Browsing by Subject "Alcohol consumption"

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  • Lainiola, Mira; Linden, Anni-Maija (2017)
    Neuroinflammation may play an important role in the development of alcohol addiction. Recent pre-clinical reports suggest that enhanced innate immune system signaling increases consumption of alcohol. Our aim was to study whether consequences of lipopolysaccharide (LPS)-induced sickness reaction increase long-term alcohol intake. Adult male C57BL/6j mice, housed in individually ventilated cages, were injected with LPS intraperitoneally (i.p.) and allowed to recover from an acute sickness reaction for 1 week before analysis of their alcohol intake in two different drinking models. Effects of LPS challenge were tested in a continuous two-bottle free choice test with increasing concentrations of alcohol and in a drinking in the dark (DID) binge model. In addition, the effect of repeatedly administered LPS during abstinence periods between binge drinking was analyzed in the DID model. In addition, the DID model was used to study the effects of the microglia inhibitor minocycline (50 mg/kg/day, 4 days) and purinergic P2X7 receptor antagonist Brilliant Blue G (75 mg/kg/day, 7 days) on alcohol intake. In contrast to previous findings, pretreatment with a 1-mg/kg dose of LPS did not significantly increase ethanol consumption in the continuous two-bottle choice test. As a novel finding, we report that increasing the LPS dose to 1.5 mg/kg reduced consumption of 18 and 21% (v/v) ethanol. In the DID model, pretreatment with LPS (0.2-1.5 mg/kg) did not significantly alter 15% or 20% ethanol consumption. Neither did repeated LPS injections affect binge alcohol drinking. Minocycline reduced alcohol, but also water, intake regardless of LPS pretreatment. No data on effects of P2X7 antagonists on alcohol consumption have been previously published; therefore, we report here that subchronic Brilliant Blue G had no effect on alcohol intake in the DID model. As a conclusion, further studies are needed to validate this LPS model of the interaction between immune system activation and alcohol consumption. (C) 2017 Elsevier Inc. All rights reserved.
  • McMinn, Megan A.; Gray, Linsay; Harkanen, Tommi; Tolonen, Hanna; Pitkanen, Joonas; Molaodi, Oarabile R.; Leyland, Alastair H.; Martikainen, Pekka (2020)
    Background: In the context of declining levels of participation, understanding differences between participants and non-participants in health surveys is increasingly important for reliable measurement of health-related behaviors and their social differentials. This study compared participants and non-participants of the Finnish Health 2000 survey, and participants and a representative sample of the target population, in terms of alcohol-related harms (hospitalizations and deaths) and all-cause mortality. Methods: We individually linked 6,127 survey participants and 1,040 non-participants, aged 30-79, and a register-based population sample (n = 496,079) to 12 years of subsequent administrative hospital discharge and mortality data. We estimated age-standardized rates and rate ratios for each outcome for non-participants and the population sample relative to participants with and without sampling weights by sex and educational attainment. Results: Harms and mortality were higher in non-participants, relative to participants for both men (rate ratios = 1.5 [95% confidence interval = 1.2, 1.9] for harms; 1.6 [1.3, 2.0] for mortality) and women (2.7 [1.6, 4.4] harms; 1.7 [1.4, 2.0] mortality). Non-participation bias in harms estimates in women increased with education and in all-cause mortality overall. Age-adjusted comparisons between the population sample and sampling weighted participants were inconclusive for differences by sex; however, there were some large differences by educational attainment level. Conclusions: Rates of harms and mortality in non-participants exceed those in participants. Weighted participants' rates reflected those in the population well by age and sex, but insufficiently by educational attainment. Despite relatively high participation levels (85%), social differentiating factors and levels of harm and mortality were underestimated in the participants.
  • Pachito, Daniela V.; Pega, Frank; Bakusic, Jelena; Boonen, Emma; Clays, Els; Descatha, Alexis; Delvaux, Ellen; De Bacquer, Dirk; Koskenvuo, Karoliina; Kroeger, Hannes; Lambrechts, Marie-Claire; Latorraca, Carolina O. C.; Li, Jian; Cabrera Martimbianco, Ana L.; Riera, Rachel; Rugulies, Reiner; Sembajwe, Grace; Siegrist, Johannes; Sillanmäki, Lauri; Sumanen, Markku; Suominen, Sakari; Ujita, Yuka; Vandersmissen, Godelieve; Godderis, Lode (2021)
    Background: The World Health Organization (WHO) and the International Labour Organization (ILO) are developing Joint Estimates of the work-related burden of disease and injury (WHO/ILO Joint Estimates), with contributions from a large network of experts. Evidence from mechanistic data suggests that exposure to long working hours may increase alcohol consumption and cause alcohol use disorder. In this paper, we present a systematic review and meta-analysis of parameters for estimating the number of deaths and disability-adjusted life years from alcohol consumption and alcohol use disorder that are attributable to exposure to long working hours, for the development of the WHO/ILO Joint Estimates. Objectives: We aimed to systematically review and meta-analyse estimates of the effect of exposure to long working hours (three categories: 41-48, 49-54 and >55 h/week), compared with exposure to standard working hours (35-40 h/week), on alcohol consumption, risky drinking (three outcomes: prevalence, incidence and mortality) and alcohol use disorder (three outcomes: prevalence, incidence and mortality). Data sources: We developed and published a protocol, applying the Navigation Guide as an organizing systematic review framework where feasible. We searched electronic bibliographic databases for potentially relevant records from published and unpublished studies, including the WHO International Clinical Trials Register, Ovid MEDLINE, PubMed, Embase, and CISDOC on 30 June 2018. Searches on PubMed were updated on 18 April 2020. We also searched electronic grey literature databases, Internet search engines and organizational websites; hand searched reference list of previous systematic reviews and included study records; and consulted additional experts. Study eligibility and criteria: We included working-age (15 years) and unpaid domestic workers. We considered for inclusion randomized controlled trials, cohort studies, case-control studies and other nonrandomized intervention studies with an estimate of the effect of exposure to long working hours (41-48, 49-54 and 55 h/week), compared with exposure to standard working hours (35-40 h/week), on alcohol consumption (in g/week), risky drinking, and alcohol use disorder (prevalence, incidence or mortality). Study appraisal and synthesis methods: At least two review authors independently screened titles and abstracts against the eligibility criteria at a first stage and full texts of potentially eligible records at a second stage, followed by extraction of data from publications related to qualifying studies. Two or more review authors assessed the risk of bias, quality of evidence and strength of evidence, using Navigation Guide and GRADE tools and approaches adapted to this project. Results: Fourteen cohort studies met the inclusion criteria, comprising a total of 104,599 participants (52,107 females) in six countries of three WHO regions (Americas, South-East Asia, and Europe). The exposure and outcome were assessed with self-reported measures in most studies. Across included studies, risk of bias was generally probably high, with risk judged high or probably high for detection bias and missing data for alcohol consumption and risky drinking. Compared to working 35-40 h/week, exposure to working 41-48 h/week increased alcohol consumption by 10.4 g/week (95% confidence interval (CI) 5.59-15.20; seven studies; 25,904 participants, I2 71%, low quality evidence). Exposure to working 49-54 h/week increased alcohol consumption by 17.69 g/week (95% confidence interval (CI) 9.16-26.22; seven studies, 19,158 participants, I2 82%, low quality evidence). Exposure to working >55 h/week increased alcohol consumption by 16.29 g/week (95% confidence interval (CI) 7.93-24.65; seven studies; 19,692 participants; I2 82%, low quality evidence). We are uncertain about the effect of exposure to working 41-48 h/week, compared with working 35-40 h/week on developing risky drinking (relative risk 1.08; 95% CI 0.86-1.36; 12 studies; I2 52%, low certainty evidence). Working 49-54 h/week did not increase the risk of developing risky drinking (relative risk 1.12; 95% CI 0.90-1.39; 12 studies; 3832 participants; I2 24%, moderate certainty evidence), nor working >55 h/week (relative risk 1.11; 95% CI 0.95-1.30; 12 studies; 4525 participants; I2 0%, moderate certainty evidence). Subgroup analyses indicated that age may influence the association between long working hours and both alcohol consumption and risky drinking. We did not identify studies for which we had access to results on alcohol use disorder. Conclusions: Overall, for alcohol consumption in g/week and for risky drinking, we judged this body of evidence to be of low certainty. Exposure to long working hours may have increased alcohol consumption, but we are uncertain about the effect on risky drinking. We found no eligible studies on the effect on alcohol use disorder. Producing estimates for the burden of alcohol use disorder attributable to exposure to long working hours appears to not be evidence-based at this time. Protocol identifier: https://doi.org/10.1016/j.envint.2018.07.025. PROSPERO registration number: CRD42018084077