27 September 2018 In Cardiovascular System

BACKGROUND/OBJECTIVES: Low/moderate alcohol consumption seems to be protective against cardiovascular disease (CVD). This study aimed to investigate the association of wine/beer consumption with the 10-year CVD incidence.

SUBJECTS/METHODS: During 2001-2002, 3042 CVD-free adults consented to participate in the ATTICA study; of them 2583 completed the 10-year follow-up (85% participation rate), but precise information about fatal/nonfatal CVD incidence (myocardial infarction, angina pectoris, cardiac ischemia, heart failure, chronic arrhythmias, and stroke) was available in 2020 participants (overall retention rate 66%). Alcohol/ethanol intake and the alcoholic beverages consumed were assessed; participants were categorized into three groups (no use; 1 glass/week).

RESULTS: Alcohol drinking was reported by 56% of the participants who did not develop a CVD event and 49% of those who had (p = 0.04); whereas ethanol intake was 14 +/- 16 g among those who did not had an event vs. 21 +/- 18 g among those who had a CVD event (p < 0.001). A strong inverse and similar association between low wine/beer intake (20 g/day had CVD-risk HRs (95% CI) of 0.60 (0.40-0.98), 1.22 (0.60-1.14), and 1.81 (0.70-4.61), respectively.

CONCLUSIONS: This study revealed similar results of low wine/beer consumption against CVD incidence, mainly due to its implication on low-grade chronic inflammation.

06 September 2018 In Cardiovascular System

BACKGROUND: Studies have shown that alcohol intake trajectories differ in their associations with biomarkers of cardiovascular functioning, but it remains unclear if they also differ in their relationship to actual coronary heart disease (CHD) incidence. Using multiple longitudinal cohort studies, we evaluated the association between long-term alcohol consumption trajectories and CHD.

METHODS: Data were drawn from six cohorts (five British and one French). The combined analytic sample comprised 35,132 individuals (62.1% male; individual cohorts ranging from 869 to 14,247 participants) of whom 4.9% experienced an incident (fatal or non-fatal) CHD event. Alcohol intake across three assessment periods of each cohort was used to determine participants' intake trajectories over approximately 10 years. Time to onset for (i) incident CHD and (ii) fatal CHD was established using surveys and linked medical record data. A meta-analysis of individual participant data was employed to estimate the intake trajectories' association with CHD onset, adjusting for demographic and clinical characteristics.

RESULTS: Compared to consistently moderate drinkers (males: 1-168 g ethanol/week; females: 1-112 g ethanol/week), inconsistently moderate drinkers had a significantly greater risk of incident CHD [hazard ratio (HR) = 1.18, 95% confidence interval (CI) = 1.02-1.37]. An elevated risk of incident CHD was also found for former drinkers (HR = 1.31, 95% CI = 1.13-1.52) and consistent non-drinkers (HR = 1.47, 95% CI = 1.21-1.78), although, after sex stratification, the latter effect was only evident for females. When examining fatal CHD outcomes alone, only former drinkers had a significantly elevated risk, though hazard ratios for consistent non-drinkers were near identical. No evidence of elevated CHD risk was found for consistently heavy drinkers, and a weak association with fatal CHD for inconsistently heavy drinkers was attenuated following adjustment for confounding factors.

CONCLUSIONS: Using prospectively recorded alcohol data, this study has shown how instability in drinking behaviours over time is associated with risk of CHD. As well as individuals who abstain from drinking (long term or more recently), those who are inconsistently moderate in their alcohol intake have a higher risk of experiencing CHD. This finding suggests that policies and interventions specifically encouraging consistency in adherence to lower-risk drinking guidelines could have public health benefits in reducing the population burden of CHD. The absence of an effect amongst heavy drinkers should be interpreted with caution given the known wider health risks associated with such intake.

TRIAL REGISTRATION: ClinicalTrials.gov, NCT03133689

06 September 2018 In Cardiovascular System

BACKGROUND: Excessive alcohol intake has been shown to be associated with cardiovascular disease via metabolic pathways. However, the relationship between alcohol intake and obesity has not been fully elucidated. We aimed to examine the association of alcohol consumption with fat deposition and anthropometric measures.

METHODS: From 2006-2008, we conducted a cross-sectional study in a population-based sample of Japanese men aged 40 to 79 years. Areas of abdominal visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) were calculated using computed tomography imaging. Based on a questionnaire, we classified participants into five groups according to weekly alcohol consumption, excluding former drinkers: non-drinkers (0 g/week), 0.1-160.9, 161-321.9, 322-482.9 and >==483 g/week. Multivariable linear regression was used to estimate adjusted means of obesity indices for each group.

RESULTS: We analyzed 998 men (mean age and body mass index [BMI], 63.8 years and 23.6 kg/m(2), respectively). Higher weekly alcohol consumption was strongly and significantly associated with higher abdominal VAT area, percentage of VAT, and VAT-to-SAT ratio (all P for trend <0.001), and also with waist circumferences and waist-to-hip ratio (P for trend, 0.042 and 0.007, respectively). These associations remained significant after further adjustment for BMI. Whereas, alcohol consumption had no significant association with abdominal SAT area.

CONCLUSIONS: Higher alcohol consumption was associated with higher VAT area, VAT% and VAT-to-SAT ratio, independent of confounders including BMI, in general Japanese men. These results suggest that alcohol consumption may have a potential adverse effect on visceral fat deposition.

27 July 2018 In Cardiovascular System

Moderate alcohol consumption has been associated with a lower risk of coronary artery disease (CAD) in the general population but has not been well studied in US veterans. We obtained self-reported alcohol consumption from Million Veteran Program participants. Using electronic health records, CAD events were defined as 1 inpatient or 2 outpatient diagnosis codes for CAD, or 1 code for a coronary procedure. We excluded participants with prevalent CAD (n = 69,995) or incomplete alcohol information (n = 8,449). We used a Cox proportional hazards model to estimate hazard ratios and 95% confidence intervals for CAD, adjusting for age, gender, body mass index, race, smoking, education, and exercise. Among 156,728 participants, the mean age was 65.3 years (standard deviation = 12.1) and 91% were men. There were 6,153 CAD events during a mean follow-up of 2.9 years. Adjusted hazard ratios (95% confidence intervals) for CAD were 1.00 (reference), 1.02 (0.92 to 1.13), 0.83 (0.74 to 0.93), 0.77 (0.67 to 0.87), 0.71 (0.62 to 0.81), 0.62 (0.51 to 0.76), 0.58 (0.46 to 0.74), and 0.95 (0.85 to 1.06) for categories of never drinker; former drinker; current drinkers of 0.5 to 1 drink/day, >1 to 2 drinks/day, >2 to 3 drinks/day, and >3 to 4 drinks/day; and heavy drinkers (>4 drinks/day) or alcohol use disorder, respectively. For a fixed amount of ethanol, intake at >/=3 days/week was associated with lower CAD risk compared with </=1 day/week. Beverage preference (beer, wine, or liquor) did not influence the alcohol-CAD relation. Our data show a lower risk of CAD with light-to-moderate alcohol consumption among US veterans, and drinking frequency may provide a further reduction in risk.

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