Effect Of Alcohol Use Disorder Research Articles

Alcohol use disorder and risk of specific methods of suicide death in a national cohort.

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.

Associations of history of alcohol use disorder with loneliness, social support, and mental health during the COVID-19 pandemic

This study examined the effects of alcohol use disorder (AUD) and treatment history on changes in loneliness, social support, and mental health symptoms from before to during the pandemic, and tested loneliness and social support as mediators of the AUD-mental health associations. Participants (n = 427) enrolled in the NIAAA COVID-19 Pandemic Impact on Alcohol Study were categorized into three groups: healthy control (62.3%), nontreatment AUD (14.1%), and treatment AUD (23.7%). Multilevel generalized linear models were conducted to examine changes in loneliness, social support, and mental health symptoms by group. Path analyses tested the mediating roles of loneliness and social support. Loneliness increased during the pandemic, especially in the nontreatment AUD group. Social support decreased in the healthy control and AUD treatment group. Anxiety and depressive symptoms increased in the nontreatment AUD group. Individuals with a history of AUD regardless of treatment history reported greater loneliness, which was linked to higher anxiety and depressive symptoms. Loneliness, but not social support, mediated the AUD-mental health associations. Psychosocial interventions aimed at increasing positive social engagement among individuals with AUD may help alleviate feelings of loneliness and mitigate mental health symptoms. Study findings can also help improve preparedness for future public health crises.

Bioinformatics and Systems Biology Approaches to Identify the Synergistic Effects of Alcohol Use Disorder on the Progression of Neurological Diseases

Clinical investigations showed that individuals with Alcohol Use Disorder (AUD) have worse Neurological Disease (ND) development, pointing to possible pathogenic relationships between AUD and NDs. It remains difficult to identify risk factors that are predisposing between AUD and NDs. In order to fix these issues, we created the bioinformatics pipeline and network-based approaches for employing unbiased methods to discover genes abnormally stated in both AUD and NDs and to pinpoint some of the common molecular pathways that might underlie AUD and ND interaction. We found 100 differentially expressed genes (DEGs) in both the AUD and ND patient’s tissue samples. The most important Gene Ontology (GO) terms and metabolic pathways, including positive control of cytotoxicity caused by T cells, proinflammatory responses, antigen processing and presentation, and platelet-triggered interactions with vascular and circulating cell pathways were then extracted using the overlapped DEGs. Protein-protein interaction analysis was used to identify hub proteins, including CCL2, IL1B, TH, MYCN, HLA-DRB1, SLC17A7, and HNF4A, in the pathways that have been reported as playing a function in these disorders. We determined several TFs (HNF4A, C4A, HLA-B, SNCA, HLA-DMB, SLC17A7, HLA-DRB1, HLA-C, HLA-A, and HLA-DPB1) and potential miRNAs (hsa-mir-34a-5p, hsa-mir-34c-5p, hsa-mir-449a, hsa-mir-155-5p, and hsa-mir-1-3p) were crucial for regulating the expression of AUD and ND which could serve as prospective targets for treatment. Our methodologies discovered unique putative biomarkers that point to the interaction between AUD and various neurological disorders, as well as pathways that could one day be the focus of therapeutic intervention.

Mediational pathways between aggregate genetic liability and nonfatal suicide attempt: A Swedish population-based cohort.

Despite recent progress in the genetics of suicidal behavior, the pathway by which genetic liability increases suicide attempt risk is unclear. We investigated the mediational pathways from family/genetic risk for suicide attempt (FGRSSA ) to suicide attempt by considering the roles of psychiatric illnesses. In a Swedish cohort, we evaluated time to suicide attempt as a function of FGRSSA and the mediational effects of alcohol use disorder, drug use disorder, attention-deficit/hyperactivity disorder, major depression, anxiety disorder, bipolar disorder, and non-affective psychosis. Analyses were conducted by sex in three age periods: 15-25 years (Nfemales = 850,278 and Nmales = 899,366), 26-35 years (Nfemales = 800,189 and Nmales = 861,774), and 36-45 years (Nfemales = 498,285 and Nmales = 535,831). The association between FGRSSA and suicide attempt was mediated via psychiatric disorders. The highest mediation effects were observed for alcohol use disorder in males (15-25 years, HRtotal = 1.60 [1.59; 1.62], mediation = 14.4%), drug use disorder in females (25-36 years, HRtotal = 1.46 [1.44; 1.49], mediation = 11.2%), and major depression (25-36 years) in females (HRtotal = 1.46 [1.44; 1.49], mediation = 7%) and males (HRtotal = 1.50 [1.47;1.52], mediation = 4.7%). While the direct effect of FGRSSA was higher at ages of 15-25, the mediation via psychiatric disorders was more prominent in later adulthood. Our study informs about the psychiatric illnesses via which genetic liability operates to impact suicide attempt risk, with distinct contributions according to age and sex.

Acute taurine reduced alcohol intake and preference in alcohol-experienced, but not in alcohol-näive rats by central mechanisms

Taurine is a non-essential β sulfonated amino acid involved in a plethora of biological functions in the mammalian central nervous system. Taurine is easily accessible in energy drinks for human consumption. Previous preclinical and clinical reports suggest that acute systemic administration of taurine could inhibit some of the behavioral and metabolic effects of alcohol use disorder. Overall, both in rodent and human studies, acute taurine administration reduced voluntary alcohol intake. This study aimed to assess the pharmacological effects of taurine (intracerebroventricular; i.c.v.) on ethanol intake/preference of rats either control (i.e., alcohol naïve) or forced ethanol intake (since juvenile age with a chronic intermittent access model). In addition, to explore anxiety-like behavior (through defensive burying behavior test) as pharmacological control of taurine. We found that acute (i.c.v.) taurine reduced alcohol consumption, i.e., taurine significantly decreased both alcohol intake and preference in adult male Wistar rats. Moreover, taurine elicits an anxiolytic-like effect in all administered groups independently of previous alcohol exposure.

An Examination of Alcohol Use Disorder Among the Characters of Patricia Highsmith

Alcohol Use Disorder (AUD) is a chronic disease with specific traits that connect to behavior, psychology, and physiology. This disease is especially prevalent among those within creative professions, which prompted further study into the effects of AUD on an alcoholic’s creative work. An examination of the incorporation of AUD within a female alcoholic author's work, particularly through the lens of Patricia Highsmith’s fictional characters, to cope with behaviors associated with AUD has yet to be accomplished, leading to this study’s purpose. A content analysis was conducted utilizing four indicating behaviors of AUD–codependency, neuroticism, binge drinking, and alcoholic terminology usage–that served as coding categories for 30 short stories analyzed. Data analysis showed that AUD was noticeably projected onto the fictional characters of Patricia Highsmith, with a total of 270 indicators identified. Implicit indicators–codependency and neuroticism–were projected within general written situations, and explicit indicators–binge drinking and alcoholic terminology usage–were projected within written situations that naturally trigger alcoholic behavior. Thus, it was suggested that AUD was projected onto the fictional characters of Patricia Highsmith in varying ways so as to cope with her alcoholic tendencies.

Alcohol use disorder (AUD) is associated with enhanced sensitivity to cellular lipopolysaccharide challenge.

Inflammation has been associated with alcohol use disorder (AUD). A novel method to characterize AUD-related immune signaling involves probing Toll-like receptor (TLR)-4 stimulated monocyte production of intracellular cytokines (ICCs) via lipopolysaccharide (LPS). We evaluated relationships between AUD and ICC production at rest and after LPS stimulation. We analyzed blood samples from 36 participants (AUD N = 14; Controls N = 22), collected across time, with ICC expression assessed at rest (i.e., unstimulated) and following stimulation with LPS (i.e., a total of 5 repeated unstimulated or stimulated measures/participant). Markers assessed included tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), TNF-α and IL-6 co-expression, and interferon (IFN). For each marker, we constructed linear mixed models with AUD, LPS, and timepoint as fixed effects (BMI as covariate), allowing for random slope and intercept. AUD × LPS was included as an interaction. For TLR4-stimulated monocyte production of TNF-α, there were effects of AUD (p < 0.01), LPS (p < 0.001), and AUD × LPS interaction (p < 0.05), indicating that individuals with AUD showed greater unstimulated- and stimulated monocyte expression of TNF-α. Similarly, for TLR4-stimulated monocyte co-expression of TNF-α and IL-6, there were effects of AUD (p < 0.01), LPS (p < 0.001), and AUD × LPS interaction (p < 0.05). No AUD or LPS effects were found for IL-6. Timepoint effects were observed on IL-6 and TNF-α/IL-6 co-expression (p < 0.001). Finally, for IFN there were also effects of AUD (p < 0.05), LPS (p < 0.001), and AUD × LPS (p < 0.001). Individuals with AUD showed greater resting or unstimulated levels of intracellular monocyte expression of TNF-α and IL-6/TNF-α co-expression than controls. AUD was associated with increases in TLR4-stimulated monocyte production of TNF-α and co-production of IL-6 and TNF-α. This is, to our knowledge, the first study to investigate relationships between AUD and monocyte production of proinflammatory cytokines, at rest and in response to TLR4 stimulation with LPS. The study extends previous findings on the roles of proinflammatory cytokines in AUD and serves as a critical proof of concept for the use of this method to probe neuroimmune mechanisms underlying AUD.

Which risk factors significantly influence the outcome of traumatic brain injured patients with alcohol use disorder?

Every year, approximately 10 million people worldwide suffer a traumatic brain injury that leads to hospitalization or mortality. Chronic and acute alcohol intoxication increase the risk of developing traumatic brain injury. Alcohol use disorder (AUD) as a predictor of outcome in neurosurgical patients and the definition of risk factors have been sparsely addressed so far. This study aims to improve the understanding of the effects of alcohol use disorder in the context of neurosurgical therapy. This study included patients admitted to Münster University Hospital with a traumatic brain injury and alcohol use disorder from January 1, 2010, to December 31, 2018. Univariate and multivariate analyses were performed to identify risk factors for a poorer outcome, assessed by the Glasgow Outcome Score. Of the 197 patients included, 156 (79%) were male, and 41 (21%) were female, with a median age of 49 years (IQR 38-58 years). In multivariate analyses, age (p < 0.001), the occurrence of a new neurologic deficit (p < 0.001), the development of hydrocephalus (p = 0.005), and CT-graphic midline shift due to intracerebral hemorrhage (p = 0.008) emerged as significant predictors of a worse outcome (GOS 1-3). In addition, the level of blood alcohol concentration correlated significantly with the occurrence of seizures (p = 0.009). Early identification of risk factors in patients with alcohol use disorder and traumatic brain injury is crucial to improve the outcome. In this regard, the occurrence of hydrocephalus or seizures during the inpatient stay should be considered as cause of neurological deterioration in this patient group.

Cytosine methylation in GABA B1 receptor identifies alcohol-related changes for men in blood and brain tissues

Alcohol use alters the reward signaling processes contributing to the development of addiction. We studied the effects of alcohol use disorder (AUD) on brain regions and blood of deceased women and men to examine sex-dependent differences in epigenetic changes associated with AUD. We investigated the effects of alcohol use on the gene promoter methylation of GABBR1 coding for GABAB receptor subunit 1 in blood and brain. We chose six brain regions associated with addiction and the reward pathway (nucleus arcuatus, nucleus accumbens, the mamillary bodies, amygdala, hippocampus and anterior temporal cortex) and performed epigenetic profiling of the proximal promoter of the GABBR1 gene of post-mortem brain and blood samples of 17 individuals with AUD pathology (4 female, 13 male) and 31 healthy controls (10 female, 21 male). Our results show sex-specific effects of AUD on GABBR1 promoter methylation. Especially, CpG -4 showed significant tissue-independent changes and significantly decreased methylation levels for the AUD group in the amygdala and the mammillary bodies of men. We saw prominent and consistent change in CpG-4 across all investigated tissues. For women, no significant loci were observed. We found sex-dependent differences in GABBR1 promoter methylation in relation to AUD. CpG-4 hypomethylation in male individuals with AUD is consistent for most brain regions. Blood shows similar results without reaching significance, potentially serving as a peripheral marker for addiction-associated neuronal adaptations. Further research is needed to discover more contributing factors in the pathological alterations of alcohol addiction to offer sex-specific biomarkers and treatment.

The impact of AUD on death for men with different IQ-scores: a register-based cohort study of 645 955 men.

To investigate whether the effect of alcohol use disorder (AUD) on death by natural and unnatural causes, respectively, differs according to intelligence quotient (IQ) scores. We followed 654 955 Danish men, including 75 267 brothers, born between 1939 and 1959 from their 25th birthday, 1 January 1970, or date of conscription (whichever came last) until 31 December 2018. The exposure of AUD was defined by first registered treatment (diagnosis since 1969, prescription medicine since 1994, or other treatment since 2006), and the outcomes of death by natural and unnatural causes, respectively, were obtained from nationwide registers since 1970. Information on IQ score was retrieved at conscription from the Danish Conscription Database. In total, 86 106 men were defined with an AUD. AUD combined with the highest, middle, and lowest IQ score tertiles, respectively, were associated with a 5.90 (95% confidence interval [CI] 5.75; 6.01), 6.88 (95% CI: 6.73; 7.04), and 7.53 (95% CI: 7.38; 7.68) times higher hazard of death by natural causes compared with no AUD and the highest IQ score tertile. The risk of death by unnatural causes was comparable for men with AUD regardless of IQ score tertile. A within-brother analysis showed that the impact of AUD on death by natural and unnatural causes, respectively, did not vary between men with different IQ score tertiles, but were hampered by statistical uncertainty. Our study indicates a need of special focus on men with lower levels of IQ score and AUD for prevention of death by natural causes.

Impact of alcohol use disorder severity on human immunodeficiency virus (HIV) viral suppression and CD4 count in three international cohorts of people with HIV.

Alcohol use has been linked to worse human immunodeficiency virus (HIV) immunologic/virologic outcomes, yet few studies have explored the effects of alcohol use disorder (AUD). This study assessed whether AUD severity is associated with HIV viral suppression and CD4 count in the three cohorts of the Uganda Russia Boston Alcohol Network for Alcohol Research Collaboration on HIV/AIDS (URBAN ARCH) Consortium. People with HIV (PWH) in Uganda (n= 301), Russia (n= 400), and Boston (n= 251), selected in-part based on their alcohol use, were included in analyses. Logistic and linear regressions were used to assess the cross-sectional associations between AUD severity (number of DSM-5 diagnostic criteria) and (1) HIV viral suppression, and (2) CD4 count (cells/mm3 ) adjusting for covariates. Analyses were conducted separately by site. The proportion of females was 51% (Uganda), 34% (Russia), and 33% (Boston); mean age (SD) was 40.7 (9.6), 38.6 (6.3), and 52.1 (10.5), respectively. All participants in Uganda and all but 27% in Russia and 5% in Boston were on antiretroviral therapy. In Uganda, 32% met criteria for AUD, 92% in Russia, and 43% in Boston. The mean (SD) number of AUD criteria was 1.6 (2.4) in Uganda, 5.6 (3.3) in Russia, and 2.4 (3.1) in Boston. Most participants had HIV viral suppression (Uganda 92%, Russia 57%, Boston 87%); median (IQR) CD4 count was 673 (506, 866), 351 (201, 542), and 591 (387, 881), respectively. In adjusted models, there were no associations between AUD severity and HIV viral suppression: adjusted odds ratios (AOR) (95%CI) per 1 additional AUD criterion in Uganda was 1.08 (0.87, 1.33); Russia 0.98 (0.92, 1.04); and Boston 0.95 (0.84, 1.08) or CD4 count: mean difference (95%CI) per 1 additional criterion: 5.78 (-7.47, 19.03), -3.23 (-10.91, 4.44), and -8.18 (-24.72, 8.35), respectively. In three cohorts of PWH, AUD severity was not associated with HIV viral suppression or CD4 count. PWH with AUD in the current era of antiretroviral therapy can achieve virologic control.

Analysis of the Causes, Effects, and Treatment of Alcohol Use Disorder

The number of people with alcohol problems is increasing year by year. There is a trend people of younger ages are even more affected by this issue. Alcohol use disorder is an important issue that contemporary society has started paying attention to, thereby making it one of the key topics of today's research. Researchers have made progress in determining the causes and effects of alcohol use disorder, but there are still gaps in research in certain areas, as well as a lack of unified explanations regarding the issues with cognition that alcohol problems cause. In that sense, studies have been conducted on how alcohol use disorder affects working memory, along with other aspects of cognition. Yet, these studies conclude that additional research is necessary in order to discover how the working memory abilities of people with alcohol use disorder can be increased. In studies of alcohol use disorder causes the physical and emotional aspects, experts note that decision-making processes, positive emotions, and negative experiences are common factors that lead to the disorder. To explore therapy and suggestions to treat alcohol use disorder, this paper examined the literature of negative impact of alcohol use disorders on working memory. The results of the analysis concluded that alcohol use disorder severely affects cognition, especially working memory. Further findings determine that combining behavioral therapy and medications is the best strategy patients can have when they are reluctant to stop using alcohol. The consequences of alcohol use disorder are also provided, including both the physical aspects and the cognitive impacts that affect people’s daily lives.

Study of brainstem auditory evoked response and biochemical markers in patients of alcohol use disorder

Objectives: Data available on brainstem auditory evoked response (BAER) and its correlation with biochemical parameters in patients of alcohol use disorder (AUD) in Indian population is scanty. Therefore, this study was undertaken to focus on the effects of AUD on BAER and liver enzymes. Materials and Methods: This case-control study included 40 males in the study group who had AUD and 40 healthy males in the control group in the age group of 20–60 years. The BAER was performed using octopus NCS/ EMG/EP (Clarity) machine. The levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase and serum bilirubin were estimated in all the subjects. Results: We observed a highly significant increase in the absolute latencies of waves III and V and interpeak latencies (IPL) I-III and I-V of BAER in the patients of AUD in this study. Significant increase in the liver enzymes and especially AST/ALT ratio of patients of AUD was seen which indicated towards subclinical alcoholic hepatitis. The latencies of waves of EPs (waves III, V, IPL I-III and IPL I-V) were positively correlated with the biochemical parameters and duration of AUD. Conclusion: Our findings indicated that AUD lead to the increase in brainstem transmission time and also lead to subclinical alcoholic hepatitis which is reflected by the increase in the liver enzymes. We concluded that chronic alcohol consumption affected the auditory pathways and delayed the auditory transmission time which was suggestive of possible demyelination of auditory tracts.

A Matched Control Analysis on the Effects of Alcohol Use Disorder After Primary Total Knee Arthroplasty in Medicare Patients.

Several studies have found the negative impact of alcohol use disorder (AUD), most notably coagulation derangements. We sought to investigate the effects of AUD after primary total knee arthroplasty (TKA) for (1) postoperative complications, (2) lengths of stay, and (3) costs of care. This was a retrospective database analysis of Medicare patients with AUD undergoing primary TKA performed between 2005 and 2014. Patients with AUD were matched to controls in a 1:5 ratio by age, sex, and medical comorbidities. The query yielded 354,690 TKA patients: 59,126 with AUD and 295,564 without AUD. Patients with AUD had significantly greater odds ratio (OR) of medical complications, including venous thromboembolism (VTE) within 90 days (OR: 1.41, P < 0.0001) and at 1 year (OR: 1.51, P < 0.0001) and greater 2-year implant-related complications after primary TKA. Furthermore, patients with AUD had significantly longer lengths of stay (4 versus 3 days, P < 0.0001) and incurred a significantly higher episode of care costs ($15,569.76 versus $13,763.06, P < 0.0001). The present study demonstrated a significant association between AUD and the development of VTE. We hope this research will aid in risk stratification and tailoring of VTE chemoprophylaxis and postoperative management in this at-risk group after TKA. Level III.

A matched-control analysis on the effects of alcohol use disorder following primary reverse shoulder arthroplasty

IntroductionThe purpose of this study was to determine whether alcohol use disorder (AUD) patients undergoing reverse shoulder arthroplasty (RSA) have increased: 1) lengths of stay (LOS); 2) complications; and 3) costs. MethodsThe study identified 19,168 patients in the study (n = 3198) and control (n = 15,970) cohort. In-hospital LOS, 90-day complications, and costs were assessed. ResultsAUD patients had significantly longer LOS (3- vs. 2-days, p < 0.0001), higher9 0-day medical complications (49.59 vs. 14.81%; p < 0.0001), and 90-day costs of care ($18,763.25 vs. $16,035.49, p < 0.0001). ConclusionsThe study is useful as it can allow healthcare professionals to adequately counsel these patients.

The Moderating Effect of Alcohol Use Disorder on Intimate Partner Violence Intervention Outcomes in Veterans

BackgroundVeterans report relatively high rates of intimate partner violence (IPV) due to high trauma exposure. Alcohol use disorder (AUD), which is more prevalent among veterans, is a risk factor for IPV use and recidivism following IPV intervention. Using data from a prior randomized control trial of a trauma-informed IPV intervention, we examined the moderating effect of AUD on treatment outcomes among veterans.MethodsParticipants were 61 male veterans (M age = 37.18, SD = 13.23; 82% White; 18% met criteria for AUD) who participated in the Strength at Home (SAH) IPV intervention. Generalized mixed modelling was used to examine the effects of AUD and treatment attendance on posttreatment reductions in IPV.ResultsA significant three-way interaction between time, AUD, and session attendance was observed with respect to reductions in psychological IPV. Specifically, psychological IPV decreased significantly over time, but to a lesser extent among individuals with AUD, regardless of treatment attendance.DiscussionResults indicate that participants with AUD receive less benefit from treatment with regard to coercive and controlling abusive behaviors. Findings speak to the need for adapting IPV intervention in order to address problematic alcohol use and related externalizing psychopathology.

Mother and Father Prescription Opioid Misuse, Alcohol Use Disorder, and Parent Knowledge in Pathways to Adolescent Alcohol Use.

Parenting during early adolescence is key in protecting adolescents against substance use initiation and patterned use. Parental alcohol use disorder is a robust risk factor for maladaptive parenting and adolescent alcohol use. However, it is unclear what effect parent prescription opioid misuse has on parenting and adolescent alcohol use. Associations were examined among parent alcohol use disorder, prescription opioid misuse, and parent knowledge of adolescent activities in early adolescence and their prediction of adolescent alcohol use approximately five years later. The current sample consisted of mothers (N = 457) and fathers (N = 368) drawn from a large longitudinal sample (The Adult and Family Development Project: AFDP). The average age was 11.68 in early adolescence and 16.22 in adolescence and 47% of adolescents were female. Parent knowledge was tested as a mediator of the effects of parent alcohol disorder and parent opioid misuse on adolescence alcohol use. This model was examined separately in mothers and fathers. For mothers, alcohol use disorder and prescription opioid misuse both predicted adolescent alcohol use indirectly via parent knowledge. Mothers' alcohol use disorder also directly predicted adolescent alcohol use. For fathers, no direct or indirect effects of alcohol use disorder or prescription opioid misuse were detected although a covariate effect of illicit drug use on parent knowledge emerged. The results are discussed with regards to the processes that may explain how alcohol disorder or prescription opioid misuse affect mothers' knowledge and increase risk for adolescent alcohol use.

Genome-Wide Effects of Alcohol Use Disorder on Long Non-Coding RNAs and Splicing in Brain and Liver

Alcohol use disorder (AUD) is a widespread disease, but molecular pathogenesis of AUD remains incompletely understood, and there are no efficient medications to treat AUD. Long non-coding RNAs (lncRNAs) are RNA molecules >200 nucleotides with no coding potential. LncRNAs control key transcriptional and posttranscriptional processes, thus regulating the formation of transcriptome. We tested the hypothesis that AUD affects transcriptome via changes in lncRNAome.

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.