Excess alcohol consumption is a leading contributor to the global burden of disease and a major risk factor for mortality. Yet, prior studies suggested that moderate alcohol consumption may be associated with a lower risk of cardiovascular disease (CVD) events. However, this evidence is based on data from younger individuals, and confirmation in older adults is lacking. Thus, we sought to investigate the risk of CVD events and all-cause mortality associated with alcohol consumption in initially healthy, older individuals.
For these post hoc analyses we used data from the ASPirin in Reducing Events in the Elderly (ASPREE) trial, which investigated the effect of low-dose...
BACKGROUND: We investigated the association of alcohol consumption with cardiovascular and non-cardiovascular mortality in elderly Chinese men.
METHODS: Our participants were recruited from residents living in a suburban town of Shanghai (>/=60 years of age, n = 1702). Alcohol intake was classified as non-drinkers, past drinkers (stopped drinking for >/=12 months), and current light-to-moderate (1 to 299 g/week) and heavy drinkers (>/=300 g/week). Alcoholic beverages were classified as beer/wine, rice aperitif and liquor/mix drinking.
RESULTS: During 5.9 years (median) of follow-up, all-cause, cardiovascular and non-cardiovascular deaths occurred in 211, 98 and 113 participants, respectively. The corresponding incidence rates were 23.6/1000, 10.9/1000 and 12.6/1000 person-years, respectively. Both before and after adjustment for confounding factors, compared with non-drinkers (n = 843), past drinkers (n = 241), but not the current light-to-moderate (n = 241) or heavy drinkers (n = 377), had a higher risk of all-cause (adjusted hazard ratio [HR] 1.90, 95% confidence interval [CI] 1.35-2.68, P = 0.0003) and non-cardiovascular mortality (HR 2.46, 95% CI 1.55-3.91, P = 0.0001). Similar trends were observed for cardiovascular mortality (HR 1.44, 95% CI 0.85-2.44, P = 0.18). In similar unadjusted and adjusted analyses, compared with the current beer/wine drinkers (n = 203), liquor/mix drinkers (n = 142), but not aperitif drinkers (n = 273), had a significantly higher risk of all-cause (HR 3.07, 95% CI 1.39-6.79, P = 0.006), and cardiovascular mortality (HR 10.49, 95% CI 2.00-55.22, P = 0.006). Similar trends were observed for non-cardiovascular mortality (HR 1.94, 95% CI 0.73-5.16, P = 0.18).
CONCLUSIONS: Our study showed risks of mortality associated with past drinking and liquor drinking in the elderly Chinese men.
Many studies conclude that wine consumption is related to lower risk for cardiovascular diseases partially through the amelioration of inflammatory biomarkers. The aim of the present study was to examine the effects of wine consumption on the inflammatory response and to compare these effects with the consumption of similar amount of alcohol without the wine micro-constituents in cardiovascular disease patients. Therefore, a randomized, single-blind, controlled, three-arm parallel intervention study was designed. Cardiovascular disease patients were randomly assigned to one of the three groups. In Group A participants consumed no alcohol, in Group B (ethanol group) and Group C (wine group) participants consumed 27 g of alcohol per day. Biological samples were collected at the beginning, on the 4th and 8th week and several biomarkers were measured. Peripheral blood mononuclear cells that were isolated from patients were incubated under basal and inflammatory conditions for 4 and 24 h and the secretion of interleukin 1beta (IL-1beta) and tumor necrosis factor alpha (TNFalpha) was measured. No significant difference was observed among the three groups before the initiation or during the intervention in the most soluble biomarkers. Higher TNFalpha secretion by peripheral blood mononuclear cells was observed at basal conditions in the ethanol group both at 4 and 24 h of incubation versus baseline secretion. Furthermore, lower secretion of the TauNFalpha was observed after 8 weeks of intake in the wine group versus the ethanol group, both at 4 and 24 h of incubation. In conclusion, the light to moderate wine consumption for 8 weeks revealed an attenuation of the ethanol consumption effect on cytokine secretion at basal conditions from the patients' peripheral blood mononuclear cells.
We assessed, for the first time, to what extent the composition of the gut microbiome might explain the cross-sectional association of habitual flavonoid and flavonoid-rich food intake with systolic and diastolic blood pressure (BP) in a community-based sample (N=904) from Northern Germany. Gut microbiome composition was sequenced from 16S ribosomal RNA genes. Higher total flavonoid intakes and specifically the polymer subclass were associated with lower systolic BP (SBP; β T3-T1: −2.9% [95% CI, −5.1 to −0.7], P=0.01 and −3.7% [95% CI, −5.4 to −1.0], P=0.01). In food-based analyses, a higher intake of berries (SBP, β Q4-Q1: −2.9% [95% CI, −5.2 to −0.6], P=0.01; pulse pressure, −5.5% [95% CI, −9.6 to −1.2], P=0.01) and red wine (SBP, β Q4-Q1: −2.6% [95% CI, −4.8 to −0.3], P=0.03; pulse pressure, −6.1% [95% CI, −10.1 to −2.0], P<0.01) were associated with lower SBP and pulse pressure. There were no associations with diastolic BP. In food-based analyses, higher intakes of anthocyanin-rich berries and red wine were associated with higher alpha diversity (β Q4-Q1: 0.03 [95% CI, 0.0–0.1], P=0.04 and 0.1 [95% CI, 0.03–0.1], P<0.01). Higher intakes of berries and apples/pears were associated with a lower abundance of Parabacteroides (β Q4-Q1: −0.2 [95% CI, −0.4 to −0.1], P<0.01, Q=0.07 and −0.3 [95% CI, −0.4 to −0.1], P< 0.01, Q=0.04). Structural equation modeling of these novel data suggests that microbial factors explained 15.2% to the association between flavonoid-rich foods and clinically relevant lower SBP. Further research should focus on interindividual variability in the gut microbiome in mediating the cardiovascular effects of flavonoid-rich foods.