25 August 2020 In Cancer

Alcohol is widely consumed and is known as a major risk factor for several types of cancers. Yet, it is unclear whether alcohol consumption is associated with the risk of prostate cancer (PCa) or not. We conducted linear and non-linear dose-response meta-analyses of cohort studies on alcohol consumption and PCa risk by types of alcohol (total, wine, beer, and liquor) and PCa (non-aggressive and aggressive). Pubmed and Embase were searched through April 2020 to identify relevant studies. Summary relative risk (RR) and 95% confidence interval (CI) were estimated using a random-effects model.

For non-aggressive PCa, by alcohol type, the risk increased linearly with liquor (RR per 14 g/day intake (alcohol content in standard drink) being 1.04 (95% CI = 1.02-1.06, I(2) = 0%, three studies) and non-linearly with beer (Pnon-linearity = 0.045, four studies), with increased risk observed in the lower range (RR = 1.03, 95% CI = 1.01-1.05; 14 g/day), with 1.05 (95% CI = 1.01-1.08) at 28 g/day. Wine was not significantly associated with the risk of non-aggressive PCa. For aggressive PCa, a non-linear relationship of diverse shapes was indicated for all types of alcohol in the sensitivity analysis.

Compared to non-drinking, a significant positive association was more apparent at lower dose for liquor (RR = 1.12, 95% CI = 1.04-1.20 at 14 g/day; RR = 1.16, 95% CI = 1.03-1.31 at 28 g/day; Pnon-linearity = 0.005, three studies) but at higher doses for wine (RR = 1.02, 95% CI = 0.90-1.16 at 28 g/day, RR = 1.35, 95% CI = 1.08-1.67 at 56 g/day; Pnon-linearity = 0.01, four studies).

In contrast, decreased risks were indicated at lower doses of beer (RR = 0.85, 95% CI = 0.79-0.92 at 14 g/day; RR = 0.79, 95% CI = 0.70-0.90 at 28 g/day, Pnon-linearity < 0.001, four studies). Total alcohol consumption was not associated with both types of PCa. In this study, we found heterogeneous associations between alcohol intake and PCa by types of alcohol and PCa.

05 June 2020 In Diabetes

We aimed to elucidate the effect of chronic alcohol consumption on fatty liver. We assessed the consumption of alcohol in 2429 Japanese males (mean age: 54.2 +/- 9 years); they were classified according to average consumption into non-drinkers (ND), light drinkers (LD), moderate drinkers (MD), and heavy drinkers (HD).

The prevalence of fatty liver was the lowest in the MD and highest in the ND group (p < 0.001), while obesity was not significantly different among the groups (p = 0.133). Elevated levels of alanine aminotransferase (ALT) were the lowest in the MD group (p = 0.011) along with resistance to insulin (homeostasis model assessment-insulin resistance (HOMA-IR)), which was highest in the ND group (p = 0.001).

Chronic consumption of alcohol was independently and inversely associated with fatty liver and insulin resistance after adjusting for obesity, hypertension, fasting hyperglycemia, habit of drinking sweet beverages, physical activity, and age (odds ratios are as follows: ND, 1; LD, 0.682; MD, 0.771; HD, 0.840 and ND, 1; LD, 0.724; MD, 0.701; HD, 0.800, respectively).

We found that regardless of the type of alcoholic beverage, chronic consumption of alcohol is inversely associated with insulin resistance and fatty liver in Japanese males. This study had limitations, most notably the lack of investigation into diet and nutrition.

04 May 2020 In Diabetes

We aimed to determine the association between alcohol consumption change on fasting serum glucose, insulin resistance, and beta cell function.

The study population consisted of 55,858 men from the Kangbuk Samsung Health Study. Participants were divided into non-, light, moderate, and heavy drinkers for each of the first and second health examinations based on a self-reported questionnaire on alcohol consumption. The adjusted mean values for change in fasting serum glucose (FSG), homeostatic model assessment of insulin resistance (HOMA-IR), and beta cell function (HOMA-beta) levels were determined according to alcohol consumption change by linear regression. Compared to sustained initial drinkers, those who increased alcohol intake to moderate (p < 0.001) and heavy (p < 0.001) levels had increased FSG levels.

In contrast, reduction in alcohol intake to light levels among initial heavy drinkers was associated with reduced change in FSG levels (p = 0.007) compared to sustained heavy drinkers. No significant associations were observed between changes in alcohol intake with HOMA-IR levels. Compared to sustained light drinkers, those who increased alcohol intake to moderate (p < 0.001) and heavy (p = 0.009) levels had lower increases in HOMA-beta levels.

Finally, compared to sustained heavy drinkers, those who reduced alcohol consumption to light levels had greater increases in HOMA-beta levels (p = 0.002). Increases in alcohol consumption were associated with higher blood glucose levels and worsened beta cell function. Heavy drinkers who reduce alcohol intake could benefit from improved blood glucose control via improved beta cell function.

27 March 2020 In Dementia

INTRODUCTION: Observational studies have suggested that light-to-moderate alcohol consumption decreases the risk of Alzheimer's disease, but it is unclear if this association is causal.

METHODS: Two-sample Mendelian randomization (MR) analysis was used to examine whether alcohol consumption, alcohol dependence, or Alcohol Use Disorder Identification Test (AUDIT) scores were causally associated with the risk of Late-Onset Alzheimer's disease (LOAD) or Alzheimer's disease age of onset survival (AAOS). Additionally, gamma-glutamyltransferase levels were included as a positive control.

RESULTS: There was no evidence of a causal association between alcohol consumption, alcohol dependence, or AUDIT, and LOAD. Alcohol consumption was associated with an earlier AAOS and increased gamma-glutamyltransferase blood concentrations. Alcohol dependence was associated with a delayed AAOS.

DISCUSSION: MR found robust evidence of a causal association between alcohol consumption and an earlier AAOS, but not alcohol intake and LOAD risk. The protective effect of alcohol dependence is potentially due to survivor bias.

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