Alcohol use is causally linked to the development of and mortality from numerous diseases. The aim of this study is to provide an update to a previous systematic review of meta-analyses that quantify the sex-specific dose-response risk relationships between chronic alcohol use and disease occurrence and/or mortality. An updated systematic search of multiple databases was performed in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses criteria to identify meta-analyses published from January 1, 2017, to March 8, 2021, which quantified the risk relationships between chronic alcohol use and the risk of disease occurrence and/or mortality. This systematic review was not preregistered. The comparator was people who have never consumed at least one standard drink of alcohol. Measurements included relative risks, odds ratios, and hazard ratios of disease occurrence and/or mortality based on long-term alcohol intake measured in grams per day. The systematic search yielded 5953 articles, of which 14 were included in the narrative review. All diseases showed an increased risk of occurrence as alcohol use increased. At all doses examined, alcohol had a significant detrimental effect on tuberculosis, lower respiratory infections, oral cavity and pharyngeal cancers, esophageal cancer, colorectal cancer, liver cancer, laryngeal cancer, epilepsy, hypertension, liver cirrhosis, and pancreatitis (among men). For ischemic heart disease, ischemic stroke, and intracerebral hemorrhage, protective effects from low-dose chronic alcohol use among both men and women were observed. Low-dose alcohol consumption also had a protective effect for diabetes mellitus and pancreatitis among women (approximately to 50 g/day and 30 g/day, respectively). Alcohol use increases the risk of numerous infectious and noncommunicable diseases in a dose-response manner. Higher levels of alcohol use have a clear detrimental impact on health; however, at lower levels of use, alcohol can have both disease-specific protective and detrimental effects.
CONTEXT: Effects of modest alcohol consumption remain controversial. Mendelian randomization (MR) can help to mitigate biases due to confounding and reverse causation in observational studies, and evaluate the potential causal role of alcohol consumption.
OBJECTIVE: This work aimed to evaluate dose-dependent effect of alcohol consumption on obesity and type 2 diabetes.
METHODS: Assessing 408 540 participants of European ancestry in the UK Biobank, we first tested the association between self-reported alcohol intake frequency and 10 anthropometric measurements, obesity, and type 2 diabetes. We then conducted MR analyses both in the overall population and in subpopulations stratified by alcohol intake frequency.
RESULTS: Among individuals having more than 14 drinks per week, a 1-drink-per-week increase in genetically predicted alcohol intake frequency was associated with a 0.36-kg increase in fat mass (SD = 0.03 kg), a 1.08-fold increased odds of obesity (95% CI, 1.06-1.10), and a 1.10-fold increased odds of type 2 diabetes (95% CI, 1.06-1.13). These associations were stronger in women than in men. Furthermore, no evidence was found supporting the association between genetically increased alcohol intake frequency and improved health outcomes among individuals having 7 or fewer drinks per week, as MR estimates largely overlapped with the null. These results withstood multiple sensitivity analyses assessing the validity of MR assumptions.
CONCLUSION: As opposed to observational associations, MR results suggest there may not be protective effects of modest alcohol consumption on obesity traits and type 2 diabetes. Heavy alcohol consumption could lead to increased measures of obesity as well as increased risk of type 2 diabetes.
OBJECTIVE: Alcohol drinking and tobacco smoking have impacts on lifestyle-related diseases, but their association with dementia remains a debated topic. This study aimed to examine longitudinal associations between alcohol consumption, smoking, and dementia risk in middle-aged and older Japanese people.
METHODS: This study used a cohort design with an 8-year follow-up. Participants were community-dwelling Japanese people (N = 13,802) aged 40-74 years. The baseline survey, including a self-administered questionnaire, was conducted in 2011-2013. Predictors were alcohol consumption and tobacco smoking. The outcome was incident dementia obtained from a long-term care insurance database. Covariates were demographics, lifestyle factors, body mass index, general health status, and history of stroke, diabetes, and depression.
RESULTS: Participant mean age was 59.0 years. The 1-149, 150-299, and 300-449 g ethanol/week groups had significantly lower adjusted hazard ratios (HRs) (0.62, 0.59, and 0.47, respectively) compared with the reference group, with no significant linear association. HRs increased toward 1 when past-drinkers and those with poor health status and a disease history were excluded (0.80, 0.66, and 0.82, respectively). Higher smoking levels were dose-dependently associated with a higher HR (adjusted P for trend = 0.0105), with the >/=20 cigarettes/day group having a significantly higher adjusted HR (1.80). Heavy drinkers (>/=449 g ethanol/week) with smoking habits, but not those without smoking habits, had higher dementia risk (P for interaction = 0.0046).
CONCLUSION: Light-to-moderate alcohol consumption is associated with decreased dementia risk, and smoking is dose-dependently associated with increased dementia risk, with an interaction between high alcohol consumption and smoking on dementia risk.
A large number of observational studies have found a J-shaped relationship between alcohol intake and ischemic heart disease (IHD) risk. However, some studies suggest that the alleged cardio-protective effect may be an artifact in the way that the elevated risk for abstainers is due to self-selection on risk factors for IHD. The aim of this paper is to estimate the association between alcohol and IHD-mortality on the basis of aggregate time-series data, where the problem with selection effects is not present. In addition, we will analyze SES-specific mortality to investigate whether there is any socio-economic gradient in the relationship at issue. SES was measured by educational level. We used IHD-mortality in three educational groups as outcome. Per capita alcohol consumption was proxied by Systembolaget's alcohol sales (litres of alcohol 100% per capita 15+). Swedish quarterly data on mortality and alcohol consumption spanned the period 1991Q1-2020Q4. We applied SARIMA time-series analysis. Survey data were used to construct an indicator of heavy SES-specific episodic drinking. The estimated association between per capita consumption and IHD-mortality was positive and statistically significant in the two groups with primary and secondary education, but not in the group with postsecondary education. The association was significantly stronger the lower the educational group. Although the associations were generally stronger for males than for females, these differences were not statistically significant (P > 0.05). Our findings suggest that the detrimental impact of per capita consumption on IHD-mortality was stronger the lower the educational group.