnostic interview and transition times between drinking milestones were coded ordinally. Standard genetic analyses were conducted in Mx to derive a trivariate model that provided estimates of genetic and environmental influences that were common as well as specific to the 3 transition times. Results: Heritable influences were found for rate of progression across all 3 transitions, accounting for 30 to 47% of the variance in transition times. Shared environmental contributions were evident only in rate of progression from nonuse to initiation (i.e., age at first drink). Heritable contributions to the rate of movement through successive drinking milestones were attributable to a common factor, whereas environmental influences were transition-specific. Conclusions: The current study is unique in its use of a genetically informative design to document the rate of movement between drinking milestones in a female sample and to examine genetic contributions to multiple transition times over the course of AD development. Results indicate that an earlier report of heritability for males in rate of progression from regular drinking to AD generalizes to women and to other alcohol stage transitions. Findings also suggest the need to consider stage-specific environmental contributions to alcohol outcomes in developing interventions. [ABSTRACT FROM AUTHOR]

Objective: Given the controversy surrounding the question of whether there are direct or causal effects of exposure to maternal smoking during pregnancy (SDP) on offspring outcomes such as substance use during the adolescent years, we sought to test, on a preliminary basis, within- and between-family associations of SDP and initiation of substance use early in adolescence (by age 15 years) using a discordant sibling design.Method: We used a sibling-comparison approach in a sample of 173 families drawn from the state of Missouri, wherein mothers were discordant for smoking behaviors between two different pregnancies, to test for associations of SDP and initiation of substance use in a younger adolescent cohort. The discordant sibling comparison approach allows for disentangling familial effects from direct effects of SDP through the purposeful collection of data from siblings within the same family with differential exposure.Results: There were no between- or within-family effects of SDP on initiation of any type of substance use (alcohol, marijuana, smoking, and other drug classes), suggesting that SDP does not exert a direct effect on substance use in early adolescence.Conclusions: Preliminary findings did not support an association of SDP and initiation of substance use in this younger adolescent sample. Studies such as this one can help build a body of evidence to explain whether associations of SDP and adolescent outcomes reflect a direct effect of SPD or may instead be attributable to familial confounders that are controlled in the discordant sibling design. [ABSTRACT FROM AUTHOR]

Objective: Cannabis use, particularly at an early age, has been linked to suicidal thoughts and behavior, but minimal work has examined the association between cannabis use and lifetime nonsuicidal self-injury (NSSI). The current study aims to characterize the overlap between lifetime and early cannabis use and NSSI and to examine genetic and environmental mechanisms of this association.Method: Adult male and female twins from the Australian Twin Registry (N = 9,583) were used to examine the odds of NSSI associated with lifetime cannabis use and early cannabis use (i.e., <17 years of age). These associations were also examined within monozygotic (MZ) twins discordant for cannabis use and MZ twins discordant for early cannabis use. Analyses were replicated in an independent sample of female twins (n = 3,787) accounting for the age at onset of cannabis use and NSSI.Results: Lifetime cannabis use (odds ratio [OR] = 2.84, 95% CI [2.23, 3.61]) and early cannabis use were associated with increased odds of NSSI (OR = 2.15, 95% CI [1.75, 2.65]), and this association remained when accounting for covariates. The association was only significant, however, in MZ twin pairs discordant for early cannabis use (OR = 3.20, 95% CI [1.17, 8.73]). Replication analyses accounting for the temporal ordering of cannabis use and NSSI yielded similar findings of nominal significance.Conclusions: Results suggest that NSSI is associated with cannabis involvement via differing mechanisms. For lifetime cannabis use, the lack of association in discordant pairs suggests the role of shared genes and family environment. However, in addition to such shared familial influences, person-specific and putatively causal factors contribute to the relationship between early cannabis use and NSSI. Therefore, delaying the onset of cannabis use may reduce exposure to influences that exacerbate vulnerabilities to NSSI. [ABSTRACT FROM AUTHOR]

Background: Distinctions in the relative contributions of genetic and environmental factors to initiation of cigarette smoking may explain, in part, the differences between African Americans and European Americans in the prevalence of smoking. The current investigation is the first to compare heritable and environmental influences on smoking initiation between African-American and European-American women.Methods: Data were drawn from Missouri Adolescent Female Twin Study participants and female Missouri Family Study participants (n=4498; 21% African-American, the remainder European-American). Mean ages at first and last assessments were 17.0 (SD=3.5) and 24.0 (SD=3.2), respectively. Twin-sibling modeling was conducted to estimate the proportion of variance in smoking initiation (i.e., ever trying a cigarette) attributable to additive genetic, shared environmental, special twin environmental, and unique environmental factors.Results: Additive genetic influences accounted for approximately half of the variance in smoking initiation in both African-American and European-American women. In the African-American subsample, the remaining variance was attributable primarily to unique environmental factors (46%; 95% CI: 28-71%). In the European-American subsample, only 12% (95% CI: 8-16%) of the variance was attributable to unique environmental factors, with the remainder accounted for by shared environmental (13%; 95% CI: 0-41%) and special twin environmental (24%; 95% CI: 0-52%) factors.Conclusions: The estimated heritability of smoking initiation is substantial and nearly identical for African-American and European-American women, but the type of environmental factors that contribute to risk differ by race/ethnicity. Whereas the primary environmental influences on European-American women's smoking initiation are at the family level, those that impact African-American women's smoking initiation are primarily individual-specific. [ABSTRACT FROM AUTHOR]

Objective: Research indicates that low parental monitoring increases the risk for early substance use. Because low parental monitoring tends to co-occur with other familial and neighborhood factors, the specificity of the association is challenging to establish. Using logistic regression and propensity score analyses, we examined associations between low parental monitoring and early substance use in European American (EA) and African American (AA) girls, controlling for risk factors associated with low parental monitoring.Method: Participants were 3,133 EA and 523 AA girls from the Missouri Adolescent Female Twin Study with data on parental monitoring assessed via self-report questionnaire, and with ages at first use of alcohol, tobacco, and cannabis queried in at least one of three diagnostic interviews (median ages = 15, 22, and 24 years).Results: The rate of early alcohol use was greater in EA than AA girls, whereas the proportion of AA girls reporting low parental monitoring was higher than in EA girls. EA girls who experienced low parental monitoring were at elevated risk for early alcohol, tobacco, and cannabis use, findings supported in both logistic regression and propensity score analyses. Evidence regarding associations between low parental monitoring and risk for early substance use was less definitive for AA girls.Conclusions: Findings highlight the role of parental monitoring in modifying risk for early substance use in EA girls. However, we know little regarding the unique effects, if any, of low parental monitoring on the timing of first substance use in AA girls. [ABSTRACT FROM AUTHOR]

Abstract: Little is known about the relationship between relative body weight and transition from experimentation to regular smoking in young adult women. In the current study, data from 2494 participants in wave 4 of the Missouri Adolescent Female Twin Study (aged 18–29years) who reported ever smoking a cigarette were analyzed using logistic regression. Body mass index (BMI) at time of interview was categorized according to CDC adult guidelines, and regular smoking was defined as having ever smoked 100 or more cigarettes and having smoked at least once a week for two months in a row. Since the OR''s for the overweight and obese groups did not differ significantly from one another in any model tested, these groups were combined. Forty-five percent of women who had ever smoked had become regular smokers. Testing of interactions between potential covariates and levels of the categorical BMI variable revealed a significant interaction between overweight/obesity and childhood sexual abuse (CSA; p<0.001) associated with regular smoking. Among women reporting CSA, the association between overweight/obesity and having become a regular smoker was negative (n=374; OR=0.48, 95% CI: 0.28–0.81). Both underweight and overweight/obesity were positively associated with transition to regular smoking among women who did not report CSA (n=2076; OR=1.57, 95% CI: 1.05–2.35 and OR=1.73, 95% CI: 1.35–2.20, respectively). These results suggest that experiencing CSA alters the association between BMI and regular smoking in women who have experimented with cigarettes. [Copyright &y& Elsevier]

Focuses on a study which evaluated equal environments assumption for mother-reported symptoms of child and adolescent emotional and behavioral problems of female twins in Missouri. Measures and data analyses; Similarity between monozygotic and dizygotic twins; Differences in symptom correlations for twin pairs with greater and lesser environmental similarity; Results of genetic model-fitting; Analysis of findings.

Focuses on a study which examined the difference between two attention-deficit hyperactivity disorder (ADHD) subtyping approaches to the prediction of cognitive function and educational achievement of child and adolescent twins in Missouri. Background on DSM-IV ADHD subtypes; Details of diagnostic assessment; Characteristics of samples; Results of cognitive and educational achievement scores; Discussion on school performance reports.

Background: We tested variation in the timing of child and maternal mortality associated with severe maternal AUD, as represented by recurrent arrests for driving under the influence of alcohol (rDUI).Methods: rDUI mothers (N = 1614) and Controls with no alcohol-related driving offenses (N = 109,928) who gave birth in Missouri from 2000 to 2004 were identified using vital records. Propensity score matching adjusted for birth record measures including delayed prenatal care, smoking during pregnancy, relationship with reproductive partner [married/unmarried, paternity acknowledged/unacknowledged], partner DUI status from driving records, and for socioeconomic characteristics of maternal residential census tract at birth derived from census data. Survival analysis was used to test months from childbirth to child or maternal death as a function of lifetime rDUI status.Results: Maternal rDUIs were associated with a consistently elevated probability of child mortality from birth through child age 17 after propensity score-adjustment (Hazard Ratio [HR] = 1.70, 95 % CI = 1.17-2.47). Maternal mortality was not elevated, relative to Controls, until child age 6-11 (HR = 1.58, 95 % CI = 1.05-2.35) and increased again from child age 12-17 (HR = 4.12, 95 % CI = 3.04-5.86).Conclusions: Severe maternal AUD, as characterized by rDUI, increases the risk for child mortality over that of Controls through age 17. Delays in rDUI maternal mortality until child age 6 may indicate a period when maternal referral for intervention to reduce harm to child and mother is likely to be especially effective. [ABSTRACT FROM AUTHOR]

The objective was to examine the association between maternal smoking during pregnancy (SDP) and (I) severity and (II) directionality of externalizing and internalizing symptoms in a sample of sibling pairs while rigorously controlling for familial confounds. The Missouri Mothers and Their Children Study is a family study (N = 173 families) with sibling pairs (aged 7 to 16 years) who are discordant for exposure to SDP. This sibling comparison study is designed to disentangle the effects of SDP from familial confounds. An SDP severity score was created for each child using a combination of SDP indicators (timing, duration, and amount). Principal component analysis of externalizing and internalizing behavior, assessed with the Child Behavior Checklist and Teacher Report Form, was used to create symptom severity and directionality scores. The variance in severity and directionality scores was primarily a function of differences between siblings (71% and 85%, respectively) rather than differences across families (29% and 15%, respectively). The severity score that combines externalizing and internalizing symptom severity was not associated with SDP. However, a significant within-family effect of SDP on symptom directionality (b = 0.07, p = 0.04) was observed in the sibling comparison model. The positive directionality score indicates that SDP is associated with differentiation of symptoms towards externalizing rather than internalizing symptoms after controlling for familial confounds with a sibling comparison model. This supports a potentially causal relationship between SDP and externalizing behavior.

Introduction: Maternal smoking during pregnancy (SDP) is associated with disruptive behavior. However, there is debate whether the SDP-disruptive behavior association is a potentially causal pathway or rather a spurious effect confounded by shared genetic and environmental factors., Aims and Methods: The Missouri Mothers and Their Children Study is a sibling comparison study that includes families (n = 173) selected for sibling pairs (aged 7-16 years) discordant for SDP. Critically, the sibling comparison design is used to disentangle the effects of SDP from familial confounds on disruptive behavior. An SDP severity score was created for each child using a combination of SDP indicators (timing, duration, and amount of SDP). Multiple informants (parents and teachers) reported on disruptive behavior (i.e., DSM-IV semi-structured interview, the Child Behavior Checklist, and Teacher Report Form)., Results: The variability in disruptive behavior was primarily a function of within-family differences (66%-100%). Consistent with prior genetically informed approaches, the SDP-disruptive behavior association was primarily explained by familial confounds (genetic and environmental). However, when using a multi-rater approach (parents and teachers), results suggest a potentially causal effect of SDP on disruptive behavior (b = 0.09, SE = 0.04, p = 0.03). The potentially causal effect of SDP remained significant in sensitivity analyses., Discussion: These findings suggest that familial confounding likely plays a complex role in the SDP-disruptive behavior association when examining both parent and teacher reports of behavior. Importantly, the current study highlights the importance of multiple raters, reflecting a more comprehensive measure of complex behaviors (e.g., disruptive behavior) to examine the teratogenic effects of SDP., Implications: Our study provides additional evidence that controlling for genetic and family factors is essential when examining the effect of SDP on later behavioral problems, as it explains a portion of the association between SDP and later behavioral problems. However, we found a significant association between SDP and disruptive behavior when using a multi-rater approach that capitalizes on both parent and teacher report, suggesting that parent and teacher ratings capture a unique perspective that is important to consider when examining SDP-behavior associations., (© The Author(s) 2019. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: Studies consistently report a higher prevalence of substance use disorders (SUDs) among women with eating disorders than control women. However, limited research exists on the prevalence of eating disorder symptoms and diagnoses in women with SUDs, especially in community-based populations. We examined the prevalence of eating disorder symptoms and diagnosis by the presence or absence of lifetime alcohol use disorder (AUD) and/or nicotine dependence (ND) in a community-based sample of women., Methods: 3756 women (median age = 22 years) from the Missouri Adolescent Female Twin Study completed a modified semi-structured interview assessing lifetime DSM-IV psychiatric disorders and SUDs. Logistic regression models adjusted for demographic characteristics and other psychopathology, and robust standard errors accounted for the non-independence of twin data., Results: In general, women with comorbid AUD and ND had a higher prevalence of eating disorder symptoms and diagnoses than women with AUD or ND Only, who in turn had a higher prevalence than those without either SUD. After adjustment for covariates, women with AUD and ND had significantly greater risk of broad anorexia nervosa (RRR = 3.17; 99 % CI = 1.35, 7.44), purging disorder (2.59; 1.24, 5.43), and numerous eating disorder symptoms than women with neither disorder. Significant differences emerged between individuals with both AUD and ND versus women with AUD Only or ND Only for some eating disorder symptoms., Conclusions: Women with lifetime AUD or ND diagnoses are at high risk for eating disorder symptoms and diagnoses, underscoring the importance of assessing eating disorder symptoms among women with these disorders., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Objective: The present study updates prior research, incorporating state-level administrative data to examine associations between self-reported history of alcohol dependence and birth record-derived reproductive onset, the latter assessed through peak childbearing years., Method: Participants included 542 African ancestry (AA) and 2,928 European or other ancestry (EA) female twins ascertained through Missouri birth records and recruited as part of a birth cohort study of like-sex female pairs born between 1975 and 1985. Analyses were limited to twins for whom residence in Missouri when of reproductive age could be documented, including twins who left Missouri but later returned. Cox proportional hazards regression models were estimated predicting age at first childbirth from history of alcohol dependence, separately for AA and EA twins, without and with adjustment for sociodemographic characteristics, comorbid psychopathology and other substance involvement, overweight/obesity status, and family-of-origin and childhood risk factors., Results: Among EA twins, alcohol dependence predicted both early and delayed childbearing; in adjusted models, alcohol dependence was associated with overall delayed childbearing. Associations between alcohol dependence and reproductive onset were nonsignificant among AA twins., Conclusions: Findings for EA twins are consistent with the broader literature indicating increased risk of teen motherhood associated with early-onset and problem drinking, but suggest that this may be explained by other correlated risk factors. The more robust finding, confirming relatively recent research, is of delayed childbearing associated with alcohol dependence.

Aims: To assess whether having multiple convictions for driving while under the influence of alcohol (MDUI) in women is a risk factor for maternal, infant and child mortality., Design: Retrospective cohort design using record linkage, comparing women with MDUI convictions with propensity-matched women without alcohol-related driving offences ascertained through state records, on rates of maternal, infant and child mortality., Setting: Missouri, United States., Participants: MDUI women (n = 1658) and women with no alcohol-related driving convictions (control, n = 184 252) who gave birth from 2000 to 2004., Measurements: Data were obtained from state administrative records and US Census data. The outcomes were maternal, infant and child mortality. The input variable was presence or absence of MDUI convictions. Propensity-matching variables were maternal (smoking during pregnancy, delayed prenatal care, previous child deaths, age at birth, mother Missouri-born, education, pre-pregnancy obesity, marital status), reproductive partner (un-named partner, race/ethnicity, education, DUI status) and census tract (socio-economic advantage, urbanicity) characteristics., Findings: Women with MDUI convictions had higher odds of maternal, infant and child mortality than propensity-matched controls [odds ratio (OR) = 2.65, 95% confidence interval (CI) = 2.07-3.40 and OR = 1.75, 95% CI = 1.17-2.61, respectively]., Conclusions: Having multiple convictions for driving under the influence of alcohol in women appears to be a risk factor for increased maternal, infant and child mortality., (© 2019 Society for the Study of Addiction.)

The current investigation assessed for moderating effects of childhood trauma on genetic and environmental contributions to timing of alcohol use initiation and alcohol use disorder in African American (AA) and European American (EA) women. Data were drawn from diagnostic telephone interviews conducted with 3786 participants (14.6% AA) in a longitudinal female twin study. Childhood trauma was defined alternately as child maltreatment and more broadly to include other events (e.g., witnessing violence). Phenotypic associations between childhood trauma and alcohol outcomes were estimated using logistic regression analyses. Twin modeling was conducted to test for moderating effects of childhood trauma on the contributions of genetic and environmental factors to timing of initiation and alcohol use disorder. Under both definitions, childhood trauma was associated with early initiation (relative risk ratios: 1.90, 1.72) and alcohol use disorder (odds ratios: 1.92, 1.76). Yet gene by environment effects were observed only for child maltreatment and timing of initiation in EA women, with heritable influences less prominent in those who had experienced child maltreatment (0.35, 95% CI: 0.05-0.66 vs. 0.52, 95% CI: 0.30-0.73). We found more similarities than differences in the association of childhood trauma with alcohol outcomes across racial/ethnic groups, trauma type, and stages of alcohol use. However, findings suggest that the relative contribution of genetic factors to alcohol outcomes differs by childhood maltreatment history in EA women specifically in the earliest stage of alcohol use.

Objective: The aim of the current study was to determine whether the higher rates of childhood sexual abuse (CSA) but lower rates of cigarette smoking in African-American vs. European-American women can be explained in part by a lower magnitude of association between CSA and smoking in African-American women., Methods: Data were drawn from a same-sex female twin study of substance use (n=3521; 14.3% African-American). Cox proportional hazards regression analyses using CSA to predict smoking initiation and progression to regular smoking were conducted separately by race/ethnicity. Co-twin status on the smoking outcome was used to adjust for familial influences on smoking (which may overlap with family-level influences on CSA exposure)., Results: After adjusting for co-twin status, CSA was associated with smoking initiation in European Americans (hazard ratio (HR)=1.43, 95% confidence intervals (CI): 1.26-1.62) and with smoking initiation ≤16 in African Americans (HR=1.70, CI: 1.26-2.29). CSA was associated with regular smoking onset ≤15 in European Americans (HR=1.63, CI: 1.21-2.18), with no change in HR after adjusting for co-twin status. In the African-American subsample, the HR for CSA was reduced to non-significance after adjusting for co-twin status (from HR=3.30, CI: 1.23-8.89 to HR=1.16, CI: 0.71-1.92 for regular smoking ≤15)., Conclusions: CSA is associated with moderate elevation in risk for initiating smoking among African-American and European-American women. By contrast, CSA is associated with elevated risk for (adolescent onset) regular smoking only in European-American women. Furthermore, there is significant overlap between risk conferred by CSA and familial influences on regular smoking in African-American but not European-American women., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

The goal of the current study was to examine whether the magnitude of the association between childhood physical abuse (CPA) and alcohol use disorder (AUD) varies by type of CPA assessment and race of the respondents. Data are from the Missouri adolescent female twins study and the Missouri family study (N = 4508) where 21.2% identified as African American (AA) and 78.8% as European American (EA); mean age = 23.8. Data were collected using a structured comprehensive interview which assessed CPA experiences using behavioral questions about specific abusive behaviors and trauma checklist items. Cox proportional hazards regression analyses were conducted, adjusting for additional risk factors associated with AUD, including co-occurring psychiatric disorders (defined as time-varying) and parental alcohol misuse. Overall, CPA reporting patterns were highly correlated (tetrachoric ρ = 0.73); although, only 25.8% of women who endorsed behaviorally defined CPA also endorsed checklist items whereas 72.2% of women who endorsed checklist items also endorsed behavioral questions. Racial disparities were evident, with behaviorally defined CPA increasing the hazard for AUD in EA but not AA women. Additional racial disparities in the risk for AUD were observed: increased hazard for AUD were associated with major depressive disorder in AA, and cannabis dependence and paternal alcohol problems in EA, women. Results demonstrate the relevance of the type of CPA measure in assessing CPA in studies of alcohol-related problems-behavioral items may be more inclusive of CPA exposure and more predictive of AUD- and highlight racial distinctions of AUD etiology in women. (PsycINFO Database Record, ((c) 2016 APA, all rights reserved).)

Background: Despite substantial evidence that alcohol use disorder (AUD) and bulimic behaviors (i.e., binge eating and compensatory behaviors) co-occur, insufficient information exists regarding a possible shared etiology. Moreover, although numerous twin studies of European ancestry individuals have reported moderate heritability estimates for AUD and bulimic behaviors, with little evidence for shared environmental factors, research on genetic and environmental risk in African American (AA) individuals is lacking., Methods: We investigated specific and overlapping genetic and environmental influences on AUD and bulimic behaviors in 3232 European American (EA; 55.38% monozygotic) and 549 AA (42.81% monozygotic) young adult female twins from the Missouri Adolescent Female Twin Study (age range=18-29 years). A structured clinical interview assessed lifetime DSM-5 AUD (minus craving) and bulimic behaviors. Biometrical twin modeling was conducted to generate age-adjusted estimates of genetic and environmental influences on AUD, bulimic behaviors, and their comorbidity., Results: Estimates of genetic and environmental contributions on AUD and bulimic behaviors could be equated across EA and AA women. Additive genetic effects accounted for 59% (95% CI: 50%, 66%) and 43% (33%, 52%) of the variance in AUD and bulimic behaviors, respectively, with the remainder due to non-shared environmental effects. Shared genetic factors (rg=.33 (.18, .49)) were solely responsible for the correlation between phenotypes; the non-shared environmental correlation was not significant (re=.10 (-.05, .25))., Conclusions: Findings indicate similar magnitudes of genetic and environmental effects on AUD and bulimic behaviors for EA and AA women and implicate common genetic mechanisms underlying liability to these problem behaviors., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

The objective of this study was to examine interrelationships between child maltreatment, post-traumatic stress disorder (PTSD) and body mass index (BMI) in young women. We used multinomial logistic regression models to explore the possibility that PTSD statistically mediates or moderates the association between BMI category and self-reported childhood sexual abuse (CSA), physical abuse (CPA), or neglect among 3,699 young women participating in a population-based twin study. Obese women had the highest prevalence of CSA, CPA, neglect, and PTSD (p<.001 for all). Although all three forms of child maltreatment were significantly, positively associated with overweight and obesity in unadjusted models, only CSA was significantly associated with obesity after adjusting for other forms of maltreatment and covariates (OR=2.21, 95% CI: 1.63, 3.00). CSA and neglect, but not CPA, were associated with underweight in unadjusted models; however, after adjusting for other forms of maltreatment and covariates, the associations were no longer statistically significant (OR=1.43, 95% CI: 0.90-2.28 and OR=2.16, 95% CI: 0.90-5.16 for CSA and neglect, respectively). Further adjustment for PTSD generally resulted in modest attenuation of effects across associations of child maltreatment forms with BMI categories, suggesting that PTSD may, at most, be only a weak partial mediator of these associations. Future longitudinal studies are needed to elucidate the mechanisms linking CSA and obesity and to further evaluate the role of PTSD in associations between child maltreatment and obesity., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Objective: Although prior studies have demonstrated that depression is associated with an overeating-binge eating dimension (OE-BE) phenotypically, little research has investigated whether familial factors contribute to the co-occurrence of these phenotypes, especially in community samples with multiple racial/ethnic groups. We examined the extent to which familial (i.e., genetic and shared environmental) influences overlapped between Major Depressive Disorder (MDD) and OE-BE in a population-based sample and whether these influences were similar across racial/ethnic groups., Method: Participants included 3,226 European American (EA) and 550 African American (AA) young adult women from the Missouri Adolescent Female Twin Study. An adaptation of the Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA) was administered to assess lifetime DSM-IV MDD and OE-BE. Quantitative genetic modeling was used to estimate familial influences between both phenotypes; all models controlled for age., Results: The best-fitting model, which combined racial/ethnic groups, found that additive genetic influences accounted for 44% (95% CI: 34%, 53%) of the MDD variance and 40% (25%, 54%) for OE-BE, with the remaining variances due to non-shared environmental influences. Genetic overlap was substantial (rg  = .61 [.39, .85]); non-shared environmental influences on MDD and OE-BE overlapped weakly (re  = .26 [.09, .42])., Discussion: Results suggest that common familial influences underlie MDD and OE-BE, and the magnitude of familial influences contributing to the comorbidity between MDD and OE-BE is similar between EA and AA women. If racial/ethnic differences truly exist, then larger sample sizes may be needed to fully elucidate familial risk for comorbid MDD and OE-BE across these groups., (© 2014 Wiley Periodicals, Inc.)

It is unknown whether there are racial differences in the heritability of major depressive disorder (MDD) because most psychiatric genetic studies have been conducted in samples comprised largely of white non-Hispanics. To examine potential differences between African-American (AA) and European-American (EA) young adult women in (1) Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV) MDD prevalence, symptomatology, and risk factors, and (2) genetic and/or environmental liability to MDD, we analyzed data from a large population-representative sample of twins ascertained from birth records (n = 550 AA and n = 3226 EA female twins) aged 18-28 years at the time of MDD assessment by semi-structured psychiatric interview. AA women were more likely to have MDD risk factors; however, there were no significant differences in lifetime MDD prevalence between AA and EA women after adjusting for covariates (odds ratio = 0.88, 95% confidence interval [CI]: 0.67-1.15). Most MDD risk factors identified among AA women were also associated with MDD at similar magnitudes among EA women. Although the MDD heritability point estimate was higher among AA women than EA women in a model with paths estimated separately by race (56%, 95% CI: 29-78% vs. 41%, 95% CI: 29-52%), the best fitting model was one in which additive genetic and non-shared environmental paths for AA and EA women were constrained to be equal (A = 43%, 33-53% and E = 57%, 47-67%). In spite of a marked elevation in the prevalence of environmental risk exposures related to MDD among AA women, there were no significant differences in lifetime prevalence or heritability of MDD between AA and EA young women.

The aim of the current study was to test the independent and joint contributions of 8 different types of trauma to posttraumatic stress disorder (PTSD) risk using data from a young adult female cohort. Associations of traumatic events with PTSD onset were examined using Cox proportional hazards models. Differences in risk as a function of age at trauma were tested. Childhood sexual assault, physical abuse, and neglect were stronger predictors of PTSD onset than adolescent and early adult occurrence of these events in individual models. In a model including all traumatic events, differential risk by age remained for sexual assault and physical abuse. Early sexual assault was the strongest predictor of risk, but additional traumatic events increased risk even in its presence.

Genetic and environmental contributions to the observed correlations among DSM-IV ADHD problems [inattentive (INATT) and hyperactive/impulsive (HYP/IMP) behaviors], conduct problems (CDP) and alcohol problems (AlcProb) were examined by fitting multivariate structural equation models to data from the Missouri Adolescent Female Twin Study [N=2892 twins (831 monozygotic pairs, 615 dizygotic pairs)]. Based on results of preliminary regression models, we modified the structural model to jointly estimate (i) the regression of each phenotype on significant familial/prenatal predictors, and (ii) genetic and environmental contributions to the residual variance and covariance. Results suggested that (i) parental risk factors, such as parental alcohol dependence and regular smoking, increase risk for externalizing behavior; (ii) prenatal exposures predicted increased symptomatology for HYP/IMP (smoking during pregnancy), INATT and CDP (prenatal alcohol exposure); (iii) after adjusting for measured familial/prenatal risk factors, genetic influences were significant for HYP/IMP, INATT, and CDP; however, similar to earlier reports, genetic effects on alcohol dependence symptoms were negligible; and (iv) in adolescence, correlated liabilities for conduct and alcohol problems are found in environmental factors common to both phenotypes, while covariation among impulsivity, inattention, and conduct problems is primarily due to genetic influences common to these three behaviors. Thus, while a variety of adolescent problem behaviors are significantly correlated, the structure of that association may differ as a function of phenotype (e.g., comorbid HYP/IMP and CDP vs. comorbid CDP and AlcProb), a finding that could inform different approaches to treatment and prevention.

The risks associated with early age at initiation for alcohol, cigarette, and cannabis use are well documented, yet the timing of first use has rarely been studied in genetically informative frameworks, leaving the relative contributions of genetic and environmental factors to age at initiation largely unknown. The current study assessed overlap in heritable and environmental influences on the timing of initiation across these three substances in African-American women, using a sample of 462 female twins (100 monozygotic and 131 dizygotic pairs) from the Missouri Adolescent Female Twin Study. Mean age at the time of interview was 25.1 years. Ages at first use of alcohol, cigarettes, and cannabis were gathered in diagnostic interviews administered over the telephone. Standard genetic analyses were conducted with substance use initiation variables categorized as never, late, and early onset. Variance in the timing of first use was attributable in large part to genetic sources: 44% for alcohol, 62% for cigarettes, and 77% for cannabis. Genetic correlations across substances ranged from 0.25 to 0.70. Shared environmental influences were modest for alcohol (10%) and absent for cigarettes and cannabis. Findings contrast with reports from earlier studies based on primarily Caucasian samples, which have suggested a substantial role for shared environment on substance use initiation when measured as lifetime use. By characterizing onset as timing of first use, we may be tapping a separate construct. Differences in findings may also reflect a distinct etiological pathway for substance use initiation in African-American women that could not be detected in previous studies.

The objective of this study was to determine the genetic and environmental contributions to variation in BMI over time in European-American (EA) and African-American (AA) adolescent and young adult women. Self-reported BMI (kg/m(2)) data from 2,816 EA (1,306 twin pairs, 56.5% monozygotic (MZ)) and 404 AA (178 twin pairs, 42.7% MZ) women at baseline (T1; median age 15 years) and 3,225 EA (1,511 twin pairs, 55.3% MZ) and 539 AA (252 pairs, 43.3% MZ) women at follow-up (T2; median age 22 years) from a Midwestern US, population-based twin registry were used to construct biometrical genetic models. For EA women, the majority of the variance in BMI was attributable to additive genetic effects at both time points (82% for each), with the remaining variance attributable to nonshared environment. Genetic and nonshared environment correlations between adolescent and young adult BMI were 0.87 and 0.23, respectively. Among AA women, nonadditive genetic effects comprised 68% of the variance at T1 and 73% at T2, and were highly correlated (r(D) = 0.94). The proportions of variance attributable to nonshared environment at T1 (29%) and T2 (25%) were more modestly correlated (r(E) = 0.31). The remaining variance in AA women could be attributed to additive genetic effects. Additive vs. nonadditive genetic effects contribute differentially to BMI in AA vs. EA adolescent and young adult women. Additional research is needed to better characterize the environmental and genetic factors related to BMI in persons of different races to aid understanding of the complex determinants of body weight in individuals.

The human distal gut harbours a vast ensemble of microbes (the microbiota) that provide important metabolic capabilities, including the ability to extract energy from otherwise indigestible dietary polysaccharides. Studies of a few unrelated, healthy adults have revealed substantial diversity in their gut communities, as measured by sequencing 16S rRNA genes, yet how this diversity relates to function and to the rest of the genes in the collective genomes of the microbiota (the gut microbiome) remains obscure. Studies of lean and obese mice suggest that the gut microbiota affects energy balance by influencing the efficiency of calorie harvest from the diet, and how this harvested energy is used and stored. Here we characterize the faecal microbial communities of adult female monozygotic and dizygotic twin pairs concordant for leanness or obesity, and their mothers, to address how host genotype, environmental exposure and host adiposity influence the gut microbiome. Analysis of 154 individuals yielded 9,920 near full-length and 1,937,461 partial bacterial 16S rRNA sequences, plus 2.14 gigabases from their microbiomes. The results reveal that the human gut microbiome is shared among family members, but that each person's gut microbial community varies in the specific bacterial lineages present, with a comparable degree of co-variation between adult monozygotic and dizygotic twin pairs. However, there was a wide array of shared microbial genes among sampled individuals, comprising an extensive, identifiable 'core microbiome' at the gene, rather than at the organismal lineage, level. Obesity is associated with phylum-level changes in the microbiota, reduced bacterial diversity and altered representation of bacterial genes and metabolic pathways. These results demonstrate that a diversity of organismal assemblages can nonetheless yield a core microbiome at a functional level, and that deviations from this core are associated with different physiological states (obese compared with lean).

Background: While there is substantial support in the literature for an increased prevalence of cannabis use in cigarette smokers, emerging studies allude to the possibility that cannabis users may, in turn, be at significantly elevated risk for rapid transitions in their cigarette smoking trajectories. If there is evidence in its favor, the increased rates of cigarette smoking in cannabis users may prove to be the most significant public health problem associated with cannabis use., Methods: In a sample of 3787 female twins (age range 18-29 years), we examined, using discrete-time survival analyses, whether women who reported cannabis use were at increased risk for regular cigarette smoking and progression to nicotine dependence., Results: After controlling for a large number of potential covariates, we found that women who used cannabis were at 4.4 and 2.8 increased hazards for transitioning from initiation to regular smoking and from regular smoking to nicotine dependence, respectively., Conclusions: Cannabis use is associated with transitions to more involved stages of cigarette smoking in women. This is a source of public health concern, first due to the high mortality associated with cigarette smoking and second, due to the high prevalence of cannabis use in the general population.

Background: Previous studies have reported that the current DSM-IV eating disorder (ED) criteria do not adequately describe ED symptomatology. The objective of the current study was to examine the clustering of ED symptoms in a general population sample using latent class analysis (LCA)., Method: ED symptoms from 3723 female young adult twins (mean age 22) were analyzed using LCA, and resulting classes were compared on external validators reflecting ED and other co-morbid psychiatric diagnoses, substance use disorders (SUDs), and suicidality., Results: The optimal solution consisted of five latent classes characterized as: (1) Unaffected; (2) Low Weight Gain; (3) Weight Concerned; (4) Dieters; and (5) ED. Members of the ED class had significantly higher prevalence of co-morbid psychiatric disorders, SUDs, and suicidality than the Unaffected and Low Weight Gain classes, and elevated rates of suicidality and major depression compared to the Weight Concerned and Dieter classes, which differed from each other primarily in terms of current body mass index (BMI). Dieter class members were more likely to be overweight and obese and less likely to be underweight than Weight Concerned class members. The majority of women with an ED diagnosis were assigned to the ED class, and few differences were found between ED class members with and without an ED diagnosis., Conclusions: The results add to the evidence that many women with significant ED psychopathology are not being identified by the DSM-IV ED categories.

Childhood sexual abuse (CSA) has been associated with increased risk for alcohol dependence (AD), but the extent to which CSA history may impact transitions in the course of AD development remains unclear. The current study examined the role of CSA in initiation of alcohol use and rate of progression from first drink to AD using a sample of 3536 female twins (mean age=21.6 years). Psychiatric diagnoses and alcohol use histories were obtained via telephone interviews using an adaptation of the SSAGA. The contribution of CSA to alcohol outcomes independent of familial influences was estimated by using co-twin AD status to adjust for familial liability to AD. CSA was associated with higher rates of both lifetime alcohol use and AD, but CSA-associated risk for consumption of first alcoholic drink was evident only at ages 12 and 13. Rate of transition from first alcohol use to AD did not differ by CSA status. Findings indicate that CSA and elevated risk for AD may be linked via early age at first drink and that progression from first drink to AD follows a similar course among women with and without histories of CSA.

Objective: Cannabis is the most commonly used illicit drug in developed nations. In adolescent girls especially, rates of cannabis use have increased over the last decade, urging the need to characterize the potential correlates of onset of cannabis use during emerging adulthood., Method: Using data from 1065 females (collected 1994-2005) who participated in both the baseline and follow-up wave of interviews of the Missouri Adolescent Female Twin Study, we examined the associations between correlates from the peer, parental and individual domains and new onsets of cannabis use, using logistic regression., Results: Univariate models revealed that initiation of cannabis use was associated with alcohol and cigarette use at baseline, peer attitude towards alcohol/cigarette/cannabis use, peer substance use and other aspects of impulse-disinhibited behavior. However, multivariate stepwise modeling retained only the significant influences of alcohol use at baseline and peer attitudes towards cannabis as correlates of cannabis initiation., Conclusion: Having peers with favorable attitudes towards alcohol, cigarette and cannabis use is an important correlate of initiation of cannabis use in women. Prevention and intervention efforts need to take this into account when developing drug resistance training programs for adolescents.

Objective: We investigated whether use and early-onset use of cigarettes, alcohol and cannabis contributed an increase in risk for initiation of subsequent psychoactive substances in women (N = 3729, mean age = 21.7)., Methods: Drugs were ordered in ascending order of initiation: cigarettes, alcohol, cannabis and other illicit drugs, with early-onset use of each drug used as a time-varying covariate to predict initiation of subsequent drugs. Interactions of use and early-onset use, with age of initiation of subsequent drugs, were evaluated using discrete-time Cox survival analyses., Results: The association between each substance and the early-onset of subsequent drug use was strong (ORs 1.54-19.9). Women who initiated cigarette, alcohol or cannabis use at an early age were at elevated risk for early experimentation with each subsequent drug class. Furthermore, early-onset of more than one substance contributed greater risk for initiation of subsequent drugs., Conclusion: Prevention efforts should target risk factors that contribute to early initiation of cigarette and alcohol use and may subsequently correlate with hard drug involvement.