Effect Of Alcohol Use Disorder Research Articles

Effect of alcohol use disorders and alcohol intake on the risk of subsequent depressive symptoms: a systematic review and meta-analysis of cohort studies.

Alcohol use disorders (AUD) are often comorbid with depressive symptoms. Cohort studies on the association between AUD and subsequent depressive symptoms have produced inconsistent results. Moreover, regarding alcohol intake, the risk of developing depressive symptoms might vary with alcohol intake level. We aimed to investigate the association between AUD, alcohol intake and subsequent depressive symptoms. We conducted a systematic search in PubMed, Embase and PsycINFO for cohort studies on the association between AUD or alcohol intake and subsequent depressive symptoms. We included 338 426 participants from 42 studies. Six and four studies analyzed only females and males, respectively. We combined risk estimates for developing depressive symptoms using a random-effects model. We divided alcohol intake into abstinence, light (0-84g/week), moderate (85-168g/week) and heavy drinking (>168g/week or>48g/day at least weekly). We conducted a categorical analysis to compare the risk of depressive symptoms between abstinence and different intake categories. Further, we conducted a dose-response analysis to investigate the alcohol-depression association. We analyzed 42 studies (follow-up time: 1-40years). AUD was associated with significantly increased risk of subsequent depressive symptoms [relative risk (RR)=1.57, 95% confidence interval (CI)=1.41-1.76]. Regarding alcohol intake, heavy drinking had an increased risk of depressive symptoms; however, the association was only significant when controls were limited to non-heavy drinkers (RR=1.13, 95% CI=1.05-1.22). Taking into consideration the possibility of publication bias and confounding factors made the association non-significant. We observed J-shaped associations in both categorical and dose-response analyses where light-moderate drinking had a significantly decreased risk of depression, while heavy drinking did not show a significant association with depressive symptoms compared with non-drinkers. Alcohol use disorders are associated with increased the risk of subsequent depressive symptoms. Heavy drinking does not significantly predict occurrence of depressive symptoms after adjusting for potential confounders.

Effect of alcohol use disorder on cellular aging.

Human telomeres consist of tandem repeats at chromosome ends which protect chromosomal DNA from degradation. Telomere shortening occurs as part of natural aging; however, life stressors, smoking, drug use, BMI, and psychiatric disorders could disrupt cell aging and affect telomere length (TL). In this context, studies have evaluated the effects of alcohol consumption on TL; however, results have been inconsistent, which may reflect diverse drinking cut-offs and categorizations. To help clarify this, the present study addresses the association of TL with alcohol use disorder (AUD), drinking behaviors, lifetime stress, and chronological age. TL was quantified as the telomere to albumin ratio (T/S ratio) obtained from peripheral blood DNA using the quantitative PCR assay, from 260 participants with AUD and 449 non-dependent healthy controls (HC) from an existing National Institute on Alcohol Abuse and Alcoholism (NIAAA) database. AUD participants showed shorter TL compared to HC with both, age, and AUD, as independent predictors as well as a significant AUD with age interaction effect on TL. TL was also associated with impulsiveness in AUD participants. We did not observe an association between TL and chronicity of alcohol use, alcohol doses ingested, or childhood trauma exposures in either AUD or HC, although very few HC reported a history of childhood trauma. Our results support previous findings of telomere shortening with chronic alcohol exposures and show both an effect of AUD on TL that is independent of age as well as a significant AUD by age interaction on TL. These findings are consistent with accelerated cellular aging in AUD.

Effect of Alcohol Use Disorder and Alcohol Intake on Risk of Subsequent Depression: A Dose-Response Meta-Analysis of Cohort Studies

Background: Alcohol misuse is a highly prevalent and attributed to a great burden of public health. Cross-sectional studies reported an association between alcohol misuse and depression. However, whether preceded alcohol misuse is a risk factor for subsequent depression remains undetermined. Moreover, different assessments based on the existence of alcohol use disorder (AUD) and various intake levels of alcohol may lead to different results. We did a dose-response meta-analysis to estimate the longitudinal association between AUD, alcohol intake level and depression. Methods: We searched Pubmed, Embase and PsycINFO for cohort studies investigating alcohol use on risk of subsequent depression up to April 2019. Effect of Alcohol use disorder (AUD) and alcohol intake on depression onset were analyzed separately. In analysis of alcohol intake, we first compared the risk between heavy drinking and non-heavy drinking, following by a qualitative analysis and a dose-response analysis in comparison of different levels of intake versus abstinence. A random-effects model was used to pool the summary RR and 95% confidence intervals (95%CI). Subgroup analysis and meta-regression was performed to trace heterogeneity. Publication bias was evaluated using multiple methods. Findings: Forty-two studies comprising 338426 participants were included in the current analysis. The summary RR of incident depression for AUD was 1.57 (1.41-1.76) compared to non-AUD. Summary RR of depression was 1.14 (1.06, 1.23) on heavy drinking versus non-heavy drinking. In qualitative analysis for various level of alcohol consumption compared to abstinence, light-moderate drinking was inversely associated with depression risk while heavy drinking was found to possibly elevate the risk of depression. Similarity was demonstrated in dose-response analysis, there was a non-linear association between alcohol intake and depression, with a decreased risk observed when consumption approximately between 0 and 29 g/day and an increased but non-significant risk when the intake was >42 g/day. Interpretation: Alcohol use disorder (AUD) is significantly associated with subsequent depression and heavy drinking probably enhanced the risk. Alarm and attention should be sent to alcohol problematic users especially to people with AUD, regardless of the absence of depression yet. Funding: This work was supported by the funding of National Key R&D Program of China (2018YFC1314400 and 2018YFC1314401 to YP). Declaration of Interest: The authors declare that they have no conflict of interest.

Neuroimaging in alcohol use disorder: From mouse to man.

This article provides an overview of recent advances in understanding the effects of alcohol use disorders (AUD) on the brain from the perspective of magnetic resonance imaging (MRI) research in preclinical models and clinical studies. As a noninvasive investigational tool permitting assessment of morphological, metabolic, and hemodynamic changes over time, MRI offers insight into the dynamic course of alcoholism beginning with initial exposure through periods of binge drinking and escalation, sobriety, and relapse and has been useful in differential diagnosis of neurological diseases associated with AUD. Structural MRI has revealed acute and chronic effects of alcohol on both white and gray matter volumes. MR Spectroscopy, able to quantify brain metabolites in vivo, has shed light on biochemical alterations associated with alcoholism. Diffusion tensor imaging permits microstructural characterization of white matter fiber tracts. Functional MRI has allowed for elucidation of hemodynamicresponses at rest and during task engagement. Positron emission tomography, a non-MRI imaging tool, has led to a deeper understanding of alcohol-induced receptor and neurotransmitter changes during various stages of drinking and abstinence. Together, such in vivo imaging tools have expanded our understanding of the dynamic course of alcoholism including evidence for regional specificity of the effects of AUD, hints at mechanisms underlying the shift from casual to compulsive use of alcohol, and profound recovery with sustained abstinence.

Convergence of three parcellation approaches demonstrating cerebellar lobule volume deficits in Alcohol Use Disorder.

Recent advances in robust and reliable methods of MRI-derived cerebellar lobule parcellation volumetry present the opportunity to assess effects of Alcohol Use Disorder (AUD) on selective cerebellar lobules and relations with indices of nutrition and motor functions. In pursuit of this opportunity, we analyzed high-resolution MRI data acquired in 24 individuals with AUD and 20 age- and sex-matched controls with a 32-channel head coil using three different atlases: the online automated analysis pipeline volBrain Ceres, SUIT, and the Johns Hopkins atlas. Participants had also completed gait and balance examination and hematological analysis of nutritional and liver status, enabling testing of functional meaningfulness of each cerebellar parcellation scheme. Compared with controls, each quantification approach yielded similar patterns of group differences in regional volumes: All three approaches identified AUD-related deficits in total tissue and total gray matter, but only Ceres identified a total white matter volume deficit. Convergent volume differences occurred in lobules I-V, Crus I, VIIIB, and IX. Coefficients of variation (CVs) were <20% for 46 of 56 regions measured and in general were graded: Ceres<SUIT<Hopkins. The most robust correlations were identified between poorer stability in balancing on one leg and smaller lobule VI and Crus I volumes from the Ceres atlas. Lower values of two essential vitamins—thiamine (vitamin B1) and serum folate (vitamin B9)—along with lower red blood cell count, which are dependent on adequate levels of B vitamins, correlated with smaller gray matter volumes of lobule VI and Crus I. Higher γ-glutamyl transferase (GGT) levels, possibly reflecting compromised liver function, correlated with smaller volumes of lobules VI and X. These initial results based on high resolution data produced with clinically practical imaging procedures hold promise for expanding our knowledge about the relevance of focal cerebellar morphology in AUD and other neuropsychiatric conditions.

Preclinical evaluation of avermectins as novel therapeutic agents for alcohol use disorders.

The deleterious effects of alcohol use disorders (AUDs) on human health have been documented worldwide. The enormous socioeconomic burden coupled with lack of efficacious pharmacotherapies underlies the need for improved treatment strategies. At present, there is a growing body of preclinical evidence that demonstrates the potential of avermectins [ivermectin (IVM), selamectin (SEL), abamectin (ABM), and moxidectin (MOX)] in treatment of AUDs. Avermectins are derived by fermentation of soil micro-organism, Streptomyces avermitilis, and have been extensively used for treatment of parasitic infections. From the mechanistic standpoint, avermectins are positive modulators of purinergic P2X4 receptors (P2X4Rs). P2X4Rs belong to P2X superfamily of cation-permeable ion channels gated by adenosine5'-triphosphate (ATP). Building evidence has implicated a role for P2X4Rs in regulation of ethanol intake and that ethanol can inhibit ATP-gated currents in P2X4Rs. Investigations using recombinant cell models and animal models of alcohol drinking have reported that IVM, ABM, and MOX, but not SEL, were able to antagonize the inhibitory effects of ethanol on P2X4Rs in vitro and reduce ethanol intake in vivo. Furthermore, IVM was shown to reduce ethanol consumption via P2X4R potentiation in vivo, supporting the involvement of P2X4Rs in IVM's anti-alcohol effects and that P2X4Rs can be used as a platform for developing novel anti-alcohol compounds. Taken together, these findings support the utility of avermectins as a novel class of drug candidates for treatment of AUDs.

Multi-Label Transduction for Identifying Disease Comorbidity Patterns.

Study of the untoward effects associated with the comorbidity of multiple diseases on brain morphology requires identifying differences across multiple diagnostic groupings. To identify such effects and differentiate between groups of patients and normal subjects, conventional methods often compare each patient group with healthy subjects using binary or multi-class classifiers. However, testing inferences across multiple diagnostic groupings of complex disorders commonly yield inconclusive or conflicting findings when the classifier is confined to modeling two cohorts at a time or considers class labels mutually-exclusive (as in multi-class classifiers). These shortcomings are potentially caused by the difficulties associated with modeling compounding factors of diseases with these approaches. Multi-label classifiers, on the other hand, can appropriately model disease comorbidity, as each subject can be assigned to two or more labels. In this paper, we propose a multi-label transductive (MLT) method based on low-rank matrix completion that is able not only to classify the data into multiple labels but also to identify patterns from MRI data unique to each cohort. To evaluate the method, we use a dataset containing individuals with Alcohol Use Disorder (AUD) and human immunodeficiency virus (HIV) infection (specifically 244 healthy controls, 227 AUD, 70 HIV, and 61 AUD+HIV). On this dataset, our proposed method is more accurate in correctly labeling subjects than common approaches. Furthermore, our method identifies patterns specific to each disease and AUD+HIV comorbidity that shows that the comorbidity is characterized by a compounding effect of AUD and HIV infection.

Effect of alcohol use disorder on oxytocin peptide and receptor mRNA expression in human brain: A post-mortem case-control study

Animal and human evidence supports a role for oxytocin in alcohol-seeking behaviors. There is interest, therefore, in targeting the oxytocin pathway as a new pharmacologic approach to treat alcohol use disorder. To this end, it is important to understand the effect of alcohol use disorder on endogenous oxytocin in brain regions that are relevant for the initiation and maintenance of alcohol use disorder. We examined human post-mortem brain tissue from males with alcohol use disorder (n=11) compared to nonalcohol dependent male controls (n=16). We a priori targeted five brain regions that in rodent studies, are projection areas for oxytocin neurons: nucleus accumbens, amygdala, hippocampus, ventral tegmental area and prefrontal cortex. Fold change in mRNA levels of oxytocin peptide and receptor were measured in each of the brain regions studied. Fold change for oxytocin peptide mRNA was significantly elevated in the prefrontal cortex of subjects with alcohol use disorder compared to controls (uncorrected p=0.0001; FDR-corrected p=0.001). For the entire sample of 27 subjects, there was a significant positive correlation between the fold change in oxytocin peptide mRNA in the prefrontal cortex and both daily alcohol intake (r2=0.38; p=0.002) and drinks per week (r2=0.24; p=0.02). Results are discussed in light of the previous animal and human literature on changes in the endogenous oxytocin system as an effect of chronic alcohol exposure.

Mental Health Over Time in a Military Sample: The Impact of Alcohol Use Disorder on Trajectories of Psychopathology After Deployment.

To identify trajectories of depression and posttraumatic stress (PTS) symptom groups after deployment and determine the effect of alcohol use disorder on these trajectories, depression symptoms were modeled using the 9-item Patient Health Questionnaire in 727 Ohio National Guard members, and PTS symptoms were modeled using the PTSD Checklist in 472 Ohio National Guard members. There were 55.8% who were resistant to depression symptoms across the 4 years of study, and 41.5% who were resistant to PTS symptoms. There were 18.7% and 42.2% of participants who showed resilience (experiencing slightly elevated symptoms followed by a decline, according to Bonanno etal., 2002) to depression and PTS symptoms, respectively. Mild and chronic dysfunction constituted the smallest trajectory groups across disorders. Marital status, deployment to an area of conflict, and number of lifetime stressors were associated with membership into different latent groups for depression (unstandardized β estimates range = 0.69 to 1.37). Deployment to an area of conflict, number of lifetime traumatic events and education predicted membership into different latent groups for PTS (significant unstandardized β estimate range = 0.83 to 3.17). AUD was associated with an increase in both symptom outcomes (significant unstandardized β estimate range = 0.20 to 9.45). These results suggested that alcohol use disorder may have contributed substantially to trajectories of psychopathology in this population.

Alcohol-related risk of suicidal ideation, suicide attempt, and completed suicide: a meta-analysis.

BackgroundSeveral original studies have investigated the effect of alcohol use disorder (AUD) on suicidal thought and behavior, but there are serious discrepancies across the studies. Thus, a systematic assessment of the association between AUD and suicide is required.MethodsWe searched PubMed, Web of Science, and Scopus until February 2015. We also searched the Psycinfo web site and journals and contacted authors. We included observational (cohort, case-control, and cross-sectional) studies addressing the association between AUD and suicide. The exposure of interest was AUD. The primary outcomes were suicidal ideation, suicide attempt, and completed suicide. We assessed heterogeneity using Q-test and I2 statistic. We explored publication bias using the Egger's and Begg's tests and funnel plot. We meta-analyzed the data with the random-effects models. For each outcome we calculated the overall odds ratio (OR) or risk ratio (RR) with 95% confidence intervals (CI).ResultsWe included 31 out of 8548 retrieved studies, with 420,732 participants. There was a significant association between AUD and suicidal ideation (OR=1.86; 95% CI: 1.38, 2.35), suicide attempt (OR=3.13; 95% CI: 2.45, 3.81); and completed suicide (OR=2.59; 95% CI: 1.95, 3.23 and RR=1.74; 95% CI: 1.26, 2.21). There was a significant heterogeneity among the studies, but little concern to the presence of publication bias.ConclusionsThere is sufficient evidence that AUD significantly increases the risk of suicidal ideation, suicide attempt, and completed suicide. Therefore, AUD can be considered an important predictor of suicide and a great source of premature death.

Mortality from alcohol consumption and alcohol use disorder: Findings from the Vietnam Experience Study

BackgroundTo examine the relationship of alcohol consumption, alcohol use disorder and mortality. MethodA cohort of 4316 male former Vietnam-era US army personnel participating in telephone survey and medical examination in middle age (mean age 38.3 years) in 1985–1986 was used. Alcohol consumption was reported in face-to-face interview on medical history and information on DSM-III alcohol use disorder was obtained from structured psychiatric interview (using the Diagnostic Interview Schedule). Mortality hazard during 15 years of follow-up was assessed with Cox proportional hazard regression modeling. ResultA total of 4251 individuals participated in the psychiatric interview and the medical history interview. Of these 998 were abstainers, and for the remaining 3253 we calculated weekly average consumption and monthly frequency of binge drinking. A total of 1988 had alcohol dependence, abuse or both. There were 237 deaths during follow up. A J-shaped association was found for both consumption and binging. In multivariable analysis jointly modeling average consumption and disorder, and binging and disorder, increased mortality remained significant for both very high consumption (Hazard Ratio (HR) 1.62, 95% Confidence Intervals [1.02–2.57]) for drinking 29 or more drinks per week, and frequent bingeing HR 1.81 [1.03–3.18] for bingeing 16 or more times per month). ConclusionThis study showed that alcohol consumption measures were associated with mortality, partly independent from the potential confounding effect of alcohol use disorder, which is an established risk factor for mortality. This further highlights the importance of alcohol consumption measures in public health.

Predictive Utility of Alcohol Use Disorder Symptoms Across Race/Ethnicity

Research has shown differences in alcohol use and problems across race/ethnicity. This study examines whether there are differential effects of alcohol use disorder (AUD) symptoms on drinking outcomes across race/ethnicity. Data from 1483 patients admitted to a hospital for treatment of an injury were utilized (19% Black, 45% non-Latino White, and 36% Latino). AUD symptoms and race/ethnicity reported at baseline and their interaction were the predictor variables. Drinking patterns and associated problems measured at the 6- and 12-month follow-up were the outcome variables of interest. Linear regression was the analytic method employed. Endorsement of “spending a great deal of time to obtain, use, or recover from effects of drinking,” “craving,” “failure to fulfill major role obligations,” and “alcohol use in physically hazardous situations” at baseline was associated with greater levels of subsequent alcohol use and alcohol-related problems at both 6- and 12-month follow-ups, regardless of race/ethnicity. Endorsement of “important social, occupational, or recreational activities given up because of drinking” was differentially associated with greater alcohol-related problems at both 6- and 12-month follow-ups dependent on race/ethnicity. Follow-up analyses indicated that this symptom was a significant predictor of alcohol problems among Latino and Black participants, but not non-Latino White participants. Brief interventions targeting these AUD symptoms could increase the effectiveness of brief motivational interventions among different racial/ethnic groups.

Analysis of perioperative morbidity and mortality in shoulder arthroplasty patients with preexisting alcohol use disorders

Shoulder arthroplasty is becoming increasingly popular in the United States. Given the high prevalence of alcohol abuse and its implications in postoperative morbidity and the increasing incidence of shoulder arthroplasty, it is prudent to explore the effect of alcohol use disorders (AUDs) in this patient population. In this study, we considered numerous outcome variables, including perioperative complications, in-hospital death, prolonged hospital stay, and nonroutine discharge. Using the Nationwide Inpatient Sample, we performed a retrospective cohort study to identify a population of 422,371 adults (≥18 years old) undergoing total shoulder arthroplasty or hemiarthroplasty between January 1, 2002, and December 31, 2011. We then further subdivided this cohort into those who were classified as having AUDs and those who did not. Comparisons of early postoperative outcome measures were performed by bivariate and multivariable analyses with logistic regression modeling. Compared with those without AUDs, patients undergoing shoulder arthroplasty with a preexisting AUD have a greater likelihood to experience death, pneumonia, deep venous thrombosis, acute renal failure, transfusion, prolonged length of stay, and nonroutine discharge irrespective of age, gender, race, and other medical comorbidities. Patients with a preexisting AUD are 2.7 times more likely to experience perioperative complications after shoulder arthroplasty. Patients undergoing shoulder arthroplasty with a preexisting AUD have a greater likelihood of perioperative complications and health care resource utilization after shoulder arthroplasty. Presurgical alcohol screening may prove effective in identifying at-risk patients, and providing interventions before surgery may effectively limit the complication profile.

Consequences of Receipt of a Psychiatric Diagnosis for Completion of College

Consequences of Receipt of a Psychiatric Diagnosis for Completion of College

Cognitive impairment in dual diagnosis inpatients with schizophrenia and alcohol use disorder

Cognitive impairment has been found independently among individuals with schizophrenia and individuals with alcohol use disorders. Less is known about the nature and severity of cognitive impairment in patients with a dual diagnosis, though the co-occurrence of these disorders may further exacerbate cognitive impairment. The study investigates the possible additive effect of alcohol use disorder and schizophrenia on cognitive impairment among patients diagnosed with schizophrenia. Participants were inpatients with schizophrenia ( n = 30), inpatients with a dual diagnosis of schizophrenia and alcohol use disorder ( n = 30), and matched controls ( n = 30): all completed a comprehensive neuropsychological battery. Both patient groups were significantly impaired, relative to controls, across the battery. Dual diagnosis patients were significantly more impaired than schizophrenia patients on delayed verbal memory, and executive functioning, primarily set-shifting, working memory, and planning, and had higher psychiatric morbidity scores. The findings provide support for an additive effect of the two disorders on cognitive impairment. These cognitive deficits may affect capacity to engage in treatment, increase risk of relapse, and adversely affect treatment outcomes. An understanding of the cognitive profile of people with dual diagnosis may help to tailor treatment delivery to meet their specific needs, enhance cognitive strengths, accommodate deficits and improve treatment outcomes.

Alcohol use disorders and cognitive abilities in young adulthood: a prospective study.

The effect of alcohol use disorder (AUD) on cognitive and neuropsychological abilities was investigated in a prospective study of 68 freshmen who met past-year criteria for AUD on 2 or more occasions during their college years and 66 matched controls. At baseline, participants were administered a total of 14 subtests from the Wechsler Adult Intelligence Scale-Revised, Wechsler Memory Scale, and Halstead-Reitan Neuropsychological Battery. At 7-year follow-up, most measures were readministered, along with the Reflective Judgment Interview, Watson-Glaser Critical Thinking Appraisal, and Plant Test. Analyses revealed few differences between AUD and control groups. However, visuospatial deficits may be present among AUD participants with poor baseline visuospatial performance. Alcohol exposure measures yielded similar patterns to those shown with AUD.

Psychiatric Comorbidity and Self-Efficacy to Resist Heavy Drinking in Alcoholic and Nonalcoholic Adolescents

The authors examined both the nonspecific effects of psychopathology and the interactions of alcohol use disorders with other specific comorbid psychiatric conditions in an adolescent population on perceived self-efficacy to resist heavy drinking. The results suggest that nonspecific psychopathology, manifested in the form of any common psychiatric disorder, is associated with decreased situational confidence to resist heavy drinking across various situations. Main effects of alcohol use disorders, and several other specific psychiatric disorders, and specific comorbid interactions were also associated with decreased situational confidence. These results have implications for the etiology, prevention, and treatment of adolescents who abuse alcohol.