05 December 2018 In General Health

BACKGROUND: Problem drinking carries significant health burdens, including an increased risk of hypertension. The effect of chronic alcohol intake on blood pressure (BP) in women is understudied and poorly understood.

OBJECTIVES: We sought to examine the relationships between drinking habits and BP in hypertensive women.

METHODS: We analyzed drinking habits in 113 women followed in the Brigham and Women's Hospital Hypertension Clinic for at least one year.

RESULTS: Among these women with well-controlled hypertension, baseline diastolic BP was significantly lower in moderate drinkers compared with women who rarely or never drank. Changes in both systolic and diastolic BP over 12 months showed a significant negative association with changes in percent drinking days. In contrast, there was a trend toward higher baseline systolic BP among those women who consumed more drinks per drinking day.

CONCLUSIONS: Among these women with controlled hypertension, our data failed to demonstrate an association between drinking beyond recommended limits and higher disease burden. These findings parallel the widely reported difference between drinking frequency, associated with a host of positive health outcomes, and drinking intensity, associated with negative outcomes. Novel to this report is an observed reduction in blood pressure over the one-year follow-up period accompanying an increased drinking frequency in treated hypertensive women. Cautions include the suggestion that a greater number of drinks per drinking day was associated with higher baseline pressure. These data imply that drinking within sensible limits has no negative impact on chronic hypertension. In fact, for women with well-controlled hypertension, such a habit may impart benefit.

18 May 2018 In General Health

BACKGROUND: Low-risk limits recommended for alcohol consumption vary substantially across different national guidelines. To define thresholds associated with lowest risk for all-cause mortality and cardiovascular disease, we studied individual-participant data from 599 912 current drinkers without previous cardiovascular disease.

METHODS: We did a combined analysis of individual-participant data from three large-scale data sources in 19 high-income countries (the Emerging Risk Factors Collaboration, EPIC-CVD, and the UK Biobank). We characterised dose-response associations and calculated hazard ratios (HRs) per 100 g per week of alcohol (12.5 units per week) across 83 prospective studies, adjusting at least for study or centre, age, sex, smoking, and diabetes. To be eligible for the analysis, participants had to have information recorded about their alcohol consumption amount and status (ie, non-drinker vs current drinker), plus age, sex, history of diabetes and smoking status, at least 1 year of follow-up after baseline, and no baseline history of cardiovascular disease. The main analyses focused on current drinkers, whose baseline alcohol consumption was categorised into eight predefined groups according to the amount in grams consumed per week. We assessed alcohol consumption in relation to all-cause mortality, total cardiovascular disease, and several cardiovascular disease subtypes. We corrected HRs for estimated long-term variability in alcohol consumption using 152 640 serial alcohol assessments obtained some years apart (median interval 5.6 years [5th-95th percentile 1.04-13.5]) from 71 011 participants from 37 studies.

FINDINGS: In the 599 912 current drinkers included in the analysis, we recorded 40 310 deaths and 39 018 incident cardiovascular disease events during 5.4 million person-years of follow-up. For all-cause mortality, we recorded a positive and curvilinear association with the level of alcohol consumption, with the minimum mortality risk around or below 100 g per week. Alcohol consumption was roughly linearly associated with a higher risk of stroke (HR per 100 g per week higher consumption 1.14, 95% CI, 1.10-1.17), coronary disease excluding myocardial infarction (1.06, 1.00-1.11), heart failure (1.09, 1.03-1.15), fatal hypertensive disease (1.24, 1.15-1.33); and fatal aortic aneurysm (1.15, 1.03-1.28). By contrast, increased alcohol consumption was log-linearly associated with a lower risk of myocardial infarction (HR 0.94, 0.91-0.97). In comparison to those who reported drinking >0-100-200-350 g per week had lower life expectancy at age 40 years of approximately 6 months, 1-2 years, or 4-5 years, respectively.

INTERPRETATION: In current drinkers of alcohol in high-income countries, the threshold for lowest risk of all-cause mortality was about 100 g/week. For cardiovascular disease subtypes other than myocardial infarction, there were no clear risk thresholds below which lower alcohol consumption stopped being associated with lower disease risk. These data support limits for alcohol consumption that are lower than those recommended in most current guidelines.

FUNDING: UK Medical Research Council, British Heart Foundation, National Institute for Health Research, European Union Framework 7, and European Research Council.

03 May 2018 In Cardiovascular System
BACKGROUND: Compelling evidence suggests that excessive alcohol consumption increases the risk of atrial fibrillation (AF), but the effect of light-moderate alcohol consumption is less certain. We investigated the association between alcohol consumption within recommended limits and AF risk in a light-drinking population. METHODS AND RESULTS: Among 47 002 participants with information on alcohol consumption in a population-based cohort study in Norway, conducted from October 2006 to June 2008, 1697 validated AF diagnoses were registered during the 8 years of follow-up. We used Cox proportional hazard models with fractional polynomials to analyze the association between alcohol intake and AF. Population attributable risk for drinking within the recommended limit (ie, at most 1 drink per day for women and 2 drinks per day for men without risky drinking) compared with nondrinking was also calculated. The average alcohol intake was 3.8+/-4.8 g/d. The adjusted hazard ratio for AF was 1.38 (95% confidence interval, 1.06-1.80) when we compared participants consuming >7 drinks per week with abstainers. When we modeled the quantity of alcohol intake as a continuous variable, the risk increased in a curvilinear manner. It was higher with heavier alcohol intake, but there was virtually no association at <1 drink per day for women and <2 drinks per day for men in the absence of risky drinking. The population attributable risk among nonrisky drinkers was 0.07% (95% confidence interval, -0.01% to 0.13%). CONCLUSIONS: Although alcohol consumption was associated with a curvilinearly increasing risk of AF in general, the attributable risk of alcohol consumption within recommended limits among participants without binge or problem drinking was negligible in this population
15 December 2016 In General Health

BACKGROUND: To estimate the benchmark dose (BMD) and their 95% lower confidence limits (BMDL) of alcohol consumption as the reference level for the development of hyperuricemia based on the dose-response relationship.

METHODS: An 8-year prospective cohort study was conducted in 8097 male workers at a Japanese steel company who received annual health check-ups between 2002 and 2009. The endpoints for development of hyperuricemia were defined as a uric acid >/=7 mg/dL or taking any anti-hyperuricemic medication. The dose-response relationship of alcohol consumption was investigated using multivariate-pooled logistic regression analyses adjusted for other potential covariates. We estimated the BMD and BMDL of alcohol consumption for the development of hyperuricemia, using the parameters obtained by pooled logistic regression with a benchmark response (BMR) of 5% or 10%.

RESULTS: Mean observed years per person was 3.86 years. The incidence rate per 1000 person-years was 61.1. The odds ratio calculated for the development of hyperuricemia was 1.29 [95% confidence interval, (1.22-1.36)] with an increase in alcohol consumption per 1 gou/day (1 gou/day = alcohol 22 g/day). The estimated BMDL/BMD with a BMR of 5% was 2.5/2.8 gou/day (54.5/61.8 g/day) and with a BMR of 10% was 4.0/4.6 gou/day (88.9/100.9 g/day).

CONCLUSIONS: The present study showed that alcohol consumption of 2.5 gou/day (=ethanol 55 g/day) caused a distinct increase in the risk of hyperuricemia. Valuable information for preventing alcohol-induced hyperuricemia was obtained by a long-term follow-up study of a large cohort.

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