Social workers, including social work researchers, are called on to challenge social injustices and pursue social change. Research has shown a strong association between trauma and adversity and marginalized populations, exposing the unequal distribution of trauma and its effects throughout society. Given the focus on marginalized populations in social work, the social justice orientation of the field, and the intersection of trauma with marginalized populations, a framework to guide social work researchers in conducting trauma-informed, socially just research with marginalized populations is warranted. Therefore, this article provides a framework integrating trauma theory, trauma-informed principles, and intersectionality as a guide for social work research. The proposed framework is illustrated using a case study of low-income, predominantly African American men recruited from a criminal justice setting, acknowledging facilitators and barriers to implementation. The article concludes with a discussion of the implications for researchers and doctoral student training.

Introduction Women with substance use disorders enter treatment with limited personal network resources and reduced recovery support. This study examined the impact of personal networks on substance use by 12 months post treatment intake. Methods Data were collected from 284 women who received substance abuse treatment. At six month follow up, composition, support availability and structure of personal networks were examined. Substance use was measured by women’s report of any use of alcohol or drugs. Hierarchical multivariate logistic regression was conducted to examine the contribution of personal network characteristics on substance use by 12 months post treatment intake. Results Higher numbers of substance using alters (network members) and more densely connected networks at six month follow-up were associated with an increased likelihood of substance use by 12 months post treatment intake. A greater number of isolates in women’s networks was associated with decreased odds of substance use. Women who did not use substances by 12 months post treatment intake had more non-users among their isolates at six months compared to those who used substances. No association was found between support availability and likelihood of substance use. Conclusions Both network composition and structure could be relevant foci for network interventions e.g. helping women change network composition by reducing substance users as well as increasing network connections. Isolates who are not substance users may be a particular strength to help women cultivate within their network to promote sustained sobriety post treatment.

Background Early identification of individuals at high risk for alcohol use disorder (AUD) coupled with prompt interventions could reduce the incidence of AUD. In this study, we investigated whether Polygenic Risk Scores (PRS) can be used to evaluate the risk for AUD and AUD severity (as measured by the number of DSM‐5 AUD diagnostic criteria met) and compared their performance with a measure of family history of AUD. Methods We studied individuals of European ancestry from the Collaborative Study on the Genetics of Alcoholism (COGA). DSM‐5 diagnostic criteria were available for 7203 individuals, of whom 3451 met criteria for DSM‐IV alcohol dependence or DSM‐5 AUD and 1616 were alcohol‐exposed controls aged ≥21 years with no history of AUD or drug dependence. Further, 4842 individuals had a positive first‐degree family history of AUD (FH+), 2722 had an unknown family history (FH?), and 336 had a negative family history (FH−). PRS were derived from a meta‐analysis of a genome‐wide association study of AUD from the Million Veteran Program and scores from the problem subscale of the Alcohol Use Disorders Identification Test in the UK Biobank. We used mixed models to test the association between PRS and risk for AUD and AUD severity. Results AUD cases had higher PRS than controls with PRS increasing as the number of DSM‐5 diagnostic criteria increased (p‐values ≤ 1.85E−05) in the full COGA sample, the FH+ subsample, and the FH? subsample. Individuals in the top decile of PRS had odds ratios (OR) for developing AUD of 1.96 (95% CI: 1.54 to 2.51, p‐value = 7.57E−08) and 1.86 (95% CI: 1.35 to 2.56, p‐value = 1.32E−04) in the full sample and the FH+ subsample, respectively. These values are comparable to previously reported ORs for a first‐degree family history (1.91 to 2.38) estimated from national surveys. PRS were also significantly associated with the DSM‐5 AUD diagnostic criterion count in the full sample, the FH+ subsample, and the FH? subsample (p‐values ≤6.7E−11). PRS remained significantly associated with AUD and AUD severity after accounting for a family history of AUD (p‐values ≤6.8E−10). Conclusions Both PRS and family history were associated with AUD and AUD severity, indicating that these risk measures assess distinct aspects of liability to AUD traits.

Predictive models for recovering from alcohol use disorder (AUD) and identifying related predisposition biomarkers can have a tremendous impact on addiction treatment outcomes and cost reduction. Our sample (N = 1376) included individuals of European (EA) and African (AA) ancestry from the Collaborative Study on the Genetics of Alcoholism (COGA) who were initially assessed as having AUD (DSM-5) and reassessed years later as either having AUD or in remission. To predict this difference in AUD recovery status, we analyzed the initial data using multimodal, multi-features machine learning applications including EEG source-level functional brain connectivity, Polygenic Risk Scores (PRS), medications, and demographic information. Sex and ancestry age-matched stratified analyses were performed with supervised linear Support Vector Machine application and were calculated twice, once when the ancestry was defined by self-report and once defined by genetic data. Multifeatured prediction models achieved higher accuracy scores than models based on a single domain and higher scores in male models when the ancestry was based on genetic data. The AA male group model with PRS, EEG functional connectivity, marital and employment status features achieved the highest accuracy of 86.04%. Several discriminative features were identified, including collections of PRS related to neuroticism, depression, aggression, years of education, and alcohol consumption phenotypes. Other discriminated features included being married, employed, medication, lower default mode network and fusiform connectivity, and higher insula connectivity. Results highlight the importance of increasing genetic homogeneity of analyzed groups, identifying sex, and ancestry-specific features to increase prediction scores revealing biomarkers related to AUD remission.

doi: medRxiv preprint NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice.

Background There are gaps in the literature on service use (help‐seeking and treatment utilization) for alcohol problems among those with alcohol use disorder (AUD). First, policy changes and cultural shifts (e.g., insurance) related to AUD have occurred over the last few decades, making it important to study generational differences. Second, multiple studies have found that females receive fewer services than males, and exploring whether these sex differences persist across generations can inform public health and research endeavors. The current study examined service use for alcohol problems among individuals with AUD. The aims were as follows: (i) to describe service use for alcohol problems; (ii) to assess generational differences (silent [b. 1928 to 1945], boomer [b. 1946 to 1964], generation X [b. 1965 to 1980], millennial [b. 1981 to 1996]) in help‐seeking and treatment utilization; and (iii) to examine sex differences across generations. Methods Data were from affected family members of probands who participated in the Collaborative Study on the Genetics of Alcoholism (N = 4,405). First, frequencies for service use variables were calculated across generations. Pearson chi‐square and ANOVA were used to test for differences in rates and types of service use across generations, taking familial clustering into account. Next, Cox survival modeling was used to assess associations of generation and sex with time to first help‐seeking and first treatment for AUD, and time from first onset of AUD to first help‐seeking and first treatment. Interactions between generation and sex were tested within each Cox regression. Results Significant hazards were found in all 4 transitions. Overall, younger generations used services earlier than older generations, which translated into higher likelihoods of these behaviors. Regardless of generation, younger females were less likely to use services than males. Conclusions There are generational and sex differences in service use for alcohol problems among individuals with AUD. Policy and clinical implications are discussed.

Prenatal cocaine exposure (PCE) may increase adolescent substance use through alterations of neurotransmitter systems affecting fetal brain development. The relationship between PCE and substance use at 15 and 17 years was examined. Subjects (365: 186 PCE; 179 non-cocaine exposed (NCE)) supplied biologic and self-report data using the Youth Risk Behavior Surveillance System (YRBSS) and Computerized Diagnostic Interview Schedule for Children (C-DISC 4) at ages 15 and 17. The relationship between PCE and substance use was assessed using General Estimating Equation (GEE) analyses controlling for confounding factors including violence exposure and preschool lead level. Teens with PCE vs. NCE teens were 2 times more likely to use tobacco (OR = 2.1; 95% CI 1.21–3.63; p < .001) and marijuana (OR = 1.85; CI 1.18–2.91; p < .001) and have a substance use disorder at age 17 (OR = 2.51; CI 1.00–6.28; p < .05). Evaluation of PCE status by gender revealed an association between PCE and marijuana use that was more pronounced for boys than girls at 17 years. Violence exposure was also a significant predictor of alcohol (p < .001), tobacco (p < .05), and marijuana (p < .0006) use and substance abuse/dependence (p < .01). Externalizing behavior at age 12 fully mediated the effects of PCE on substance use disorder at age 17 and partially mediated effects of PCE on tobacco use, but did not mediate effects on marijuana use. The percentage of substance use reported increased between 15 and 17 years, with no differences between the PCE and NCE groups. Data suggest specialized drug use prevention measures for children with PCE may benefit this high risk group.

No abstract