21 February 2020 In General Health

The primary aim of this systematic review was to establish the prevalence, character, and risk factors of peripheral neuropathy amongst chronic alcohol abusers and to identify the most appropriate management strategies.

In this review, possible pathogenetic mechanisms are also discussed. A systematic, computer-based search was conducted using the PubMed database. Data regarding the above parameters were extracted. 87 articles were included in this review, 29 case-control studies, 52 prospective/retrospective cohort studies and 2 randomised control trials, 1 cross sectional study, and 3 population-based studies.

The prevalence of peripheral neuropathy amongst chronic alcohol abusers is 46.3% (CI 35.7- 57.3%) when confirmed via nerve conduction studies. Alcohol-related peripheral neuropathy generally presents as a progressive, predominantly sensory axonal length-dependent neuropathy.

The most important risk factor for alcohol-related peripheral neuropathy is the total lifetime dose of ethanol, although other risk factors have been identified including genetic, male gender, and type of alcohol consumed. At present, it is unclear what the pathogenetic mechanisms for the development of neuropathy amongst those who chronically abuse alcohol are, and therefore, it is unknown whether it is attributed to the direct toxic effects of ethanol or another currently unidentified factor.

There is presently sparse data to support a particular management strategy in alcohol-related peripheral neuropathy, but the limited data available appears to support the use of vitamin supplementation, particularly of B-vitamin regimens inclusive of thiamine

09 August 2019 In General Health

BACKGROUND: Alcohol consumption is a common modifiable lifestyle factor. Alcohol may be a risk factor for frailty, however, there is limited evidence in the literature.

OBJECTIVE: The objectives of this study were to examine the association of alcohol consumption with the risk of incident frailty.

METHODS: This is a prospective panel study of 2544 community-dwelling people aged 60 years and older in England. Frailty status defined by frailty phenotype criteria was measured at baseline and 4 years later. Participants free of frailty at baseline were divided into 5 groups based on quantity of self-reported alcohol consumption per week with cut-points at 0, 7, 14, and 21 UK units per week. Adjusted odds ratios (OR) were calculated for incident frailty according to the alcohol consumption using logistic regression models.

RESULTS: Compared with the low consumption group (>0 and 21 units per week) had a significantly lower incident frailty risk (unadjusted OR 0.45, 95% CI 0.270.75, P < .01), which became nonsignificant on adjustment for sociodemographic factors (OR 0.64, 95% CI 0.371.13, P = .12).

CONCLUSIONS/IMPLICATIONS: We found that nondrinkers were more likely than those with low alcohol consumption to develop frailty, but this appeared to be explained by poorer baseline health status. No evidence was found for an association between high levels of alcohol consumption and becoming frail. Future studies with information on life-course history of alcohol use, especially for those classified as nondrinkers in old age, are warranted.

24 June 2019 In General Health
Studies indicate an inverse association between moderate alcohol consumption and chronic inflammatory diseases; however, the association between alcohol consumption and chronic obstructive pulmonary disease (COPD) incidence has not been widely studied. We investigated the associations of total alcohol consumption and intake of specific alcoholic beverages with risk of COPD in a population-based prospective cohort study, the Cohort of Swedish Men (n = 44,254). Alcohol consumption was assessed with a self-administered questionnaire in 1997. During follow-up (1998-2014), 2,177 COPD cases were ascertained. Moderate alcohol consumption was associated with the lowest risk of COPD. A J-shaped association was observed for ethanol consumption (P for nonlinearity = 0.003) and beer consumption (P for nonlinearity < 0.001); for wine consumption, a U-shaped association was observed (P for nonlinearity < 0.001). Defining a "standard drink" as 12 g of ethanol, the multivariable-adjusted hazard ratios were 0.77 (95% confidence interval (CI): 0.66, 0.90) and 0.92 (95% CI: 0.81, 1.05) for beer consumption of 4.1-6.0 and >6.0 standard drinks/week (SDW) versus <1.0 SDW, respectively; 0.80 (95% CI: 0.69, 0.93) and 1.00 (95% CI: 0.83, 1.21) for wine consumption of 2.0-4.0 and >4.0 SDW versus <1.0 SDW, respectively; and 1.10 (95% CI: 0.98, 1.24) and 1.20 (95% CI: 0.99, 1.44) for liquor consumption of 2.0-4.0 and >4.0 SDW versus <1.0 SDW, respectively. In conclusion, our findings suggest that moderate beer and wine consumption, but not liquor consumption, may decrease risk of COPD. Additional studies are needed to confirm these associations.
24 June 2019 In Cardiovascular System

BACKGROUND: In addition to its established harmful effects on the liver and other organs, heavy alcohol use confers deleterious effects on the cardiovascular (CV) system, as well. However, data have emerged that light/moderate alcohol consumption (1 drink/day for women and 1-2 drinks/day for men) may be protective against CV disease.

OBJECTIVE/METHODS: English articles regarding the CV effects of alcohol/ethanol were reviewed by search in Medline, Scopus, and Google Scholar.

RESULTS: A J-shaped curve has been proposed to illustrate a differential effect of alcohol on the CV system with the lowest point on the curve (light/moderate drinking) corresponding to optimal exposure to alcohol, which may confer cardioprotection, the rather neutral effect of non-drinking, and the highest risk of heavy and/or binge drinking reflecting the consequence of harmful exposure. However, staying at the nadir of this J-shaped curve appears difficult. Furthermore, concern and distrust have also been raised about the quality of evidence for such "cardioprotection", emphasizing the need for further randomized controlled trials. Another concern relates to the risk of moderate drinking leading to problem drinking, since alcohol is the most common addictive substance.

CONCLUSION: Optimal exposure to alcohol (light/moderate use) means that one needs to stay at the nadir of the J-shaped curve for alcohol use to avail oneself of possible cardioprotection, and this may not be an easy thing to accomplish and/or adhere to, especially if one "likes" alcohol drinking. However, the evidence of "cardioprotection" conferred by alcohol has also been refuted, due to lack of randomized controlled trials.

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