22 September 2022 In Dementia

Alcohol consumption has been associated with the risk of mild cognitive impairment (MCI) in observational studies. The result is inconsistent and whether the association is causal remains unknown. To examine the causal effect of alcohol consumption on MCI in rural China, this study used a cross-sectional dataset that included 1966 observations collected in rural China, of which 235 observations' genotyping were collected. All participants accepted the MCI evaluation using Mini-Cog and were asked about the participants' alcohol consumption behavior. The causal effect of alcohol consumption on MCI was investigated by Mendelian randomization (MR) of genetic variation in the aldehyde dehydrogenase 2 (ALDH2 rs671) gene. The risk of MCI in Chinese rural areas was 43%. Alcohol consumption was causally associated with a higher risk of MCI under MR design. Parameter estimates of drinking or not (b = 0.271, p = 0.007, 95% CI = 0.073 to 0.469), drinking frequency during the past 30 days (b = 0.016, p = 0.003, 95% CI = 0.005 to 0.027), and the weekly ethanol consumption (b = 0.132, p = 0.004, 95% CI = 0.042 to 0.223) were all positive and statistically significant at the 5% level. In conclusion, there was a high risk of MCI in rural China, and alcohol consumption was causally associated with a higher risk of MCI.

26 August 2022 In General Health

Alcohol consumption is associated with the development of cardiovascular diseases, cancer, and liver disease. The biological mechanisms are still largely unclear. Here, we aimed to use an agnostic approach to identify phenotypes mediating the effect of alcohol on various diseases.

METHODS: We performed an agnostic association analysis between alcohol consumption (red and white wine, beer/cider, fortified wine, and spirits) with over 7800 phenotypes from the UK biobank comprising 223,728 participants. We performed Mendelian randomisation analysis to infer causality. We additionally performed a Phenome-wide association analysis and a mediation analysis between alcohol consumption as exposure, phenotypes in a causal relationship with alcohol consumption as mediators, and various diseases as the outcome.

RESULTS: Of 45 phenotypes in association with alcohol consumption, 20 were in a causal relationship with alcohol consumption. Gamma glutamyltransferase (GGT; beta = 9.44; 95% CI = 5.94, 12.93; Pfdr = 9.04 x 10(-7)), mean sphered cell volume (beta = 0.189; 95% CI = 0.11, 0.27; Pfdr = 1.00 x 10(-4)), mean corpuscular volume (beta = 0.271; 95% CI = 0.19, 0.35; Pfdr = 7.09 x 10(-10)) and mean corpuscular haemoglobin (beta = 0.278; 95% CI = 0.19, 0.36; Pfdr = 1.60 x 10(-6)) demonstrated the strongest causal relationships. We also identified GGT and physical inactivity as mediators in the pathway between alcohol consumption, liver cirrhosis and alcohol dependence.

CONCLUSION: Our study provides evidence of causality between alcohol consumption and 20 phenotypes and a mediation effect for physical activity on health consequences of alcohol consumption.

26 August 2022 In Drinking Patterns

BACKGROUND: Heavy alcohol consumption increases the risk of several chronic diseases. In this multicohort study, we estimated the number of life-years without major chronic diseases according to different characteristics of alcohol use.

METHODS: In primary analysis, we pooled individual-level data from up to 129,942 adults across 12 cohort studies with baseline data collection on alcohol consumption, drinking patterns, and history between 1986 and 2005 (the IPD-Work Consortium). Self-reported alcohol consumption was categorised according to UK guidelines - non-drinking (never or former drinkers); moderate consumption (1-14 units); heavy consumption (>14 units per week). We further subdivided moderate and heavy drinkers by binge drinking pattern (alcohol-induced loss of consciousness). In addition, we assessed problem drinking using linked data on hospitalisations due to alcohol abuse or poisoning. Follow-up for chronic diseases for all participants included incident type 2 diabetes, coronary heart disease, stroke, cancer, and respiratory disease (asthma and chronic obstructive pulmonary disease) as ascertained via linkage to national morbidity and mortality registries, repeated medical examinations, and/or self-report. We estimated years lived without any of these diseases between 40 and 75 years of age according to sex and characteristics of alcohol use. We repeated the main analyses using data from 427,621 participants in the UK Biobank cohort study.

FINDINGS: During 1.73 million person-years at risk, 22,676 participants in IPD-Work cohorts developed at least one chronic condition. From age 40 to 75 years, never-drinkers [men: 29.3 (95%CI 27.9-30.8) years, women 29.8 (29.2-30.4) years)] and moderate drinkers with no binge drinking habit [men 28.7 (28.4-29.0) years, women 29.6 (29.4-29.7) years] had the longest disease-free life span. A much shorter disease-free life span was apparent in participants who experienced alcohol poisoning [men 23.4 (20.9-26.0) years, women 24.0 (21.4-26.5) years] and those with self-reported heavy overall consumption and binge drinking [men: 26.0 (25.3-26.8), women 27.5 (26.4-28.5) years]. The pattern of results for alcohol poisoning and self-reported alcohol consumption was similar in UK Biobank. In IPD-Work and UK Biobank, differences in disease-free years between self-reported moderate drinkers and heavy drinkers were 1.5 years or less.

INTERPRETATION: Individuals with alcohol poisonings or heavy self-reported overall consumption combined with a binge drinking habit have a marked 3- to 6-year loss in healthy longevity. Differences in disease-free life between categories of self-reported weekly alcohol consumption were smaller. Funding: Medical Research Council, National Institute on Aging, NordForsk, Academy of Finland, Finnish Work Environment Fund.

15 June 2022 In Dementia

BACKGROUND: Low-to-moderate alcohol consumption appears to have potential health benefits. Existing evidence concludes that wine may be associated with a lower incidence of certain diseases. This systematic review and meta-analysis aim to examine evidence on the association between wine consumption and cognitive decline and to analyze whether this association varies depending on the wine consumption level or is affected by individual and study characteristics, including mean age, percentage of women participants, and follow-up time.

METHODS: In this systematic review and meta-analysis, we undertook a search in MEDLINE (via PubMed), Scopus, Cochrane, and Web of Science databases for longitudinal studies measuring the association between wine consumption and cognitive decline from their inception to May 2021. Effect sizes were calculated using the DerSimonian and Laird and Hartung-Knapp-Sidik-Jonkman methods.

RESULTS: The search retrieved 6,055 articles, 16 of which were included in this systematic review. In total, 12 studies were included in the meta-analysis. The studies were published between 1997 and 2019. They were conducted in nine different countries. The sample size of the included studies ranged from 360 to 10,308 with a mean age of 70 years old. Using the DerSimoniand and Laird method, the pooled RR for the effect of wine consumption on cognitive decline was 0.72 (95% CI 0.63-0.80; I (2) = 82.4%; tau(2): 0.0154). Using the Hartung-Knapp-Sidik-Jonkman method, the RR was 0.65 (95% CI 0.52-0.79; I (2) = 94,531%; tau(2): 0.057).

CONCLUSIONS: This study may show a protective effect of wine consumption against cognitive decline. However, it would be important for future research to differentiate the types of wine within consumption.

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