Alcohol and alcoholism最新文献

Aims: This study aimed to test whether the alcohol harm paradox (AHP) is observed in Brazil by investigating (i) the association between educational attainment and alcohol-related consequences (ARC) and (ii) the contribution of average alcohol volume consumed (AVC), past-month heavy episodic drinking (HED), smoking, body mass index (BMI), and depression in accounting for the disparities in ARC.

Methods: We analysed data from the 2019 Brazilian National Health Survey, a nationally representative household survey. The composite ARC outcome was considered present when an individual reported a past-year episode of activity failure, amnesia, and concern by others due to alcohol consumption. Adjusted binary logistic regression models were fitted using a hierarchical approach to calculate the odds ratios (OR) and respective 95% confidence intervals (CI), and to assess the contribution of each set of variables in attenuating the educational differences in ARC.

Results: Those from the lowest educational strata (incomplete elementary school) exhibited higher odds of ARC than their counterparts (OR: 2.03; 95% CI: 1.73-2.37). Although smoking, BMI, and depression attenuated the educational gradient (i.e. reduced the difference between reference and riskier categories) in ARC by ~13%, the adjustment for AVC and HED amplified inequalities by 0.3% and 5.7%, respectively.

Conclusion: We found evidence of the AHP in Brazil. Educational inequalities in ARC were scarcely attenuated by behavioural factors, and a suppression effect was noted when adjusting for AVC and HED.

Aims: The treatment with the antibiotic rifampicin (Rif) led to a decrease in the frequency of neurodegenerative pathologies. There are suggestions that the mechanism of action of Rif may be mediated by its effect on toll-like receptor (TLR)4-dependent pathways. We evaluated the expression status of TLR4-dependent genes during abstinence from long-term alcohol treatments in the nucleus accumbens (NAc) of the rat brain, and also studied the effects of Rif to correct these changes.

Methods: The long-term alcohol treatment was performed by intragastric delivery of ethanol solution. At the end of alcohol treatment intraperitoneal injections of Rif (100 mg/kg) or saline were made. Extraction of the brain structures was performed on the 10th day of abstinence from alcohol. We used the SYBR Green qPCR method to quantitatively analyze the relative expression levels of the studied genes.

Results: The long-term alcohol treatment promotes an increase in the level of TLR4 mRNA and mRNA of its endogenous ligand high-mobility group protein B1 during abstinence drop alcohol in NAc of rats. The use of Rif in our study led to a decrease in the increased expression of high-mobility group protein B1, Tlr4, and proinflammatory cytokine genes (Il1β, Il6) in the NAc of the rat brain during abstinence of long-term alcohol treatment. In addition, Rif administration increased the decreased mRNA levels of anti-inflammatory cytokines (Il10, Il11).

Conclusion: The data obtained indicate the ability of Rif to correct the mechanisms of the TLR4 system genes in the NAc of the rat brain during alcohol abstinence.

Aims: To examine the cross sectional and longitudinal associations between the Alcohol Use Disorders Identification Test-Concise (AUDIT-C) and differences in high-density lipoprotein (HDL) in a psychiatrically ill population.

Methods: Retrospective observational study using electronic health record data from a large healthcare system, of patients hospitalized for a mental health/substance use disorder (MH/SUD) from 1 July 2016 to 31 May 2023, who had a proximal AUDIT-C and HDL (N = 15 915) and the subset who had a repeat AUDIT-C and HDL 1 year later (N = 2915). Linear regression models examined the association between cross-sectional and longitudinal AUDIT-C scores and HDL, adjusting for demographic and clinical characteristics that affect HDL.

Results: Compared with AUDIT-C score = 0, HDL was higher among patients with greater AUDIT-C severity (e.g. moderate AUDIT-C score = 8.70[7.65, 9.75] mg/dl; severe AUDIT-C score = 13.02 [12.13, 13.90] mg/dL[95% confidence interval (CI)] mg/dl). The associations between cross-sectional HDL and AUDIT-C scores were similar with and without adjusting for patient demographic and clinical characteristics. HDL levels increased for patients with mild alcohol use at baseline and moderate or severe alcohol use at follow-up (15.06[2.77, 27.69] and 19.58[2.77, 36.39] mg/dL[95%CI] increase for moderate and severe, respectively).

Conclusions: HDL levels correlate with AUDIT-C scores among patients with MH/SUD. Longitudinally, there were some (but not consistent) increases in HDL associated with increases in AUDIT-C. The increases were within range of typical year-to-year variation in HDL across the population independent of alcohol use, limiting the ability to use HDL as a longitudinal clinical indicator for alcohol use in routine care.

Introduction: Alcohol ingestion influences metabolism during a subsequent exercise session, as evidenced by increased blood lactate concentration during fixed-intensity exercise. Therefore, augmented blood concentrations of alcohol may interfere with the anaerobic metabolism during high-intensity, short-duration exercise bout, thereby leading to impaired athletic performance.

Objective: This study investigated whether the acute ingestion of alcohol as ethanol modulates performance parameters derived from the power-duration relationship in a 3-min all-out cycling test that allows for identifying the power output related to heavy and severe exercise intensities.

Methods: Twenty-four recreationally active cyclists (16 men and 8 women) ingested a beverage containing either 0.4 g ethanol.kg-1 body mass (EtOH) or a placebo (PLA) solution. Thirty minutes following ingestion, they completed a 3-min all-out test to measure power output and determine the end-test power (EP) and the work done above EP (WEP).

Results: Alcohol ingestion decreased WEP by 16% (EtOH: 5.6 ± 2.5 kJ vs. PLA: 6.7 ± 2.4 kJ; P = .003) but did not change EP (EtOH: 211 ± 44 W vs. PLA: 212 ± 44 W; P = .671). The alcohol-mediated effect in WEP was not influenced when controlling for participants' sex or accuracy in identifying the beverage ingested.

Conclusion: Our data indicate that alcohol ingestion impaired the anaerobic work capacity, as evidenced by the reduction in WEP during the 3-min all-out test. Moreover, the ability to exercise at an intensity above the heavy domain may be decreased after ingestion of a moderate alcohol dose.

Aims: This study aimed to compare reward, relief, and habit treatment-seeking individuals on recent drinking, alcohol use disorder (AUD) phenomenology, and mood. The second aim of the study was to evaluate the predictive validity of reward, relief, and habit profiles.

Method: Treatment-seeking individuals with an AUD (n = 169) were recruited to participate in a medication trial for AUD (NCT03594435). Reward, relief, and habit drinking groups were assessed using the UCLA Reward Relief Habit Drinking Scale. Group differences at baseline were evaluated using univariate analyses of variance. A subset of participants were enrolled in a 12-week, double-blind, placebo-controlled medication trial (n = 102), and provided longitudinal drinking and phenomenology data. The predictive validity of group membership was assessed using linear regression analyses.

Results: At baseline, individuals who drink primarily for relief had higher craving and negative mood than those who drink for reward and habit. Prospectively, membership in the relief drinking group predicted greater alcohol use, greater heavy drinking, and fewer days abstinent compared to those in the reward drinking group. Membership in the relief drinking group also predicted greater alcohol craving, more alcohol-related consequences, and more anxiety symptoms over 12 weeks compared to those in the reward drinking group.

Conclusions: This study provides support for reward and relief drinking motive profiles in treatment-seeking individuals with an AUD. Membership in the relief drinking motive group was predictive of poorer drinking outcomes and more negative symptomology over 12 weeks, indicating that individuals who drink for relief may be a particularly vulnerable sub-population of individuals with AUD.

Aims: To outline the demographic, clinical, laboratory characteristics, and treatment outcomes of tuberculosis (TB) patients who used substances.

Methods: This retrospective cohort study compared 50 TB patients who used substances with a matched random sample of 100 TB patients who did not use substances between 2007 and 2017. Treatment failure was defined as a sputum smear or culture that tested positive after 5 months of treatment, loss to follow-up, unevaluated patients, or death.

Results: TB patients who used substances were typically younger, experienced homelessness, smokers, and had fewer chronic diseases than those who did not use substances. They also were hospitalized for longer periods, their treatment durations were longer, had higher rates of multidrug resistant strains, increased rates of treatment failure, and higher mortality. Individuals whose treatment failed predominantly originated from the former Soviet Union, experienced homelessness, and had chronic diseases compared with those whose treatment was successful. In the multivariate analysis, homelessness [odds ratios (OR) = 6.7], chronic diseases (OR = 12.4), and substance use (OR = 4.0) were predictors of treatment failures.

Conclusions: TB patients who used substances were more likely to have treatment failure. Targeted interventions, including early diagnosis and enhanced support during treatment, are essential to achieve treatment success in this vulnerable population, in addition to TB-alcohol/drug collaborative activities.

Aim: We examined the acute effects of a moderate alcohol dose (48 g) ingested before prolonged cycling on acute physiological responses in eight healthy males (mean ± SD; 23 ± 2 years; 1.77 ± 0.04 m; 75.8 ± 4.1 kg).

Methods: In a randomized order, euhydrated participants completed two experimental sessions with the sequence of 150-min seated at rest, 90-min of cycling at 50% of the maximal rate of oxygen consumption ($dot{textrm V}textrm O$2max), 120-min seated at rest. Participants drank 250 mL of flavored squash with or without alcohol (vodka; ~16 g) at 10, 40, and 70 min of the initial resting phase, giving a cumulative fluid intake of 750 mL with 48 g of alcohol. Heart rate, blood glucose, breath alcohol concentration, and respiratory gasses were recorded throughout the entire trial with cumulative urine volume recorded during both rest phases.

Results: Total carbohydrate (control = 115 ± 19 g: alcohol = 119 ± 21 g; P = 0.303) and lipid (control = 17 ± 4 g: alcohol = 20 ± 7 g; P = 0.169) oxidation was similar between conditions. Average heart rate was 7% higher in the alcohol condition (control = 111 ± 12 bpm; alcohol = 119 ± 11 bpm; P = 0.003). Blood glucose concentrations were similar between conditions during (P = 0.782) and after exercise (P = 0.247). Urine output was initially increased between conditions following alcohol ingestion before diminishing (P < 0.001) with no difference in total cumulative urine output (P = 0.331).

Conclusion: Consuming an alcoholic drink containing 48 g of alcohol in the hour before moderate intensity sub-maximal aerobic exercise led to detectable increases in heart rate and rate of urine production with no effect on substrate use.

Aims: Chronic alcohol consumption is well known to cause peripheral neuropathy, affecting both small and large nerve fibers. The aim of this study was to correlate biochemical and neurophysiological findings and investigate possible biomarkers and risk factors for pathogenetic mechanisms of neuropathy in patients diagnosed with alcohol use disorder (AUD).

Methods: Ninety patients diagnosed with AUD were enrolled in this prospective study over a period of 3 years. Serum biochemical parameters, as well as thiamine blood levels, were determined upon admission. Every subject was assessed by clinical neurological examination, followed by Nerve Conduction Studies, Quantitative Sensory Testing, and Sympathetic Skin Response. Fifty age and gender-matched patients without a diagnosis of AUD were used as the control group.

Results: Peripheral neuropathy was diagnosed in 54 patients (60%). Among them, pure large fiber neuropathy was found in 18 patients, pure small fiber neuropathy in 12 patients, and both large and small fiber neuropathy was diagnosed in 24 patients. Elevated liver enzymes and fasting glucose levels upon admission were significantly correlated with neuropathy. Lower blood thiamine levels (than reference) were found in seven patients and were not correlated with neuropathy.

Conclusions: Our study suggests that alcohol-related liver dysfunction and hyperglycemia may contribute as risk factors of peripheral neuropathy in patients diagnosed with AUD, while blood thiamine levels do not correlate with neuropathy. Moreover, we suggest that liver enzymes and the De Ritis ratio could be potentially used as biomarkers for the incidence and severity of alcohol-related neuropathy.

Topiramate (TPM), a GABA/glutamate modulator, has shown positive results for treating alcohol use disorder (AUD), but causes significant cognitive adverse effects. TPM causes cognitive side effects by reducing glutathione levels in the frontal lobe. N-acetyl cysteine (NAC) increases level of intracellular glutathione. We hypothesized that combining NAC with TPM may mitigate the possible cognitive side effects of TPM, as well as working synergistically in reducing alcohol consumption more efficaciously than using TPM alone. A 12-week, double-blind randomized trial assessing the effects of combining NAC (1200 mg/day) with TPM (200 mg/day) vs TPM alone (i) cognitive side effects caused by TPM, (ii) percentage of heavy drinking days (PHDD) and percentage of days abstinent (PDA) using weekly calendar, and (iii) craving outcomes using the obsessive-compulsive drinking scale. Seventeen participants were randomized into the study (nine received TPM + NAC and eight matching TPM + Placebo). Cognitive adverse events were not significantly different between the treatment arms (P = 0.581). There was no difference in PHDD (P = 0.536) and in PDA over the entire study period (P = 0.892). However, both treatment groups at study end, compared with the baseline, significantly reduced their PHDD and increased their PDA. As for cravings: TPM + NAC group has shown higher level in automaticity of drinking (P = 0.029) and interference due to drinking (P = 0.014) subscales compared with the TPM + Placebo group. No difference was observed between groups in terms of Drinking Obsessions and Alcohol Consumption subscales. This pilot study indicates that combining NAC with TPM is overall safe, but the addition of NAC has no significant benefit over placebo in the incidence of TPM-related cognitive impairment, and alcohol drinking. Furthermore, craving outcomes may become worse with the addition of NAC.