Childhood interpersonal violence and adult alcohol, cannabis, and tobacco use disorders: variation by race/ethnicity?

Meyers, Jacquelyn L.; Sartor, Carolyn E.; Werner, Karel; Koenen, Karestan C.; Grant, Bridget F.; Hasin, Deborah S.

doi:10.1017/s0033291717003208

Cited by 25 publications

(21 citation statements)

References 61 publications

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“…Early trauma [14] and later traumatic life events [15] have been associated with an increased likelihood of cannabis use. Independent contributions of childhood physical and sexual abuse to cannabis use were observed with no effect of witnessing parental violence [16]. Moreover, it has also been shown that childhood trauma predicts the transition from cannabis initiation to cannabis use disorder [17].…”

Section: Introductionmentioning

confidence: 95%

The interplay between childhood trauma, cognitive biases, and cannabis use on the risk of psychosis in nonclinical young adults in Poland

et al. 2020

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Background. Childhood traumatic events are risk factors for psychotic-like experiences (PLEs). However, the mechanisms explaining how trauma may contribute to the development of PLEs are not fully understood. In our study, we investigated whether cannabis use and cognitive biases mediate the relationship between early trauma and PLEs. Methods. A total sample of 6,772 young adults (age 26.6 ± 4.7, 2,181 male and 3,433 female) was recruited from the general population to participate in an online survey. We excluded 1,158 individuals due to a self-reported lifetime diagnosis of any mental disorder. The online survey included selected items from the following questionnaires: Traumatic Experience Checklist (TEC, 3 items), Childhood Experience of Care and Abuse Questionnaire (CECA.Q, 3 items), Cannabis Problems Questionnaire (CPQ, 10 items), Davos Assessment of Cognitive Biases Scale (DACOBS-18, 9 items), and Prodromal Questionnaire-16 (PQ-16). Mediation analyses were performed with respect to different categories of traumatic experiences (emotional, physical and sexual abuse as well as emotional neglect). Results. Our results showed significant associations of any time of childhood trauma with higher scores of cannabis use (CPQ), cognitive biases (DACOBS), and PLEs (PQ-16) (p < 0.001). We found a direct effect of childhood trauma on PLEs as well as significant indirect effect mediated through cannabis use and cognitive biases. All models tested for the effects of specific childhood adversities revealed similar results. The percentage of variance in PQ-16 scores explained by serial mediation models varied between 32.8 and 34.2% depending on childhood trauma category. Conclusion. Cannabis use and cognitive biases play an important mediating role in the relationship between childhood traumatic events and the development of PLEs in a nonclinical young adult population.

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Section: Introductionmentioning

confidence: 95%

The interplay between childhood trauma, cognitive biases, and cannabis use on the risk of psychosis in nonclinical young adults in Poland

et al. 2020

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“…In contrast, contextual triggering 5 was used to describe a detrimental environment combining with a genetic predisposition toward a negative outcome. For example, adverse experiences have been shown to exacerbate genetic influences on substance use and disorders 18–20 , including CUD 17,21,22 . We note that even the association of Alcohol Dehydrogenase 1B (Class I), Beta Polypeptide ( ADH1B )-rs1229984 with alcohol use/problems, and Cholinergic Receptor Nicotinic Alpha 5 Subunit ( CHRNA5 )-rs16969968 with cigarette smoking, two of the most robust and replicable genetic effects in the substance use literature, have been found to differ as a function of trauma exposure 13,23,24 .…”

Section: Introductionmentioning

confidence: 99%

Psychosocial moderation of polygenic risk for cannabis involvement: the role of trauma exposure and frequency of religious service attendance

et al. 2019

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Cannabis use and disorders (CUD) are influenced by multiple genetic variants of small effect and by the psychosocial environment. However, this information has not been effectively incorporated into studies of gene–environment interaction (GxE). Polygenic risk scores (PRS) that aggregate the effects of genetic variants can aid in identifying the links between genetic risk and psychosocial factors. Using data from the Pasman et al. GWAS of cannabis use (meta-analysis of data from the International Cannabis Consortium and UK Biobank), we constructed PRS in the Collaborative Study on the Genetics of Alcoholism (COGA) participants of European (N: 7591) and African (N: 3359) ancestry. The primary analyses included only individuals of European ancestry, reflecting the ancestral composition of the discovery GWAS from which the PRS was derived. Secondary analyses included the African ancestry sample. Associations of PRS with cannabis use and DSM-5 CUD symptom count (CUDsx) and interactions with trauma exposure and frequency of religious service attendance were examined. Models were adjusted for sex, birth cohort, genotype array, and ancestry. Robustness models were adjusted for cross-term interactions. Higher PRS were associated with a greater likelihood of cannabis use and with CUDsx among participants of European ancestry (p < 0.05 and p < 0.1 thresholds, respectively). PRS only influenced cannabis use among those exposed to trauma (R2: 0.011 among the trauma exposed vs. R2: 0.002 in unexposed). PRS less consistently influenced cannabis use among those who attend religious services less frequently; PRS × religious service attendance effects were attenuated when cross-term interactions with ancestry and sex were included in the model. Polygenic liability to cannabis use was related to cannabis use and, less robustly, progression to symptoms of CUD. This study provides the first evidence of PRS × trauma for cannabis use and demonstrates that ignoring important aspects of the psychosocial environment may mask genetic influences on polygenic traits.

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“…Given that the majority of previous genetic association studies and G × E research has focused on European Americans (Dick et al, 2017; Popejoy & Fullerton, 2016), little is known about G × E in relation to alcohol use problems in other groups such as African Americans (Chartier, Karriker-Jaffe, Cummings, & Kendler, 2017). Given differences in rates of alcohol use and related consequences across racial/ethnic groups (Chartier & Caetano, 2010; Mulia, Greenfield, & Zemore, 2009), as well as potential racial/ethnic differences in pathways of risk to alcohol and related problems (Akins, Smith, & Moshe, 2010; Meyers et al, 2018), it is important to study G × E processes that impact risk for alcohol use disorders in all racial groups so that all can benefit from the research and intervention/prevention efforts. This also aligns with a cultural genomics approach by examining the interplay of genes and environments across and within different cultural groups (Causadias & Korous, 2018).…”

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confidence: 99%

Examining interactions between genetic risk for alcohol problems, peer deviance, and interpersonal traumatic events on trajectories of alcohol use disorder symptoms among African American college students

Kuo

Meyers

et al. 2018

Dev Psychopathol

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Numerous studies have demonstrated that genetic and environmental factors interact to influence alcohol problems. Yet prior research has primarily focused on samples of European descent and little is known about gene-environment interactions in relation to alcohol problems in non-European populations. In this study, we examined whether and how genetic risk for alcohol problems and peer deviance and interpersonal traumatic events independently and interactively influence trajectories of alcohol use disorder symptoms in a sample of African American students across the college years (N = 1,119; Mage = 18.44 years). Data were drawn from the Spit for Science study where participants completed multiple online surveys throughout college and provided a saliva sample for genotyping. Multilevel growth curve analyses indicated that alcohol dependence genome-wide polygenic risk scores did not predict trajectory of alcohol use disorder symptoms, while family history of alcohol problems was associated with alcohol use disorder symptoms at the start of college but not with the rate of change in symptoms over time. Peer deviance and interpersonal traumatic events were associated with more alcohol use disorder symptoms across college years. Neither alcohol dependence genome-wide polygenic risk scores nor family history of alcohol problems moderated the effects of these environmental risk factors on alcohol use disorder symptoms. Our findings indicated that peer deviance and experience of interpersonal traumatic events are salient risk factors that elevate risk for alcohol problems among African American college students. Family history of alcohol problems could be a useful indicator of genetic risk for alcohol problems. Gene identification efforts with much larger samples of African descent are needed to better characterize genetic risk for alcohol use disorders, in order to better understand gene-environment interaction processes in this understudied population.

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Childhood interpersonal violence and adult alcohol, cannabis, and tobacco use disorders: variation by race/ethnicity?

Cited by 25 publications

References 61 publications

The interplay between childhood trauma, cognitive biases, and cannabis use on the risk of psychosis in nonclinical young adults in Poland

The interplay between childhood trauma, cognitive biases, and cannabis use on the risk of psychosis in nonclinical young adults in Poland

Psychosocial moderation of polygenic risk for cannabis involvement: the role of trauma exposure and frequency of religious service attendance

Examining interactions between genetic risk for alcohol problems, peer deviance, and interpersonal traumatic events on trajectories of alcohol use disorder symptoms among African American college students

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