25 August 2020 In Drinking Patterns

BACKGROUND: Some of the previously reported health benefits of low-to-moderate alcohol consumption may derive from health status influencing alcohol consumption rather than the opposite. We examined whether health status changes influence changes in alcohol consumption, cessation included.

METHODS: Data came from 571 current drinkers aged >/=60 years participating in the Seniors-ENRICA cohort in Spain. Participants were recruited in 2008-2010 and followed-up for 8.2 years, with four waves of data collection. We assessed health status using a 52-item deficit accumulation (DA) index with four domains: functional, self-rated health and vitality, mental health, and morbidity and health services use. To minimise reverse causation, we examined how changes in health status over a 3-year period (wave 0-wave 1) influenced changes in alcohol consumption over the subsequent 5 years (waves 1-3) using linear/logistic regression, as appropriate.

RESULTS: Compared with participants in the lowest tertile of DA change (mean absolute 4.3% health improvement), those in the highest tertile (7.8% worsening) showed a reduction in alcohol intake (beta: -4.32 g/day; 95% CI -7.00 to -1.62; p trend=0.002) and were more likely to quit alcohol (OR: 2.80; 95% CI 1.54 to 5.08; p trend=0.001). The main contributors to decreasing drinking were increased functional impairment and poorer self-rated health, whereas worsening self-rated health, onset of diabetes or stroke and increased prevalence of hospitalisation influenced cessation.

CONCLUSIONS: Health deterioration is related to a subsequent reduction and cessation of alcohol consumption contributing to the growing evidence challenging the protective health effect previously attributed to low-to-moderate alcohol consumption

26 June 2020 In Cardiovascular System

BACKGROUND: The causal role of alcohol consumption for cardiovascular disease remains unclear. We used Mendelian randomization (MR) to predict the effect of alcohol consumption on 8 cardiovascular diseases.

METHODS: Up to 94 single-nucleotide polymorphisms were used as instrumental variables for alcohol consumption. Genetic association estimates for cardiovascular diseases were obtained from large-scale consortia and UK Biobank. Analyses were conducted using the inverse variance-weighted, weighted median, MR-PRESSO, MR-Egger, and multivariable MR methods.

RESULTS: Genetically predicted alcohol consumption was consistently associated with stroke and peripheral artery disease across the different analyses. The odds ratios (ORs) per 1-SD increase of log-transformed alcoholic drinks per week were 1.27 ([95% CI, 1.12-1.45] P=2.87x10(-4)) for stroke and 3.05 ([95% CI, 1.92-4.85] P=2.30x10(-6)) for peripheral artery disease in the inverse variance-weighted analysis. There was some evidence for positive associations of genetically predicted alcohol consumption with coronary artery disease (OR, 1.16 [95% CI, 1.00-1.36]; P=0.052), atrial fibrillation (OR, 1.17 [95% CI, 1.00-1.37]; P=0.050), and abdominal aortic aneurysm (OR, 2.60 [95% CI, 1.15-5.89]; P=0.022) in the inverse variance-weighted analysis. These associations were somewhat attenuated in multivariable MR analysis adjusted for smoking initiation. There was no evidence of associations of genetically predicted alcohol consumption with heart failure (OR, 1.00 [95% CI, 0.68-1.47]; P=0.996), venous thromboembolism (OR, 1.04 [95% CI, 0.77-1.39]; P=0.810), and aortic valve stenosis (OR, 1.03 [95% CI, 0.56-1.90]; P=0.926).

CONCLUSIONS: This study provides evidence of a causal relationship between higher alcohol consumption and increased risk of stroke and peripheral artery disease. The causal role of alcohol consumption for other cardiovascular diseases requires further research.

24 January 2020 In Cardiovascular System

Alcohol has a hormetic physiological behavior that results in either increased or decreased cardiovascular risk depending on the amount consumed, drinking frequency, pattern of consumption, and the outcomes under study or even the type of alcoholic beverage consumed.

However, the vast majority of studies elucidating the role of alcohol in cardiovascular and in the global burden of disease relies on epidemiological studies of associative nature which carry several limitations. This is why the cardiovascular benefits of low-moderate alcohol consumption are being questioned and perhaps might have been overestimated.

Thus, the aim of this review was to critically discuss the current knowledge on the relationship between alcohol intake and cardiovascular disease. Besides new evidence associating low and moderate alcohol consumption with decreased risk of cardiovascular disease, several questions remain unanswered related to the concrete amount of safe consumption, the type of alcoholic beverage, and the age-, sex-, and genetic/ethnical-specific differences in alcohol consumption.

24 June 2019 In Cardiovascular System

PURPOSE: To provide evidence of the relationship of Mediterranean diet (MD) on incidence/mortality for cardiovascular disease (CVD), coronary/ischemic heart disease (CHD)/acute myocardial infarction (AMI) and stroke (ischemic/hemorrhagic) by sex, geographic region, study design and type of MD score (MDS).

METHODS: We performed a systematic review and meta-analysis of observational studies. Pooled relative risks (RRs) were calculated using random-effects models.

RESULTS: We identified 29 articles. The RR for the highest versus the lowest category of the MDS was 0.81 (95% CI 0.74-0.88) for the 11 studies that considered unspecified CVD, consistent across all strata. The corresponding pooled RR for CHD/AMI risk was 0.70 (95% CI 0.62-0.80), based on 11 studies. The inverse relationship was consistent across strata of study design, end point (incidence and mortality), sex, geographic area, and the MDS used. The overall RR for the six studies that considered unspecified stroke was 0.73 (95% CI 0.59-0.91) for the highest versus the lowest category of the MDS. The corresponding values were 0.82 (95% CI 0.73-0.92) for ischemic (five studies) and 1.01 (95% CI 0.74-1.37) for hemorrhagic stroke (four studies).

CONCLUSIONS: Our findings indicate and further quantify that MD exerts a protective effect on the risk of CVD. This inverse association includes CHD and ischemic stroke, but apparently not hemorrhagic stroke.

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