Search

Background: The current study examines the association of perceived racial and social class discrimination with cannabis involvement among Black youth and young adults., Methods: This secondary analysis used data from the Missouri Family Study (MOFAM), a high-risk longitudinal family study of alcohol use disorder, oversampled for Black families. Offspring (n = 806) and their mothers were interviewed by telephone. Cox proportional hazards regression analyzes were used to examine associations of racial and social class discrimination (experienced by offspring and their mothers) with offspring cannabis involvement. Two stages of cannabis involvement were analyzed: timing of 1) initiation and 2) transition from initiation to first cannabis use disorder (CUD) symptom., Results: The study found that offspring report of experiencing racial (HR: 1.28, CI: 1.01-1.62) and social class discrimination (HR: 1.45, CI: 1.14-1.84) were associated with cannabis initiation in our fully adjusted model. Mothers' report of discrimination predicted a lower hazard of cannabis initiation among offspring (HR: 0.79, CI: 0.64-0.98). Offspring social class discrimination (HR: 2.45, CI: 1.71-3.51) predicted an increased hazard of transition from initiation to first CUD symptom, while offspring racial discrimination (HR: 0.57, CI: 0.39-0.85) was associated with lower hazard of transition in our fully adjusted model., Conclusions: As rates for cannabis use among Black youth are disproportionately rising, there is a critical need to identify pathways to its use among Black youth. These findings suggest racial and social class discrimination may be important targets in efforts to prevent cannabis involvement among Black youth and emerging adults., (Copyright © 2022. Published by Elsevier B.V.)

Background: This study aimed to characterize the associations of racial and socioeconomic discrimination with timing of alcohol initiation and progression from initiation to problem drinking in Black youth., Methods: Data were drawn from a high-risk family study of alcohol use disorder. Mothers and their offspring (N = 806; M age  = 17.87, SD age  = 3.91; 50% female) were assessed via telephone interview. Cox proportional hazards regression analyses were used to examine associations between discrimination and timing of first drink and progression from first drink to problem drinking in two separate models. Predictor variables were considered in a step-wise fashion, starting with offspring racial and socioeconomic discrimination, then adding (2) maternal racial and/or socioeconomic discrimination experiences; (3) religious service attendance and social support as potential moderators; and (4) psychiatric and psychosocial risk factors and other substance use., Results: Offspring racial discrimination (HR: 2.01, CI: 1.17-3.46 ≤ age 13) and maternal experiences of discrimination (HR: 0.79, CI: 0.67-0.93) were associated with timing of initiation in the unadjusted model only; offspring socioeconomic discrimination predicted timing of initiation among female offspring, even after adjusting for all covariates (HR: 1.49, CI: 1.14-1.93). Socioeconomic discrimination predicted a quicker transition from first use to problem drinking exclusively in the unadjusted model (HR: 1.70, CI: 1.12-2.58 ≤ age 18). No moderating effects of religious service attendance or social support were observed for either alcohol outcome., Conclusions: Findings suggest socioeconomic discrimination is a robust risk factor for initiating alcohol use in young Black female youth and should be considered in the development of targeted prevention programs., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Background: Childhood maltreatment is a known risk factor for cannabis initiation and problem use, but the extent to which this association is attributable to shared familial influences is unknown. We estimate the magnitude of associations between childhood maltreatment, timing of cannabis initiation, and cannabis-related problems, in European-American (EA) and African-American (AA) women, and parse the relative influence of additive genetic (A), shared environmental (C), and individual-specific environmental (E) factors on these constructs and their covariation., Methods: Data were from diagnostic telephone interviews conducted with 3786 participants (14.6% AA) in a population-based study of female twins. Logistic regression analyses and twin modeling were used to test for associations, and estimate the relative contributions of genetic and environmental influences to childhood maltreatment and cannabis outcomes and their covariation., Results: Maltreatment was significantly associated with increased likelihood of cannabis initiation before age 15 among EAs (OR=6.33) and AAs (OR=3.93), but with increased likelihood of later initiation among EAs only (OR=1.68). Maltreatment was associated with cannabis problems among both groups (EA OR=2.32; AA OR=2.03). Among EA women, the covariation between maltreatment and cannabis outcomes was primarily attributable to familial environment (rC=0.67-0.70); among AAs, only individual-specific environment contributed (rE=0.37-0.40)., Conclusion: Childhood maltreatment is a major contributor to early initiation of cannabis as well as progression to cannabis problems in both AA and EA women. Distinctions by race/ethnicity are not in the relative contribution of genetic factors, but rather in the type of environmental influences that contribute to stages of cannabis involvement., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Background: Use of cigarettes and cannabis frequently co-occurs. We examine the role of genetic and environmental influences on variation in and covariation between tobacco cigarette and cannabis use across European-American (EA) and African-American (AA) women., Methods: Data on lifetime cannabis and cigarette use were drawn from interviews of 956 AA and 3557 EA young adult female twins and non-twin same sex female full siblings. Twin modeling was used to decompose variance in and covariance between cigarette and cannabis use into additive genetic, shared, special twin and non-shared environmental sources., Results: Cigarette use was more common in EAs (75.3%, 95% C.I. 73.8-76.7%) than AAs (64.2%, 95% C.I. 61.2-67.2%) while cannabis use was marginally more commonly reported by AAs (55.5%, 95% C.I. 52.5-58.8%) than EAs (52.4%, 95% C.I. 50.7-54.0%). Additive genetic factors were responsible for 43-66% of the variance in cigarette and cannabis use. Broad shared environmental factors (shared+special twin) played a more significant role in EA (23-29%) than AA (2-15%) women. In AA women, the influence of non-shared environment was more pronounced (42-45% vs. 11-19% in EA women). There was strong evidence for the same familial influences underlying use of both substances (rA=0.82-0.89; rC+T=0.70-0.75). Non-shared environmental factors were also correlated but less so (rE=0.48-0.66). No racial/ethnic differences were apparent in these sources of covariation., Conclusion: Heritability of cigarette and cannabis use is comparable across racial/ethnic groups. Differences in the contribution of shared and non-shared environmental influences indicate that different factors may shape substance use in EA and AA women., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Introduction: To examine the contribution of trauma exposure to cannabis initiation and transition to first cannabis use disorder (CUD) symptom in African-American (AA) and European-American (EA) emerging adults., Methods: Data are from the Missouri Adolescent Female Twins Study [(N=3787); 14.6% AA; mean age=21.7 (SD 3.8)]. Trauma exposures (e.g. sexual abuse, physical abuse, witnessing another person being killed or injured, experiencing an accident, and experiencing a disaster) were modeled as time-varying predictors of cannabis initiation and transition to CUD symptom using Cox proportional hazards regression. Other substance involvement and psychiatric disorders were considered as time-varying covariates., Results: Analyses revealed different trauma-related and psychiatric predictors for cannabis use supporting racially distinct etiologic models of cannabis involvement. For AA women, history of witnessing injury/death or experiencing a life-threatening accident was associated with cannabis initiation across the complete emerging adult risk period while sexual abuse predicted cannabis initiation only before 15 years old. For EA women, history of sexual or physical abuse and major depressive disorder (MDD) predicted cannabis initiation and physical abuse and MDD predicted transition from initiation to first CUD symptom. No association was discovered between trauma exposures and transition to first CUD symptom in AA women., Conclusions: Results reveal trauma exposures as important contributors to cannabis initiation and to a lesser extent transition to CUD symptom, with different trauma types conferring risk for cannabis involvement in AA and EA women. Findings suggest the importance of considering racial/ethnic differences when developing etiologic models of cannabis involvement., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

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., (Copyright © 2015 Elsevier Ireland Ltd. 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.)

Background: We examined timing of substance involvement as a joint function of parental history of alcoholism and parental separation during childhood., Method: Data were drawn from a large cohort of female like-sex twins [n=613 African Ancestry (AA), n=3550 European or other ancestry (EA)]. Cox proportional hazards regression was conducted predicting age at first use of alcohol, first alcohol intoxication, first use and regular use of cigarettes, and first use of cannabis and other illicit drugs from dummy variables coding for parental alcoholism and parental separation. Propensity score analysis was also conducted comparing intact and separated families by predicted probability of parental separation., Results: In EA families, increased risk of substance involvement was found in both alcoholic and separated families, particularly through ages 10 or 14 years, with risk to offspring from alcoholic separated families further increased. In AA families, associations with parental alcoholism and parental separation were weak and with few exceptions statistically nonsignificant. While propensity score findings confirmed unique risks observed in EA families, intact and separated AA families were poorly matched on risk-factors presumed to predate parental separation, especially parental alcoholism, requiring cautious interpretation of AA survival-analytic findings., Conclusion: For offspring of European ancestry, parental separation predicts early substance involvement that is not explained by parental alcoholism nor associated family background characteristics. Additional research is needed to better characterize risks associated with parental separation in African American families., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

Objective: The objective of this study was to determine whether race/ethnicity was associated with time to smoking initiation and time from first cigarette to onset of DSM-IV nicotine dependence (ND) after adjusting for familial and individual psychosocial risk factors., Methods: Cox proportional hazards models with time-dependent covariates were used to analyze data from 1376 offspring aged 12-33 years from 532 families at high risk for substance use problems due to paternal alcohol problems and 235 low risk families. Fifty-six percent of the sample self-identified as African-American (AA) and 44% were mainly of European descent., Results: Controlling for covariates, AAs began smoking at older ages (HR=0.58; 95% CI: 0.48-0.70) and had longer times between smoking initiation and onset of ND compared to non-AAs (HR=0.25, 95% CI: 0.16-0.39 for ND onset occurring <18 years and HR=0.49, 95% CI: 0.30-0.80 for ND onsets ≥ age 18). After additionally controlling for number of cigarettes smoked daily, the racial/ethnic effects for onset of ND were attenuated, but remained statistically significant for ND onset <18 (HR=0.34, 95% CI: 0.19-0.61); however, the estimate was no longer significant for later ND onset (HR=0.84, 95% CI: 0.50-1.41)., Conclusions: AA adolescents and young adults initiate smoking at older ages and have longer transition periods between initiation and onset of ND compared to non-AAs, even after controlling for many relevant psychiatric and psychosocial covariates; however, racial/ethnic differences in time to onset of nicotine dependence in late adolescence and young adulthood may be explained by differences in daily quantity smoked., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

The objective of this study was to examine the underlying factorial architecture of lifetime DSM-IV alcohol use disorder (AUD) criteria in a population-based sample of adolescent and emerging adult female twins who had ever used alcohol (n=2832; aged 18-25 years), and to determine whether thresholds and factor loadings differed by age. Item response modeling was applied to DSM-IV AUD criteria. Compound criteria (e.g., persistent desire or unsuccessful attempts to quit or cut down) were included as separate items. Of the remaining 16 items, tolerance and use despite physical problems were the most and least commonly endorsed items, respectively. Underlying the items was a single factor representing liability to AUDs. Factor loadings ranged from 0.67 for blackouts to 0.90 for time spent using/recovering from effects. Some items assessing different DSM-IV criteria had very similar measurement characteristics, while others assessing the same criterion showed markedly different thresholds and factor loadings. Compared to that of women aged 21-25 years, the threshold for hazardous use was higher in women aged 18-20 years, but lower for used longer than intended and persistent desire to cut down. After accounting for threshold differences, no variations in discrimination across age groups were observed. In agreement with the extant literature, our findings indicate that the factorial structure of AUD is unidimensional, with no support for the abuse/dependence distinction. Individual components of compound criteria may differ in measurement properties; therefore pooling information from such divergent items will reduce information about the AUD construct., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Background: Previous reports in adults have suggested that the effects experienced after cannabis use can be described in terms of positive and negative subtypes that are heritable and are associated with abuse and dependence. This study extends existing research by inclusion of adolescents and young adults in an offspring of twins design which makes it possible to take into account genetic and environmental risks for substance use disorder., Methods: Data were collected from 725 twin members of the Vietnam Era Twin Registry, 839 of their 12-32 year old biological offspring and 427 mothers. Offspring who had ever used cannabis (n=464) were asked the degree to which they typically experienced 13 subjective effects shortly after using cannabis. Latent class analysis (LCA) was used to derive subjective effect classes and logistic regression models were computed to test associations between subjective effect class and heavy cannabis use, abuse and dependence after adjusting for familial risk and psychopathology and sociodemographics., Results: The best fitting LCA model included 4 classes of responders which were characterized as 'high responders' (39%), 'positive responders' (28%), 'mixed/relaxed' (22%), and 'low responders' (11%). Compared to low responders, members of other classes were heavier users (OR range 3.0-11.8). Compared to mixed/relaxed responders and positive responders, high responders were more likely to have cannabis abuse and dependence., Conclusions: Subjective reactions to cannabis use are associated with use to heavy use, abuse and dependence in adolescents and young adults. This association exists above and beyond the genetic vulnerability for problem cannabis use.

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.

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.