Elevated risk of alcohol use disorder in Japanese men living with HIV: Psychosocial determinants and protective role of sense of coherence.

To assess whether parental alcohol use disorder (AUD) is associated with higher risks of living in a non-intact family and assess whether non-intact family structure is associated with higher risks of AUD in the offspring. Prospective cohort study. Danish nation-wide registries. A total of 9948 parental AUD offspring and 98 136 reference offspring from the Danish population. Family structure assessed at birth and at each birthday until age 15 as intact or non-intact (with mother only, father only or neither parent); years lived in an intact family defined as total number of years lived with both parents from birth until the 15th birthday; AUD defined as registration in medical, treatment and cause of death registries. Data were analyzed by Cox regression. At birth, 30.9% [95% confidence interval (CI) = 29.1-32.6] of parental AUD offspring and 10.7% (95% CI = 10.3-11.0) of reference offspring lived in a non-intact family. At age 15, the numbers were 84.6% (95% CI = 83.9-85.3) and 38.4% (95% CI = 38.1-38.7). Parental AUD was associated with a higher risk of offspring AUD [hazard ratio (HR) = 1.88, 95% CI = 1.74-2.02]. Offspring were at lower risk of AUD if they lived 15 years in an intact family compared with offspring who never lived in an intact family (HR = 0.67, 95% CI = 0.52-0.87 for those with parental AUD, and HR = 0.53, 95% CI = 0.48-0.59 for those whose parents did not have AUD). Findings were inconclusive as to whether or not an association was present between family structure and AUD among offspring with parental AUD and reference offspring. The prevalence of non-intact family structure appears to be higher in offspring of parents with alcohol use disorder (AUD) than among offspring from the general population. Parental AUD appears to be associated with increased risk of offspring AUD, and non-intact family structure appears to be associated with increased risk of offspring AUD regardless of parental AUD.

Abstinence from alcohol is often considered a critical element of recovery from alcohol use disorder. Yet, low risk drinking may be more desirable for some patients. There is mixed literature on whether low risk drinking is achievable and stable. Low risk drinking outcomes during treatment and outcomes 3 years after treatment were examined using data from the outpatient arm in Project MATCH (n = 877). Drinking outcomes were defined by repeated measures latent class analysis of weekly abstinence, low risk drinking days (<4/5 drinks for women/men), and heavy drinking days (≥4/5 drinks for women/men) during 12 weeks of treatment. Functioning outcome measures included psychosocial functioning, alcohol use, and alcohol-related consequences. Mixture modeling was used to examine the association between drinking classes and functioning outcomes. We identified 7 classes based on drinking during treatment: persistent heavy drinking, abstinence to heavy drinking, abstinence and heavy drinking, heavy drinking to mostly abstinent, low risk and heavy drinking, abstinence and low risk drinking, and abstinence. As compared with heavier drinkers, individuals who achieved mostly abstinence or low risk drinking, even with some heavy drinking episodes during treatment, had significant improvements in alcohol use, alcohol-related consequences, and psychosocial functioning 3 years after treatment. Those who were mostly abstinent or engaged in low risk drinking during treatment did not differ on any outcomes at 3 years after treatment. Findings indicate that low risk drinking is achievable for some individuals during treatment and that improvement in functioning among low risk drinkers can be observed at 3 years after treatment. (PsycINFO Database Record

Does the genetic aptitude for educational attainment (GAEA) moderate the genetic risk for alcohol use disorder (AUD) and drug use disorder (DUD)? In the native Swedish population, born 1960-1980 and followed through 2017 (n = 1 862 435), the family genetic risk score (FGRS) for AUD and DUD and GAEA were calculated from, respectively, the educational attainment and risk for AUD and DUD, of 1st through 5th degree relatives from Swedish national registers. Analyses utilized Aalen's linear hazards models. Risk for AUD was robustly predicted by the main effects of FGRSAUD [b = 6.32 (95% CI 6.21-6.43), z = 64.9, p < 0.001) and GAEA [b = -2.90 (2.83-2.97), z = 44.1, p < 0.001] and their interaction [b = -1.93 (1.83-2.03), z = 32.9, p < 0.001]. Results were similar for the prediction of DUD by the main effects of FGRSDUD [b = 4.65 (CI 4.56-4.74), z = 59.4, p < 0.001] and GAEA [-2.08 (2.03-2.13), z = 46.4, p < 0.001] and their interaction [b = -1.58 (1.50-1.66)), z = 30.2, p < 0.001]. The magnitude of the interactions between GAEA and FGRSAUD and FGRSDUD in the prediction of, respectively, AUD and DUD was attenuated only slightly by the addition of educational attainment to the model. The genetic propensity to high educational attainment robustly moderates the genetic risk for both AUD and DUD such that the impact of the genetic liability to AUD and DUD on the risk of illness is substantially attenuated in those with high v. low GAEA. This effect is not appreciably mediated by the actual level of educational attainment. These naturalistic findings could form the basis of prevention efforts in high-risk youth.

Differences in the connectivity of large-scale functional brain networks among individuals with alcohol use disorders (AUD), as well as those at risk for AUD, point to dysfunctional neural communication and related cognitive impairments. In this study, we examined how polygenic risk scores (PRS), derived from a recent GWAS of DSM-IV Alcohol Dependence (AD) conducted by the Psychiatric Genomics Consortium, relate to longitudinal measures of interhemispheric and intrahemispheric EEG connectivity (alpha, theta, and beta frequencies) in adolescent and young adult offspring from the Collaborative Study on the Genetics of Alcoholism (COGA) assessed between ages 12 and 31. Our findings indicate that AD PRS (p-threshold < 0.001) was associated with increased fronto-central, tempo-parietal, centro-parietal, and parietal-occipital interhemispheric theta and alpha connectivity in males only from ages 18–31 (beta coefficients ranged from 0.02–0.06, p-values ranged from 10−6–10−12), but not in females. Individuals with higher AD PRS also demonstrated more performance deficits on neuropsychological tasks (Tower of London task, visual span test) as well as increased risk for lifetime DSM-5 alcohol and opioid use disorders. We conclude that measures of neural connectivity, together with neurocognitive performance and substance use behavior, can be used to further understanding of how genetic risk variants from large GWAS of AUD may influence brain function. In addition, these data indicate the importance of examining sex and developmental effects, which otherwise may be masked. Understanding of neural mechanisms linking genetic variants emerging from GWAS to risk for AUD throughout development may help to identify specific points when neurocognitive prevention and intervention efforts may be most effective.

To determine whether genetic risk factors for major depression (MD) and alcohol use disorder (AUD) interact with a potent stressor - death of spouse, parent, and sibling - in predicting episodes of, respectively, MD and AUD. MD and AUD registrations were assessed from national Swedish registries. In individuals born in Sweden 1960-1970, we identified 7586, 388 459, and 34 370 with the loss of, respectively, a spouse, parent, and sibling. We started following subjects at age 18 or the year 2002 with end of follow-up in 2018. We examined time to event - a registration for MD within 6 months or AUD within a year - on an additive scale, using the Nelson-Aalen estimator. Genetic risk was assessed by the Family Genetic Risk Score (FGRS). In separate models controlling for the main effects of death of spouse, parent, and sibling, FGRS, and sex, significant interactions were seen in all analyses between genetic risk for MD and death of relative in prediction of subsequent MD registration. A similar pattern of results, albeit with weaker interaction effects, was seen for genetic risk for AUD and risk for AUD registration. Genetic risk for bipolar disorder (BD) and anxiety disorders (AD) also interacted with event exposure in predicting MD. Genetic risk for both MD and AUD act in part by increasing the sensitivity of individuals to the pathogenic effects of environmental stressors. For prediction of MD, similar effects are also seen for genetic risk for AD and BD.

This cross-sectional study examined whether COVID-19-related disruption of occupational, social/leisure, and family roles was associated with alcohol use disorder (AUD) risk among adults in South Korea. We analyzed data from 936 adults aged 20-69 years who participated in the 2022 Chungnam Provincial Mental Health Survey. COVID-19-related disruption was assessed across three role domains and categorized as low, moderate, or high. AUD risk was defined using the Korean version of the Alcohol Use Disorders Identification Test. Multivariable logistic regression was used to estimate adjusted odds ratios (aORs), controlling for sociodemographic characteristics and depressive symptoms. Overall, 129 participants (13.8%) screened positive for AUD risk. The crude prevalence of AUD risk increased across disruption categories: 11.0% in the low-disruption group, 12.3% in the moderate-disruption group, and 20.8% in the high-disruption group. In the fully adjusted model, high disruption was associated with higher odds of AUD risk compared with low disruption (aOR = 1.93, 95% CI: 1.10-3.39; p = 0.021), whereas moderate disruption was not statistically significant. These findings suggest that substantial pandemic-related role disruption may be associated with increased AUD risk, although causal inference is limited by the cross-sectional design.

Sexual orientation disparities in psychiatric and drug use disorders among a nationally representative sample of women with alcohol use disorders

Alcohol use disorder (AUD) is among the strongest correlates of suicide death, but it is unclear whether AUD status is differentially associated with risk of suicide by particular methods. The authors used competing risks models to evaluate the association between AUD status and risk of suicide by poisoning, suffocation, drowning, firearm, instruments, jumping, or other means in a large Swedish cohort born 1932-1995 (total N = 6,581,827; 48.8% female). Data were derived from Swedish national registers, including the Cause of Death Register and a range of medical registers. After adjusting for sociodemographic factors and familial liability to suicidal behavior, AUD was positively associated with risk of suicide for each method evaluated (cumulative incidence differences: 0.006-1.040 for females, 0.046-0.680 for males), except the association with firearm suicide in females. AUD was most strongly associated with risk of suicide by poisoning. Sex differences in the effects of AUD and family liability were observed for some, but not all, methods. Furthermore, high familial liability for suicidal behavior exacerbated AUD's impact on risk for suicide by poisoning (both sexes) and suffocation and jumping (males only), while the inverse interaction was observed for firearm suicide (males only). AUD increases risk of suicide by all methods examined and is particularly potent with respect to risk of suicide by poisoning. Differences in risk related to sex and familial liability to suicidal behavior underscore AUD's nuanced role in suicide risk. Future research should investigate targeted means restriction effectiveness among persons with AUD.

Direct-acting antiviral (DAA) treatment for hepatitis C virus (HCV) infection is associated with lower mortality and is effective in individuals with alcohol use disorder (AUD). However, despite recommendations, patients with AUD may be less likely to receive DAAs. To assess the association between alcohol use and receipt of DAA treatment among patients with HCV within the Veterans Health Administration (VHA). This cohort study included 133 753 patients with HCV born from 1945 to 1965 who had completed the Alcohol Use Disorders Identification Test-Consumption (AUDIT-C) questionnaire and had at least 1 outpatient visit in the VHA from January 1, 2014, through May 31, 2017, with maximal follow-up of 3 years until May 31, 2020; DAA receipt; or death, whichever occurred first. Alcohol use categories generated using responses to the AUDIT-C questionnaire and International Classification of Diseases, Ninth Revision and International Statistical Classification of Diseases and Related Health Problems, Tenth Revision diagnoses: current AUD, abstinent with AUD history, at-risk drinking, lower-risk drinking, and abstinent without AUD history. Demographic, other clinical, and pharmacy data were also collected. Associations between alcohol use categories and DAA receipt within 1 and 3 years estimated using Cox proportional hazards regression stratified by calendar year. Of 133 753 patients (130 103 men [97%]; mean [SD] age, 60.6 [4.5] years; and 73 493 White patients [55%]), 38% had current AUD, 12% were abstinent with a history of AUD, 6% reported at-risk drinking, 14% reported lower-risk drinking, and 30% were abstinent without a history of AUD. Receipt of DAA treatment within 1 year was 7%, 33%, 53%, and 56% for patients entering the cohort in 2014, 2015, 2016, and 2017, respectively. For patients entering in 2014, those with current AUD (hazard ratio [HR], 0.72 [95%, CI, 0.66-0.77]) or who were abstinent with an AUD history (HR, 0.91 [95% CI, 0.84-1.00]) were less likely to receive DAA treatment within 1 year compared with patients with lower-risk drinking. For those entering in 2015-2017, patients with current AUD (HR, 0.75 [95% CI, 0.70-0.81]) and those who were abstinent with an AUD history (HR, 0.76 [95% CI, 0.68-0.86]) were less likely to receive DAA treatment within 1 year compared with patients with lower-risk drinking. This cohort study suggests that individuals with AUD, regardless of abstinence, were less likely to receive DAA treatment. Improved access to DAA treatment for persons with AUD is needed.

Risk and resilience for alcohol use disorder revealed in brain functional connectivity

The purpose of this study was to clarify the mediational pathways from genetic risk for alcohol use disorder (AUD) to AUD itself. Using information on AUD status from first- through fourth-degree relatives obtained from national registries, we created a genetic risk score for AUD for the Swedish population. We first tested a simple mediational path model in males and females separately, with early onset externalizing psychopathology (EPP), internalizing psychopathology (IPP), and poor educational attainment (EA). We then tested a more complex model in a smaller, older sample of males that contained additional self-report measures from late adolescence. In our basic model, the largest mediational pathway from AUD genetic risk to AUD in both sexes was via high EPP followed by low EA and high IPP. The EPP pathway was considerably stronger in males, the low EA pathway was modestly stronger in females, and the IPP pathway was identical in both sexes. Our more complex model replicated the strong externalizing pathway to AUD, showing that it connected to key downstream risk factors such as early drug and alcohol use and low resilience. Our models concurred in showing that the strongest mediational pathway for genetic risk to AUD includes externalizing symptoms and disorders, which in turn predict further key downstream risk factors. Pathways through lower EA and IPP had smaller effects. IPP had mixed effects (partly predisposing and partly protective) on downstream risk factors. The largest sex difference was a stronger externalizing pathway to genetic risk to AUD in males than in females.

Back to table of contents Previous article Next article Clinical and Research NewsFull AccessMarriage May Decrease Future Risk of Alcohol Use DisorderMark MoranMark MoranSearch for more papers by this authorPublished Online:1 Jun 2016https://doi.org/10.1176/appi.pn.2016.6a24AbstractThe protective effect of marriage endured even when statistical analysis controlled for such factors as age, parental education, early-onset externalizing syndromes, or positive family history of alcohol use disorder.Men and women in a first marriage to a spouse with no history of alcohol use disorder (AUD) are much less likely to experience AUD themselves, according to a report published last month in AJP in Advance and released at APA’s 2016 Annual Meeting in Atlanta. iStock/digitalskilletThe study found that marriage generally was protective against the risk of alcohol use disorder: married men and women had, respectively, a 60 percent and 71 percent lower risk for onset of alcohol use disorder compared with individuals who remained single.“These results are consistent with the hypothesis that the psychological and social aspects of marriage, and in particular health-monitoring spousal interactions, strongly protect against the development of alcohol use disorder,” Kenneth Kendler, M.D., a professor of psychiatry and human and molecular genetics at the Virginia Institute for Psychiatric and Behavioral Genetics and Virginia Commonwealth University, and colleagues wrote.Kendler and colleagues from the Lund University in MalmɆ, Sweden, used a variety of Swedish national birth, health, and crime registries to assess the relationship between first marriage and subsequent registration for AUD in a large population-based Swedish cohort (n=3,220,628). They also sought to determine the degree to which this association can be explained by parental education, family history, and early history of criminal behavior or drug abuse. Of the more than 3.2 million individuals included in the sample, 72,252 met the criteria for AUD.They found that while marriage to a spouse without AUD was strongly protective, marriage to a spouse with lifetime AUD significantly increased the risk for subsequent AUD registration in both men and women. “As expected, we found a substantial main effect of those with a positive family history having a stronger risk for alcohol use disorder,” the researchers stated. “More interestingly, we found robust evidence that the protective effects of marriage were stronger in those with a family history compared to those without. This effect is consistent with recent findings that severe problem drinkers show the greatest decrease in drinking after the transition to marriage. Those at highest risk for alcohol problems appear to be the most likely to benefit from the protective effects of marriage.”The protective effect of marriage endured even when statistical analysis controlled for such contributing factors as age, parental education, early-onset externalizing syndromes, or positive family history of AUD, the authors noted.Marc Galanter, M.D., a professor of psychiatry at New York University School of Medicine and an expert in alcohol use disorders, who reviewed the report for Psychiatric News, noted that lead author Kendler has done past important research on genetic vulnerability to alcoholism. “The current study illustrates how environmental issues can be comparably influential,” he said. “The study shows how spousal influence can have a beneficial effect, making alcohol use disorder much less likely to emerge.“This reflects spousal influence in a naturalistic setting, but in a clinical setting psychiatrists can utilize spousal, family, and other relationships to help promote recovery,” he said. ■“Effect of Marriage on Risk for Onset of Alcohol Use Disorder: A Longitudinal and Co-Relative Analysis in a Swedish National Sample” can be accessed here. ISSUES NewArchived

The economic burden of chronic diseases with co-occurring depression and alcohol use disorder for people in the Western Cape, South Africa

When sober, problematic drinkers display exaggerated reactivity to threats that are uncertain (U-threat). Since this aversive affective state can be alleviated via acute alcohol intoxication, it has been posited that individuals who exhibit heightened reactivity to U-threat at baseline are motivated to use alcohol as a means of avoidance-based coping, setting the stage for excessive drinking. To date, however, no study has attempted to characterize the dispositional nature of exaggerated reactivity to U-threat and test whether it is a vulnerability factor or exclusively a disease marker of problematic alcohol use. The current investigation utilized a family study design to address these gaps by examining whether (1) reactivity to U-threat is associated with risk for problematic alcohol use, defined by family history of alcohol use disorder (AUD) and (2) reactivity to U-threat is correlated amongst adult biological siblings. A total of 157 families, and 458 individuals, participated in the study and two biological siblings completed a threat-of-shock task designed to probe reactivity to U-threat and predictable threat (P-threat). Startle potentiation was collected as an index of aversive responding. Within biological siblings, startle potentiation to U-threat [intraclass correlation (ICC) = 0.35] and P-threat (ICC = 0.63) was significantly correlated. In addition, independent of an individuals' own AUD status, startle potentiation to U-threat, but not P-threat, was positively associated with risk for AUD (i.e. AUD family history). This suggests that heightened reactivity to U-threat may be a familial vulnerability factor for problematic drinking and a novel prevention target for AUD.

Parents impact their offspring's brain development, neurocognitive function, risk, and resilience for alcohol use disorder (AUD) via both genetic and socio-environmental factors. Individuals with AUD and their unaffected children manifest low parietal P3 amplitude and low frontal theta (FT) power, reflecting heritable neurocognitive deficits associated with AUD. Likewise, children who experience poor parenting tend to have atypical brain development and greater rates of alcohol problems. Conversely, positive parenting can be protective and critical for normative development of self-regulation, neurocognitive functioning and the neurobiological systems subserving them. Yet, the role of positive parenting in resiliency toward AUD is understudied and its association with neurocognitive functioning and behavioral vulnerability to AUD among high-risk offspring is less known. Using data from the Collaborative Study on the Genetics of Alcoholism prospective cohort (N= 1256, mean age [SD]=19.25 [1.88]), we investigated the associations of closeness with mother and father during adolescence with offspring P3 amplitude, FT power, and binge drinking among high-risk offspring. Self-reported closeness with mother and father between ages 12 and 17 and binge drinking were assessed using the Semi-Structured Assessment for the Genetics of Alcoholism. P3 amplitude and FT power were assessed in response to target stimuli using a Visual Oddball Task. Multivariate multiple regression analyses showed that closeness with father was associated with larger P3 amplitude (p= 0.002) and higher FT power (p= 0.01). Closeness with mother was associated with less binge drinking (p= 0.003). Among male offspring, closeness with father was associated with larger P3 amplitude, but among female offspring, closeness with mother was associated with less binge drinking. These associations remained statistically significant with father's and mothers' AUD symptoms, socioeconomic status, and offspring impulsivity in the model. Among high-risk offspring, closeness with parents during adolescence may promote resilience for developing AUD and related neurocognitive deficits albeit with important sex differences.