26 May 2021 In Liver Disease
BACKGROUND & AIMS: Increasingly populations are both overweight/obese and consume alcohol. The risk of liver disease from the combination of these factors is unclear. We performed a systematic review and meta-analysis to address this important gap in evidence. Protocol registered with PROSPERO(CRD42016046508). METHODS: We performed electronic searches of Ovid Medline, Embase Classic + Embase, until 17th June 2020 for cohort studies of adults without pre-existing liver disease. Primary outcome was morbidity/mortality from chronic liver disease. Exposures were alcohol consumption categorised as within or above UK recommended limits (14 units/112 g per week) and BMI categorised as normal, overweight or obese. Non-drinkers were excluded. A Poisson regression log-linear model was used to test for statistical interaction between alcohol and BMI and to conduct a one-stage meta-analysis. RESULTS: Searches identified 3129 studies-16 were eligible. Of these, nine cohorts (1,121,514 participants) had data available and were included in the analysis. The Poisson model showed no significant statistical interaction between alcohol consumption and BMI on the risk of chronic liver disease. Compared to normal weight participants drinking alcohol within UK recommended limits, relative risk of chronic liver disease in overweight participants drinking above limits was 3.32 (95% CI 2.88 to 3.83) and relative risk in obese participants drinking above limits was 5.39 (95% CI 4.62 to 6.29). CONCLUSIONS: This meta-analysis demonstrated a significantly increased risk of chronic liver disease in participants who were both overweight/obese and consumed alcohol above UK recommended limits. This evidence should inform advice given to patients and risk stratification by healthcare professionals.
26 May 2021 In General Health
OBJECTIVES: Previous studies have reported inconsistent results on the relationship between alcohol intake and the risk of systemic lupus erythematosus (SLE). Therefore, we conducted a systematic review and meta-analysis to illustrate the potential role of alcohol intake on the progression of SLE. METHODS: An electronic search of the PubMed, EmBase, and the Cochrane library databases was conducted from their inception up to March 2020. Observational studies that investigated the role of alcohol intake on the risk of SLE were eligible for inclusion in this study. The pooled odds ratio (OR) with 95% confidence interval (CI) was calculated as an effect estimate using the random-effects model. RESULTS: Seven case-control studies (n = 3, 251) and three cohort studies (n = 322, 479) were selected for the final meta-analysis. Mild (OR: 0.85; 95% CI: 0.53-1.38; p = 0.515) or heavy (OR: 0.63; 95% CI: 0.37-1.09; p = 0.102) alcohol intake were not associated with the risk of SLE, while moderate alcohol intake could protect against the risk of SLE (OR: 0.71; 95% CI: 0.55-0.93; p = 0.012). Sensitivity analysis suggested that heavy alcohol intake was associated with a reduced risk of SLE (OR: 0.47; 95% CI: 0.32-0.67; p
25 August 2020 In Cardiovascular System
BACKGROUND AND AIMS: The alcohol-hypertension relation has been well documented, but whether women have protective effect or race and type of beverage consumed affect the association remain unclear. To quantify the relation between total or beverage-specific alcohol consumption and incident hypertension by considering the effect of sex and race. METHODS AND RESULTS: Articles were identified in PubMed and Embase databases with no restriction on publication date. Pooled relative risks (RRs) and 95% confidence intervals (CIs) were calculated by random effects models. Restricted cubic splines were used to model the dose-response association. This study involved 22 articles (31 studies) and included 414,477 participants. The hypertension risk was different among liquor, wine, and beer at 5.1-10 g/d of ethanol consumption (P-across subgroups = 0.002). The hypertension risk differed between men (RR: 1.14, 95% CI: 1.07, 1.20) and women (RR: 0.98, 95% CI: 0.89, 1.06) at 10 g/d (P-across subgroups = 0.005). We found a linear alcohol-hypertension association among white (P-linearity = 0.017), black people (P-linearity = 0.035), and Asians (P-linearity
25 August 2020 In Cardiovascular System
BACKGROUND/AIMS: There are inconsistencies in the effects of low to moderate dose alcohol consumption on the development of hypertension in adult men. We hypothesized that a region-specific effect might participate in this heterogeneity. METHODS: We conducted a systematic review and meta-analysis to evaluate the effect of alcohol dose on hypertension incidence using contemporary data through December 2017. Subjects were categorized according to their level of alcohol consumption as non-drinkers (reference) and low- (0.01 to 20.0 g/day), moderate- (20.1 to 40.0 g/day), moderate- to high- (40.1 to 60.0 g/day), and high-dose (> 60.0 g/day) drinkers. We defined hypertension as a blood pressure >/= 140/90 mmHg and/or the use of anti-hypertensive drugs. RESULTS: In total, 11 articles (seven Asian and four Western) were selected for our analysis. Among Asian men, a significantly elevated risk was observed even in the low alcohol dose group in comparison with the group with no alcohol consumption, and the risk increased in a dose-dependent manner (pooled relative risks [95% confidence intervals (CI)]: 1.25 [1.13 to 1.38], 1.48 [1.27 to 1.72], 1.75 [1.43 to 2.15], and 1.78 [1.51 to 2.09]). Among Western men, a similar dose-response relationship was noted in general (p for subgroup difference > 0.1), but a significantly elevated risk was evident only in the high-dose group (pooled relative risks [95% CI]: 1.22 [0.85 to 1.74], 1.57 [0.90 to 2.75], 1.47 [0.44 to 4.91], and 1.49 [1.02 to 2.18]). CONCLUSION: Even low doses of alcohol can lead to the development of hypertension, particularly in Asian men. Our findings could serve as additional evidence for developing an appropriate preventive strategy in each region.
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