Onset Of Alcohol Use Disorders Research Articles

Childhood Violence, High School Academic Environment, and Adult Alcohol Use Among Latinas and Black Women: A Structural Equation Modeling Study.

Young Latinas and Black women drink less than women of other racial/ethnic groups but experience more alcohol-related problems in midlife. This study aims to identify modifiable factors to prevent adult onset of alcohol use disorder (AUD) in this population. Data were collected at six time points as part of the Harlem Longitudinal Development Study from 365 Latinas (47%) and Black (53%) women (mean age at time 1 = 14, standard deviation 1.3). Structural equation modeling was used to test hypothesized pathways from childhood physical and sexual abuse to AUD via depressive mood, anxiety disorders, and somatic complaints in the 20s. We also tested the moderation effect of the high school academic environment by including in the structural equation model two latent variable interaction terms between the school environment and each of the abuse variables. Childhood physical and sexual abuse was positively associated with depressive mood, anxiety disorders, and somatic complaints when participants were in the 20s. Depressive mood mediated childhood abuse and AUD when women were in the 30s. The high school academic environment attenuated the effect of physical, but not sexual abuse, on depressive mood (β = -0.59, B = -9.38, 95% CI [-14.00, -4.76]), anxiety symptoms (β = -0.61, B = -14.19, 95% CI [-21.76, -6.61]), appetite loss (β = -0.41, B = -10.52, 95% CI [-15.61, -5.42]), and sleeplessness (β = -0.50, B = -9.56, 95% CI [-13.95, -5.17]) in the early 20s. Our findings underscore the need to invest in early violence prevention interventions and in education to ensure equitable access to quality, academically oriented, and safe schools.

Pattern of Risks for Psychiatric and Substance Use Disorders in the Offspring of Parents With Alcohol Use Disorder.

The authors sought to clarify the components of the familial liability to alcohol use disorder (AUD) by examining parent-offspring transmission in a large Swedish population sample. To this end, 1,244,516 offspring in intact families with a mean age at follow-up of 37.7 years (SD=6.8) were examined. Hazard ratios for offspring of parents with AUD were calculated using Cox models for risk of five disorders assessed from Swedish medical and criminal registries: AUD, drug use disorders, attention deficit hyperactivity disorder, major depression, and anxiety disorders. The hazard ratio for the offspring was highest for AUD (hazard ratio=2.36), followed by drug use disorder (hazard ratio=2.04), attention deficit hyperactivity disorder (hazard ratio=1.82), major depression (hazard ratio=1.43), and anxiety disorder (hazard ratio=1.43). The risks for AUD were statistically indistinguishable between the children having mothers with AUD compared with those having fathers with AUD and between sons and daughters of a parent with AUD. All risks for offspring having two parents with AUD were higher than those having one parent with AUD, but the increase with two parents with AUD was greatest for AUD, followed by drug use disorder and attention deficit hyperactivity disorder. Age at AUD onset of the parents predicted risk among the offspring more strongly for AUD and drug use disorder, followed by attention deficit hyperactivity disorder, and then major depression and anxiety disorders. Number of recurrences of the parents with AUD predicted risks for all disorders equally. The risk pattern of disorders for the offspring of not-lived-with fathers with AUD was similar to that in the main analysis of intact families. No evidence was found for sex-specific transmission of AUD or a familial female protective effect. Familial and likely genetic liability to AUD has three components: a nonspecific risk of common internalizing and externalizing disorders, a moderately specific risk of externalizing disorders, and a highly specific risk of AUD.

'We're outside the norm again because of the thing that allowed us to be inside the norm': An interpretative phenomenological analysis of the experience of developing an alcohol use disorder after bariatric surgery.

Studies indicate that bariatric surgery is associated with an increased risk of alcohol use disorder (AUD). It is considered some patients develop the disorder after surgery, without having antecedents of preoperative alcohol problems. This qualitative study aimed to explore the experiences of people who developed AUD postoperatively and understand how they make sense of the onset of this disorder. A semi-directed interview was carried out with eight adults who had undergone bariatric surgery and developed AUD de novo postoperatively. Data were analysed using interpretative phenomenological analysis. Four superordinate themes emerged: (1) 'losing control over drinking and self after surgery'; (2) 'feelings of guilt, shame and loss contrasted with perceptions of still being lucky'; (3) 'trying to make sense of the onset of AUD'; and (4) 'retrospective evaluation of bariatric surgery and preoperative information'. These themes indicated loss of control was a central aspect of participant's experiences of postoperative alcohol consumption. AUD was associated with negative emotions and cognitions, but several participants still considered themselves lucky. All tried to make sense of this disorder's onset; many felt they would not have developed AUD if they had not undergone surgery. The onset of AUD influenced their current perceptions and feelings about surgery and the preoperative information regarding AUD risks. Taken together, these results provide insight into the subjective experience of suffering from new-onset AUD post-surgery. However, more studies are necessary to gain a better understanding of the physical and psychological implications of postoperative AUD.

Neural activations during cognitive and affective theory of mind processing in healthy adults with a family history of alcohol use disorder.

Social cognition impairments are a common feature of alcohol use disorders (AUD). However, it remains unclear whether these impairments are solely the consequence of chronic alcohol consumption or whether they could be a marker of vulnerability. The present study implemented a family history approach to address this question for a key process of social cognition: theory of mind (ToM). Thirty healthy adults with a family history of AUD (FH+) and 30 healthy adults with a negative family history of AUD (FH-), matched for age, sex, and education level, underwent an fMRI cartoon-vignette paradigm assessing cognitive and affective ToM. Participants also completed questionnaires evaluating anxiety, depressive symptoms, childhood trauma, and alexithymia. Results indicated that FH+ individuals differed from FH- individuals on affective but not cognitive ToM processing, at both the behavioral and neural levels. At the behavioral level, the FH+ group had lower response accuracy for affective ToM compared with the FH- group. At the neural level, the FH+ group had higher brain activations in the left insula and inferior frontal cortex during affective ToM processing. These activations remained significant when controlling for depressive symptoms, anxiety, and childhood trauma. These findings highlight difficulties during affective ToM processing among first-degree relatives of AUD patients, supporting the idea that some of the impairments exhibited by these patients may already be present before the onset of AUD and may be considered a marker of vulnerability.

Community exposure to armed conflict and subsequent onset of alcohol use disorder.

To measure the independent consequences of community-level armed conflict beatings on alcohol use disorders (AUD) among males in Nepal during and after the 2000-2006 conflict. A population-representative panel study from Nepal, with precise measures of community-level violent events and subsequent individual-level AUD in males. Females were not included because of low AUD prevalence. Chitwan, Nepal. Four thousand eight hundred seventy-six males from 151 neighborhoods, systematically selected and representative of Western Chitwan. All residents aged 15-59 were eligible (response rate 93%). Measures of beatings in the community during the conflict (2000-2006), including the date and distance away, were gathered through neighborhood reports, geo-location and official resources, then linked to respondents' life histories of AUD (collected in 2016-2018) using the Nepal-specific Composite International Diagnostic Interview with life history calendar. Beatings nearby predict the subsequent onset of AUD during and after the armed conflict. Data were analyzed in 2021-2022. Cohort-specific, discrete-time models revealed that within the youngest cohort (born 1992-2001), those living in neighborhoods where armed conflict beatings occurred were more likely to develop AUD compared with those in other neighborhoods (odds ratio = 1.66; 95% confidence interval = 1.02-2.71). In this cohort, a multilevel matching analysis designed to simulate a randomized trial showed the post-conflict incidence of AUD for those living in neighborhoods with any armed conflict beatings was 9.5% compared with 5.3% in the matched sample with no beatings. Among male children living in Chitwan, Nepal during the 2000-2006 armed conflict, living in a neighborhood where armed conflict beatings occurred is associated with increased odds of developing subsequent alcohol use disorder. This association was independent of personal exposure to beatings and other mental disorders.

Predictors of polysubstance use in patients with severe alcohol use disorder: the role of reward craving

BackgroundDifferent craving typologies (i.e., reward, relief, obsessive) have been identified in alcohol use disorder (AUD) but have been less investigated in specific populations like AUD patients with polysubstance use (PSU). The role of dysfunctional personality traits and reward pathways has been reported in both AUD and PSU. We hypothesized that patients with AUD-PSU might show a prevalent reward craving, alongside specific sociodemographic, clinical, and personality features, and aimed at investigating differences in 423 severe AUD outpatients with and without PSU. MethodsOne hundred fifteen patients (27.1% of the sample, 67% males, 42 ± 11.6 years old) displayed PSU. Sociodemographic, clinical features and psychopathological/personality dimensions were assessed through: Craving Typologies Questionnaire (CTQ); Obsessive–Compulsive Drinking Scale (OCDS); UPPS-P Impulsive Behavior Scale (S-UPPS-P); Difficulties in Emotion Regulation Scale (DERS). A binomial logistic regression explored factors associated with PSU. ResultsWe found higher CTQ ‘reward’ scores (p < 0.001) in AUD-PSU patients, and a significant association between reward craving and PSU through logistic regression (OR:1.13; p = 0.005). Earlier AUD onset (p < 0.001), greater rates of binge drinking (p = 0.029), more legal problems (p = 0.015), but no significantly higher S-UPPS-S and DERS scores, were detected in AUD-PSU patients. ConclusionsReward craving was associated with increased risk for PSU in severe AUD patients. Given AUD-PSU participants greater severity and detrimental treatment responses imputed to PSU, identifying prevalent craving types among risk factors for PSU in AUD may help to implement therapeutic strategies. Addressing neurobiological and behavioral mechanisms through combined psychotherapies, pharmacological and neuromodulation treatments could support tailored interventions with better long-term outcome.

Central sensitization in alcohol use disorder: correlates of pain, addiction and health-related quality of life

Background Central sensitization is an important mechanism underlying many chronic pain conditions. Chronic pain and alcohol use disorder (AUD) are highly comorbid. Despite great scientific interest in brain mechanisms linking chronic pain and AUD, progress has been impeded by difficulty assessing central sensitization in AUD. Objective The present study is the first to employ a validated surrogate measure to describe central sensitization in a clinical sample with AUD. Methods Participants with AUD (n = 99) were recruited from an academic addiction treatment center. A well-established surrogate measure of central sensitization, The American College of Rheumatology Fibromyalgia Survey Criteria (ACRFMS) was administered. Participants also responded to questions about quality of life (RAND-36), and AUD. Descriptive analyses and Spearman’s rho correlations were performed. Results Chronic pain and evidence of central sensitization were prevalent. Greater central sensitization was associated with worse health-related quality of life. Participants higher in central sensitization expressed greater endorsement of pain as a reason for AUD onset, maintenance, escalation, treatment delay, and relapse. Conclusion The present study bolsters prior assertions that AUD and chronic pain might compound one another via progressive sensitization of shared brain circuitry. These results may inform future mechanistic research and precision AUD treatment.

Contagious Transmission in a Swedish National Sample of Alcohol Use Disorders as a Function of Geographical Proximity among Siblings and Propinquity-of-Rearing Defined Acquaintances.

Can Alcohol Use Disorder (AUD) be transmitted contagiously in siblings and likely acquaintances growing up close to one another ("Propinquity-of-Rearing Defined Acquaintances (PRDAs)")? PRDAs were pairs of same-age subjects growing up within 1 kilometer of each other and sharing the same school class, where one of whom (PRDA1) was first registered for AUD at age ≥15. Using adult residential location, we predicted proximity-dependent risk for an AUD first registration in a second PRDA within 3 years of PRDA1's registration. In 150,195 informative siblings, cohabitation status [HR (95% CIs) = 1.22 (1.08; 1.37)], but not proximity, predicted risk for AUD onset. In 114,375 informative PRDA pairs, a log model fit best, predicting lower risk the greater the distance (HR=0.88 95% CIs (0.84; 0.92)) with risks for AUD at 10, 50 and 100 km from affected PRDA1 cases equaling, respectively: 0.73 (0.66; 0.82),0.60 (0.51; 0.72), and 0.55 (0.45; 0.68). Within PRDA acquaintanceships, results resembled that found among PRDA pairs. The proximity-dependent contagious risk for AUD among PRDA pairs was attenuated by increasing age, lower genetic risk, and higher educational attainment. Cohabitation but not distance predicted transmission of AUD between siblings. However, contagious transmission of AUD among acquaintances growing up and attending school together was present and attenuated by increasing distance in adulthood. The impact of adult proximity on transmission was moderated by age, educational attainment, and genetic risk for AUD. Our results provide support for the validity of contagion models for AUD.

Plasma Concentrations of Neurofilament Light Chain Protein and Brain-Derived Neurotrophic Factor as Consistent Biomarkers of Cognitive Impairment in Alcohol Use Disorder.

For a long time, Substance Use Disorders (SUDs) were not considered a component in the etiology of dementia. The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders introduced substance-induced neurocognitive disorders, incorporating this notion to clinical practice. However, detection and monitoring of neurodegenerative processes in SUD patients remain a major clinical challenge, especially when early diagnosis is required. In the present study, we aimed to investigate new potential biomarkers of neurodegeneration that could predict cognitive impairment in SUD patients: the circulating concentrations of Neurofilament Light chain protein (NfL) and Brain-Derived Neurotrophic Factor (BDNF). Sixty SUD patients were compared with twenty-seven dementia patients and forty healthy controls. SUD patients were recruited and assessed using the Psychiatric Research Interview for Substance and Mental (PRISM) and a battery of neuropsychological tests, including the Montreal Cognitive Assessment test for evaluation of cognitive impairment. When compared to healthy control subjects, SUD patients showed increases in plasma NfL concentrations and NfL/BDNF ratio, as well as reduced plasma BDNF levels. These changes were remarkable in SUD patients with moderate-severe cognitive impairment, being comparable to those observed in dementia patients. NfL concentrations correlated with executive function and memory cognition in SUD patients. The parameters "age", "NfL/BDNF ratio", "first time alcohol use", "age of onset of alcohol use disorder", and "length of alcohol use disorder diagnosis" were able to stratify our SUD sample into patients with cognitive impairment from those without cognitive dysfunction with great specificity and sensibility. In conclusion, we propose the combined use of NfL and BDNF (NfL/BDNF ratio) to monitor substance-induced neurocognitive disorder.

Functional roles, regulatory mechanisms and theranostics applications of ncRNAs in alcohol use disorder.

Alcohol use disorder (AUD) is one of the most prevalent neuropsychological disorders worldwide, and its pathogenesis is convoluted and poorly understood. There is considerable evidence demonstrating significant associations between multiple heritable factors and the onset and progression of AUD. In recent years, a substantial body of research conducted by emerging biotechnologies has increasingly highlighted the crucial roles of noncoding RNAs (ncRNAs) in the pathophysiology of mental diseases. As in-depth understanding of ncRNAs and their mechanisms of action, they have emerged as prospective diagnostic indicators and preclinical therapeutic targets for a variety of psychiatric illness, including AUD. Of note, dysregulated expression of ncRNAs such as circRNAs, lncRNAs and miRNAs was routinely found in AUD individuals, and besides, exogenous regulation of partial ncRNAs has also been shown to be effective in ameliorating alcohol preference and excessive alcohol consumption. However, the exact molecular mechanism still remains elusive. Herein, we systematically summarized current knowledge regarding alterations in the expression of certain ncRNAs as well as their-mediated regulatory mechanisms in individuals with AUD. And finally, we detailedly reviewed the potential theranostics applications of gene therapy agents targeting ncRNAs in AUD mice. Overall, a deeper comprehension of functional roles and biological mechanisms of ncRNAs may make significant contributions to the accurate diagnosis and effective treatment of AUD.

Definition matters: assessment of tolerance to the effects of alcohol in a prospective cohort study of emerging adults.

Tolerance to the effects of alcohol is an important element in the diagnosis of alcohol use disorders (AUD); however, there is ongoing debate about its utility in the diagnosis AUD in adolescents and young adults. This study aimed to refine the assessment of tolerance in young adults by testing different definitions of tolerance and their associations with longitudinal AUD outcomes. Prospective cohort study. Australia. A contemporary cohort of emerging adults across Australia (n= 565, mean age = 18.9, range = 18-21 at baseline). Clinician-administered Structured Clinical Interview for DSM-IV Research Version (SCID-IV-RV) assessed for AUD criteria across five interviews, at 6-month intervals over 2.5years. Tolerance definitions were operationalized using survey-type response (yes/no), clinician judgement (SCID-IV-RV), different initial drinking quantity and percentage increase thresholds and average heavy consumption metrics. AUD persistence was operationalized by the number of times AUD was present across the 2.5-year study period (n = 491), and new-onset AUD was operationalized as any new incidence of AUD during the follow-up period (n = 461). The (i) SCID-IV-RV clinician judgement [odds ratio (OR) = 2.50, P= 0.005], (ii) an initial drinking quantity threshold of four to five drinks and 50% minimum increase (OR = 2.48, P= 0.007) and (iii) 50% increase only (OR = 2.40, P= 0.005) were the tolerance definitions more strongly associated with any new onset of AUD throughout the four follow-up time-points than other definitions. However, these definitions were not associated with persistent AUD (Ps > 0.05). Average heavy consumption definitions of tolerance were most strongly associated with persistent AUD (OR = 6.66, P= 0.001; OR = 4.65, P= 0.004) but not associated with new-onset AUD (Ps > 0.05). Initial drink and percentage change thresholds appear to improve the efficacy of change-based tolerance as an indicator for new-onset alcohol use disorder diagnosis in self-report surveys of young adults. When predicting persistent alcohol use disorder, average heavy consumption-based indicators appear to be a better way to measure tolerance than self-reported change-based definitions.

Trait sensitivity to negative feedback determines the intensity of compulsive alcohol seeking and taking in male rats.

Background:Alcohol use disorder is one of the most common psychiatric disorders, and it is a leading cause of mortality worldwide. It has been demonstrated previously that people with alcohol use disorder are less sensitive to the negative outcomes of their actions and less able to use negative feedback to guide and adjust their ongoing behaviour. However, far less is known about the aberrant processing of negative feedback before the onset of alcohol use disorder. In this study, we investigated the theoretical claim that sensitivity to negative feedback — as a stable and enduring behavioural trait — can predict vulnerability to the development of compulsive alcohol consumption in rats.Methods:We trained and tested rats in a series of probabilistic reversal learning tests, and based on this “negative feedback sensitivity screening,” we classified each rat as more or less sensitive to negative feedback. Then, in the intermittent-access 2-bottle choice paradigm, we measured alcohol consumption in the animals classified above. In the next step, using the instrumental second-order chained schedule of alcohol reinforcement task, we examined the influence of sensitivity to negative feedback on the development of compulsive alcohol seeking behaviour. Finally, we measured how trait sensitivity to negative feedback affected the extinction and reinstatement of alcohol seeking after a period of abstinence.Results:Trait sensitivity to negative feedback predicted the vulnerability of rats to the development of compulsive alcohol seeking and consumption. We also found significant differences between the more sensitive and less sensitive groups in their propensity to extinguish alcohol seeking behaviours when the alcohol was no longer available.Limitations:The findings from our study did not answer the question of whether individual differences in sensitivity to negative feedback have a genetic basis or develop in response to postnatal experiences.Conclusion:The results of our study suggest that negative feedback sensitivity screening could be used to evaluate individual vulnerability to the development and maintenance of alcohol use disorder.

The Prognostic Role of DSM-5 Alcohol Use Disorder Severity and Age of Onset in Treatment Outcome Among Adults Aged 60.

To investigate among older adults with DSM-5 alcohol use disorder (AUD) the relevance of (1) baseline DSM-5 AUD severity, (2) age of DSM-5 AUD onset, and (3) the interactions of DSM-5 AUD severity*treatment condition and age of DSM-5 AUD onset*treatment condition for the prediction of AUD treatment outcomes. The international multicenter RCT "ELDERLY-Study" compared outpatient motivational enhancement therapy (4 sessions) with outpatient motivational enhancement therapy followed by community reinforcement approach for seniors (8 sessions) in adults aged 60+ with DSM-5 AUD. Baseline and 1-, 3-, and 6-month follow-up data from the German and Danish ELDERLY-sites (n = 544) were used (6-month participation rate: 75.9%). DSM-5 AUD diagnoses were obtained using the Mini International Neuropsychiatric Interview and alcohol use using Form 90. Associations between DSM-5 AUD severity and age of onset and AUD treatment outcomes were investigated using multiple logistic regression and generalized linear models. The sample was diverse in AUD severity (severe: 54.9%, moderate: 28.2%, mild: 16.9%) and age of onset (median: 50 years; 12-78 years). Overall, with few exceptions, neither AUD severity, nor age of onset, nor their respective interactions with treatment condition significantly predicted drinking outcomes at the different follow-ups ( P ≥ 0.05). No indication was found for the need to tailor treatment content according to DSM-5 AUD severity and earlier onset in older adults.

Gender Differences in the Psychosocial Determinants Underlying the Onset and Maintenance of Alcohol Use Disorder.

A large number of different mechanisms have been linked to Alcohol Use Disorder (AUD), including psychosocial, neurocognitive, affective, and neurobiological factors. Gender has been shown to impact the presentation and progression of AUD; yet, little work has been done to parse the different mechanisms underlying AUD within the lens of gender differences. A review of the literature on adolescence revealed that psychosocial factors, in particular lack of family social support and interactions with peers, drive the onset of alcohol use more strongly in girls relative to boys. However, research done on gender differences in disease progression in adults remains limited. Our gender-specific analysis of the mechanisms underlying AUD in adults revealed that lack of social support was causally linked to negative affect, mental health symptoms, and AUD symptom severity in women, but not men. These novel results suggest that psychosocial factors may play a gender-specific role not only in the onset of use in adolescence, but also in the maintenance of addiction in adults. If confirmed, this suggests the need for investigating gender-specific recovery trajectories. In this perspective piece, we review the literature regarding gender differences in the onset and maintenance of AUD and present original data that support unique risk factors in women.

Non-coding RNA in alcohol use disorder by affecting synaptic plasticity.

Alcohol use disorder (AUD) is one of the most serious public health problems worldwide. AUD is a complex disorder, and there is ample evidence that genetic predisposition is critical to its development. Recent studies have shown that genetic predisposition leads to the onset of AUD, and alcohol metabolism can affect epigenetic inheritance, which in turn affects synaptic plasticity, alters brain function, and leads to more severe addictive behaviors. Non-coding RNAs (ncRNAs), especially microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), play an important role in alcohol addiction. This paper reviews the regulatory role of ncRNAs. ncRNAs are involved in enzyme and neurotransmitter reaction systems during alcohol use disorder. Alcohol consumption regulates the expression of ncRNAs that mediate epigenetic modification and synaptic plasticity, which play an important role in the development of chronic AUD. ncRNAs may be used not only as predictors of therapeutic responses but also as therapeutic targets of AUD. Chronic alcoholism is more likely to lead to neuroimmune disorders, including permanent brain dysfunction. AUD induced by long-term alcoholism greatly alters the expression of genes in the human genome, especially the expression of ncRNAs. Alcohol can cause a series of pathological changes by interfering with gene expression, such as through disordered miRNA-mRNA expression networks, epigenetic modifications, disordered metabolism, and even synaptic remodeling. ncRNAs are involved in the transition from moderate drinking to alcohol dependence.

Onset of alcohol use disorder among alcohol initiates by race/ethnicity.

Prevalence of alcohol use disorders (AUD) varies across racial/ethnic groups. It remains unclear whether rapid transition from first-time alcohol use to developing AUD varies by race and ethnicity. In this study, we investigate racial/ethnic differences in AUD onset among first-time alcohol drinkers and identify specific predictors of AUD onset by racial/ethnic group. The study population was non-institutionalized US residents aged 12 and older. Within four nationally representative probability samples (n ∼70,000/year) drawn from the 2015-2018 National Surveys on Drug Use and Health, we identified 9,381 individuals who initiated alcohol use within 1-12 months prior to the survey. The probability of AUD after initiation was estimated for the entire sample, followed by racial/ethnic group stratification. Bivariate and multivariable logistic regression models were used to identify predictors of AUD onset among alcohol initiates. The overall incidence estimate of AUD among alcohol initiates was 3.7% (95% CI=3.0%, 4.6%). There was no significant variation in the incidence of AUD between racial/ethnic groups. Drug use, drug use disorders, and major depressive episode were significant predictors of AUD onset among all alcohol initiates. However, these predictors were not significant among non-Hispanic/Latinx Black individuals. Drug use and drug use disorders were strong predictors of AUD onset among alcohol initiates, except among non-Hispanic/Latinx Black individuals. These findings strengthen the importance of focusing on the co-use of alcohol and other drugs and the need to further investigate the risk profile differences between racial/ethnic groups.

High Polygenic Risk Scores Are Associated With Early Age of Onset of Alcohol Use Disorder in Adolescents and Young Adults at Risk

BackgroundGenome-wide association studies have been conducted in alcohol use disorder (AUD), and they permit the use of polygenic risk scores (PRSs), in combination with clinical variables, to predict the onset of AUD in vulnerable populations. MethodsA total of 2794 adolescent/young adult subjects from the Collaborative Study on the Genetics of Alcoholism were followed, with clinical assessments every 2 years. Subjects were genotyped using a genome-wide chip. Separate PRS analyses were performed for subjects of European ancestry and African ancestry. Age of onset of DSM-5 AUD was evaluated using the Cox proportional hazard model. Predictive power was assessed using receiver operating characteristic curves and by analysis of the distribution of PRS. ResultsEuropean ancestry subjects with higher than median PRSs were at greater risk for onset of AUD than subjects with lower than median PRSs (p = 3 × 10–7). Area under the curve for the receiver operating characteristic analysis peaked at 0.88 to 0.95 using PRS plus sex, family history, comorbid disorders, age at first drink, and peer drinking; predictive power was primarily driven by clinical variables. In this high-risk sample, European ancestry subjects with a PRS score in the highest quartile showed a 72% risk for developing AUD and a 35% risk of developing severe AUD (compared with risks of 54% and 16%, respectively, in the lowest quartile). ConclusionsPredictive power for PRSs in the extremes of the distribution suggests that these may have future clinical utility. Uncertainties in interpretation at the individual level still preclude current application.

Clinical-Dynamical Features of Alcohol Use Disorder and Mood Disorders Considering the Chronology of Their Comorbidity Formation

Background. The comorbid course of Mood Disorders (MD) and Alcohol Use Disorder (AUD) is a problem actively discussed by national and foreign researchers. Scientists pay close attention to clinical and pathodynamic polymorphism of symptoms in their works. Objective of the study: to compare the Clinical-Dynamical characteristics of AUD and MD, taking into account the formation chronology of their comorbidity, in a clinical sample of the specialized psychiatric hospital. Patients and methods: the study enrolled 56 patients under treatment in Department of Affective Disorders or Addictive Disorders of Mental Health Research Institute Clinics with a comorbid diagnosis of AUD (F10.2 according to ICD-10) and MD (F31–F34.1 according to ICD10). The Clinical-Dynamic, Psychometric and Statistical Methods were used in work. Results: according to statistical analysis in the case of the primary onset of AUD a relatively later formation of the comorbidity was shown (p = 0.001, Mann–Whitney test) and a higher frequency of Dysthymia as a Secondary MD (p = 0.043, chi-square test). Inspite of relatively shorter Duration of the Disease (p = 0.001, Mann–Whitney test), Secondary AUD characterized by rapid evolution of clinical and dynamic traits: the Alcohol Tolerance and Duration of Withdrawal Symptoms are comparable to the Primary AUD (p = 0.739, Mann–Whitney test; p = 0.359, Mann–Whitney test), and slightly shorter Duration of Light Gaps (p = 0.087, Mann–Whitney test) and Heavy Drinking Days (p = 0.034, Mann–Whitney test). A Psychometric study of the severity of symptoms of Depression, Anxiety and Craving for alcohol in the dynamics of psychopharmacotherapy demonstrate their comparability both at the beginning of treatment and by the 28th day of therapy (p &gt; 0.05, Mann–Whitney test). Thereby, AUD developed in the background of a formed MD characterized by a prognostically unfavorable course of Disease.

Gender Differences among Sardinians with Alcohol Use Disorder

Sardinia is an Italian island in the Mediterranean characterized by secular isolation and the singular genetic characteristics of its inhabitants. Findings obtained in populations with diverse genetic make-up and cultural background indicate gender differences and/or similarities in drinking characteristics of patients with alcohol use disorder (AUD). Knowledge of these characteristics in AUD patients is useful to improve access to treatments. This paper investigated the drinking characteristics of 66 female and 282 male outpatients with AUD, born from 1937 to 1991, living in Sardinia, and compared their characteristics with those of AUD patients living in other countries. Most Sardinian patients were men, approximately 3 years younger than women; women consumed lower amounts of alcohol than men but did not differ from men in the severity of AUD. Men were more often single than women, while a higher proportion of women reported that their mother or spouse was affected by AUD. Anxiety and depression were more prevalent among women while a higher proportion of men were affected by substance use disorders. Women were older than men at the age of first drink, regular drinking, and onset of AUD, and progressed faster than men from regular use to AUD onset. Women did not differ from men in age at first request for care, and in the lapse from AUD onset to first request for care. Women and men waited for more than 8 and 9 years, respectively, before receiving medical treatment. Gender differences progressively decreased among younger patients. Although the scarce number of women in some cohorts limits the strength of these findings, drinking characteristics of Sardinian patients did not vary significantly from those of AUD patients living in other countries. These results suggest that the number of Sardinian women with AUD is increasing and services for treatment of AUD should (a) consider women’s specific needs, and (b) realize effective policies to reduce latency prior to accessing medical treatment for both men and women with AUD.

Drinking cultures and socioeconomic risk factors for alcohol and drug use disorders among first- and second-generation immigrants: A longitudinal analysis of Swedish population data

BackgroundFew longitudinal studies investigate predictors of substance use incidence among immigrants. The current study describes substance use disorders in immigrants to Sweden, focusing on drinking culture in the country of origin and socioeconomic status (SES), and how these intersect with generational status to influence risk. MethodsUsing pseudonymized Swedish population registry data, we track onset of alcohol use disorder and drug use disorder in a longitudinal study of 815,778 first-generation immigrants and 674,757 second-generation immigrants from 64 countries over a 6-year period. Cox regression analysis estimated risks of alcohol and drug use disorders in second-generation immigrants compared to first-generation, and moderation analyses assessed interactions of generational status with country-of-origin per capita alcohol consumption and SES. ResultsImmigrants and second-generation immigrants originating from countries with high levels of alcohol consumption had higher risks for alcohol and drug use disorders. Immigrants with high SES had lower risks for alcohol and drug use disorders. The interaction between generational status and country-of-origin alcohol consumption was significant for drug use disorder (not for alcohol use disorder), with drug use disorder risk for second-generation immigrants being highest for those from countries with the lowest level of country-of-origin per capita alcohol consumption. The interaction between generational status and SES was significant for alcohol use disorder, with low-SES second-generation immigrants showing markedly higher risk than first-generation immigrants with comparable SES. ConclusionsAmong immigrants in Sweden, second-generation immigrants are at increased risk of developing alcohol and drug use disorders, particularly if they have lower SES. Policy and community attention to these high-risk subgroups in immigrant communities is warranted.