28 April 2022 In Drinking Patterns

The present study examines how alcohol intake from wine and non-wine alcoholic beverages (non-wine) in g/d, as well as cups of coffee and tea included as continuous covariates and mutually adjusted are associated with all-cause, cancer, non-cancer and CVD mortality. Consumption was assessed in 354 386 participants of the UK Biobank cohort who drank alcohol at least occasionally and survived at least 2 years after baseline with 20 201 deaths occurring over 4.2 million person-years. Hazard ratios (HR) for mortality were assessed with Cox proportional hazard regression models and beverage intake fitted as penalised cubic splines.

A significant U-shaped association was detected between wine consumption and all-cause, non-cancer and CVD mortality. Wine consumption with lowest risk of death (nadir) ranged from 19 to 23 g alcohol/d in all participants and both sexes separately. In contrast, non-wine intake was significantly and positively associated in a dose-dependent manner with all mortality types studied except for CVD in females and with the nadir between 0 and 12 g alcohol/d.

In all participants, the nadir for all-cause mortality was 2 cups coffee/d with non-coffee drinkers showing a slightly increased risk of death. Tea consumption was significantly and negatively associated with all mortality types in both sexes. Taken together, light to moderate consumption of wine but not non-wine is associated with decreased all-cause and non-cancer mortality. A minor negative association of coffee consumption with mortality cannot be excluded whereas tea intake is associated with a consistently decreased risk of all mortality types studied.

22 March 2022 In Drinking Patterns

The present study examines how alcohol intake from wine and non-wine alcoholic beverages (non-wine) in g/d, as well as cups of coffee and tea included as continuous covariates and mutually adjusted are associated with all-cause, cancer, non-cancer and CVD mortality. Consumption was assessed in 354 386 participants of the UK Biobank cohort who drank alcohol at least occasionally and survived at least 2 years after baseline with 20 201 deaths occurring over 4.2 million person-years.

Hazard ratios (HR) for mortality were assessed with Cox proportional hazard regression models and beverage intake fitted as penalised cubic splines. A significant U-shaped association was detected between wine consumption and all-cause, non-cancer and CVD mortality. Wine consumption with lowest risk of death (nadir) ranged from 19 to 23 g alcohol/d in all participants and both sexes separately. In contrast, non-wine intake was significantly and positively associated in a dose-dependent manner with all mortality types studied except for CVD in females and with the nadir between 0 and 12 g alcohol/d.

In all participants, the nadir for all-cause mortality was 2 cups coffee/d with non-coffee drinkers showing a slightly increased risk of death. Tea consumption was significantly and negatively associated with all mortality types in both sexes. Taken together, light to moderate consumption of wine but not non-wine is associated with decreased all-cause and non-cancer mortality. A minor negative association of coffee consumption with mortality cannot be excluded whereas tea intake is associated with a consistently decreased risk of all mortality types studied.

26 January 2022 In Drinking Patterns

OBJECTIVES: To evaluate the associations of status, amount, and frequency of alcohol consumption across different alcoholic beverages with coronavirus disease 2019 (COVID-19) risk and associated mortality.

MANDATE: This study included 473,957 subjects, 16,559 of whom tested positive for COVID-19. Multivariate logistic regression analyses were used to evaluate the associations of alcohol consumption with COVID-19 risk and associated mortality. The non-linearity association between the amount of alcohol consumption and COVID-19 risk was evaluated by a generalized additive model.

RESULTS: Subjects who consumed alcohol double above the guidelines had a higher risk of COVID-19 (1.12 [1.00, 1.25]). Consumption of red wine above or double above the guidelines played protective effects against the COVID-19. Consumption of beer and cider increased the COVID-19 risk, regardless of the frequency and amount of alcohol intake. Low-frequency of consumption of fortified wine (1-2 glasses/week) within guidelines had a protective effect against the COVID-19. High frequency of consumption of spirits (>/=5 glasses/week) within guidelines increased the COVID-19 risk, whereas the high frequency of consumption of white wine and champagne above the guidelines decreased the COVID-19 risk. The generalized additive model showed an increased risk of COVID-19 with a greater number of alcohol consumption. Alcohol drinker status, frequency, amount, and subtypes of alcoholic beverages were not associated with COVID-19 associated mortality.

CONCLUSIONS: The COVID-19 risk appears to vary across different alcoholic beverage subtypes, frequency, and amount. Red wine, white wine, and champagne have chances to reduce the risk of COVID-19. Consumption of beer and cider and spirits and heavy drinking are not recommended during the epidemics. Public health guidance should focus on reducing the risk of COVID-19 by advocating healthy lifestyle habits and preferential policies among consumers of beer and cider and spirits.

22 October 2021 In General Health

Harmful alcohol use is a leading cause of premature death and is associated with age-related disease. Biological ageing is highly variable between individuals and may deviate from chronological ageing, suggesting that biomarkers of biological ageing (derived from DNA methylation or brain structural measures) may be clinically relevant. Here, we investigated the relationships between alcohol phenotypes and both brain and DNA methylation age estimates. First, using data from UK Biobank and Generation Scotland, we tested the association between alcohol consumption (units/week) or hazardous use (Alcohol Use Disorders Identification Test [AUDIT] scores) and accelerated brain and epigenetic ageing in 20,258 and 8051 individuals, respectively. Second, we used Mendelian randomisation (MR) to test for a causal effect of alcohol consumption levels and alcohol use disorder (AUD) on biological ageing. Alcohol use showed a consistent positive association with higher predicted brain age (AUDIT-C: beta = 0.053, p = 3.16 x 10(-13) ; AUDIT-P: beta = 0.052, p = 1.6 x 10(-13) ; total AUDIT score: beta = 0.062, p = 5.52 x 10(-16) ; units/week: beta = 0.078, p = 2.20 x 10(-16) ), and two DNA methylation-based estimates of ageing, GrimAge (units/week: beta = 0.053, p = 1.48 x 10(-7) ) and PhenoAge (units/week: beta = 0.077, p = 2.18x10(-10) ). MR analyses revealed limited evidence for a causal effect of AUD on accelerated brain ageing (beta = 0.118, p = 0.044). However, this result should be interpreted cautiously as the significant effect was driven by a single genetic variant. We found no evidence for a causal effect of alcohol consumption levels on accelerated biological ageing. Future studies investigating the mechanisms associating alcohol use with accelerated biological ageing are warranted.

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