25 August 2020 In Cardiovascular System
BACKGROUND: This study investigated the dose-response relationship between alcohol consumption and CVD incidence, conducting a meta-analysis of studies focusing on residents from local communities. Further, we examined whether light to moderate alcohol consumption had a protective effect on CVD incidence through a sub-group analysis. METHODS: This study conducted a meta-analysis of the relationship between alcohol consumption and CVD incidence, selecting journals published up to December 2017. The alcohol consumption level was classified into non-consumers, light (0.01-10.0 g/day), light to moderate (10.1-20.0 g/day), moderate (20.1-40.0 g/day), moderate to high (40.1-60.0 g/day), and high (> 60.0 g/day) groups. The sub-group analysis was conducted according to the number of comorbidities and age. RESULTS: Seven articles were selected in total for the meta-analysis. The mean Newcastle-Ottawa scale score was 8.14 points, suggesting studies were of high quality. There was a J-shaped dose-response relationship between alcohol consumption level and CVD incidence only in men. In general, light to moderate and moderate consumption lowered CVD incidence (Relative risk (RR) [95% confidence interval (CI)] was 0.68 [0.57-0.81] and 0.72 [0.58-0.90], respectively). In men with 3-4 comorbidities, there were no protective effects of light to moderate and moderate consumption on CVD incidence. In either groups of only men or men and women there were protective effects of light to moderate and moderate consumption on CVD incidence only in those aged between 41 and 65. DISCUSSION: We found that light to moderate and moderate alcohol consumption had a protective effect on CVD incidence, there was no protective effect either in those with at least three comorbidities or people aged 40 or younger. CONCLUSIONS: We conclude that not all local community residents experience a protective effect of light to moderate consumption on CVD incidence. As such, it is necessary to recommend a moderate amount of drinking or less for each individual.
15 December 2016 In Liver Disease

The susceptibility to developing alcohol dependence and significant alcohol-related liver injury is determined by a number of constitutional, environmental and genetic factors, although the nature and level of interplay between them remains unclear. The familiality and heritability of alcohol dependence is well-documented but, to date, no strong candidate genes conferring increased risk have emerged, although variants in alcohol dehydrogenase and acetaldehyde dehydrogenase have been shown to confer protection, predominantly in individuals of East Asian ancestry. Population contamination with confounders such as drug co-dependence and psychiatric and physical co-morbidity may explain the essentially negative genome-wide association studies in this disorder. The familiality and hereditability of alcohol-related cirrhosis is not as well-documented but three strong candidate genes PNPLA3, TM6SF2 and MBOAT7, have been identified. The mechanisms by which variants in these genes confer risk and the nature of the functional interplay between them remains to be determined but, when elucidated, will undoubtedly increase our understanding of the pathophysiology of this disease. The way in which this genetic information could potentially inform patient management has yet to be determined and tested.

25 October 2016 In Cancer

OBJECTIVE: To determine the association of prediagnostic alcohol consumption with long-term mortality from breast cancer and other causes in a cohort of women with breast cancer.

METHODS: We studied a Michigan-based cohort of 939 women aged 40-84 years, who provided complete information about the type, amount and intensity of prediagnostic alcohol consumption. Associations of alcohol consumption, based on weekly volume of alcohol consumption during the year prior to breast cancer diagnosis, with mortality were evaluated in Cox proportional hazards models, with adjustment for sociodemographic factors, body mass index, smoking, comorbidity, tumor characteristics, and treatment. Differences among covariates were assessed with Pearson chi2 , Student t -tests and Wilcoxon Rank Sum tests. All statistical tests were two-sided.

RESULTS: During a median follow-up of 11 years, 724 deaths occurred overall, with 303 from breast cancer. Fifty-five percent of the women were categorized as drinkers with volume of alcohol consumption ranging from 0.75 to 36.00 drinks/week. In multivariable models, a decreased risk of other-cause mortality was associated with low alcohol drinking (0.75-3.75 drinks/week; HR = 0.61, 95% CI = 0.47-0.78), moderate volume alcohol drinking (4.00-9.75 drinks/week; HR = 0.57, 95% CI = 0.39-0.85) and low frequency (0.75-3.75 drinks/week) beer and wine intake (HR = 0.69, 95% CI = 0.50-0.96 and HR = 0.68, 95% CI = 0.52-0.88 respectively). Although the risk of breast cancer-specific mortality was not statistically significantly associated with moderate (4.00-9.75 drinks/week) and high volume (10.00-36.00 drinks/week) alcohol drinking in the overall cohort (HR = 1.43, 95% CI = 95% 0.97-2.12 and HR = 1.53, 95% CI = 0.87-2.70 respectively), there was a positive association of alcohol consumption with breast cancer-specific mortality among current smokers (HR = 1.92, 95% CI = 1.03-3.57; Pinteraction = 0.04).

CONCLUSION: In this prospective cohort study, regular consumption of 0.75-36.00 alcoholic drinks per week during the year prior to breast cancer diagnosis was associated with a reduction in other-cause mortality and with an increase in breast cancer-specific mortality among current smokers, after taking into account clinical and sociodemographic factors.

21 September 2016 In General Health

OBJECTIVES: This study aimed to describe the cross-sectional and longitudinal association between alcohol intake and gait parameters in older persons.

METHODS: Community-dwelling persons aged 65-70 years (N = 807). Information on health, functional status, and alcohol use was self-reported at baseline and at 3-year follow-up, whereas gait speed and stride-to-stride variability were measured while walking only (single task) and under dual tasking (counting backwards).

RESULTS: Compared to light-to-moderate drinking, heavy drinking was associated with slower gait speed in single task (adj. coeff.: -.040, 95% CI: -.0.78 to -.002, p = .035). No significant association was observed between heavy drinking and gait speed variability. Nondrinkers walked significantly slower than light-to-moderate drinkers in dual task and had significantly higher gait speed variability in both single and dual task, but these associations disappeared after adjustment for comorbidity. At follow-up, 35.2% and 34.1% of the participants walked significantly slower in single and dual task, respectively. This proportion varied a little across drinking categories.

CONCLUSION: At baseline, heavy alcohol consumption was significantly associated with slower gait speed in single task. Selective survival of the fittest heavy drinkers probably explains why this association faded in longitudinal analyses. The trend of poorer gait performance in nondrinkers disappeared after adjustment for comorbidity, suggesting confounding by a worse health status.

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