Data are conflicting about the effects of alcohol intake on kidney function. This population-based study investigated associations of alcohol intake with kidney function and mortality. The study cohort included adult participants in Exam-1, Exam-2 (6-year follow-up), and Exam-3 (20-year follow-up) of the Gubbio study.
Kidney function was evaluated as estimated glomerular filtration rate (eGFR, CKD-Epi equation, mL/min x 1.73 m(2)). Daily habitual alcohol intake was assessed by questionnaires. Wine intake accounted for >94% of total alcohol intake at all exams. Alcohol intake significantly tracked over time (R > 0.66, p < 0.001). Alcohol intake distribution was skewed at all exams (skewness > 2) and was divided into four strata for analyses (g/day = 0, 1-24, 25-48, and >48). Strata of alcohol intake differed substantially for lab markers of alcohol intake (p < 0.001).
In multivariable regression, strata of alcohol intake related cross-sectionally to eGFR at all exams (Exam-1: B = 1.70, p < 0.001; Exam-2: B = 1.03, p < 0.001; Exam-3: B = 0.55, p = 0.010) and related longitudinally to less negative eGFR change from Exam-1 to Exam-2 (B = 0.133, p = 0.002) and from Exam-2 to Exam-3 (B = 0.065, p = 0.004). In multivariable Cox models, compared to no intake, intakes > 24 g/day were not associated with different mortality while an intake of 1-24 g/day was associated with lower mortality in the whole cohort (HR = 0.77, p = 0.003) and in the subgroup with eGFR < 60 mL/min x 1.73 m(2) (HR = 0.69, p = 0.033). These data indicate a positive independent association of alcohol intake with kidney function not due to a mortality-related selection.
Based on a prospective cohort study of adults from southwest China with heterogeneity in their demographical characteristics and lifestyles, we aimed to explore the association between drinking patterns and incident hypertension under the interaction of these confounding factors. The Cox proportional hazard model was used to estimate the hazard ratios (HR) and 95% confidence intervals (95% CI).
Subgroup analysis was performed according to sex, ethnicity, area, occupation, smoking, and exercise to compare the differences in the association between drinking patterns and the incidence of hypertension. Blood pressure was higher in participants with a high drinking frequency than those with a low drinking frequency (p < 0.001). We found that total drinking frequency, liquor drinking frequency, rice wine drinking frequency, and alcohol consumption were significantly associated with an increased risk of hypertension.
Compared with the non-drinking group, a heavy drinking pattern was positively correlated with hypertension. Drinking can increase the risk of hypertension, especially heavy drinking patterns, with a high frequency of alcohol intake and high alcohol consumption. From the analysis results of the longitudinal data, drinking alcohol is still an important risk factor for hypertension among Chinese subjects, especially for men, the rural population, the employed, the Han nationality, smokers, and certain exercise populations.
BACKGROUND & AIMS: Only a minority of excess alcohol drinkers develop cirrhosis. We developed and evaluated risk stratification scores to identify those at highest risk.
METHODS: Three cohorts (GenomALC-1: n = 1,690, GenomALC-2: n = 3,037, UK Biobank: relevant n = 6,898) with a history of heavy alcohol consumption (>/=80 g/day (men), >/=50 g/day (women), for >/=10 years) were included. Cases were participants with alcohol-related cirrhosis. Controls had a history of similar alcohol consumption but no evidence of liver disease. Risk scores were computed from up to 8 genetic loci identified previously as associated with alcohol-related cirrhosis and 3 clinical risk factors. Score performance for the stratification of alcohol-related cirrhosis risk was assessed and compared across the alcohol-related liver disease spectrum, including hepatocellular carcinoma (HCC).
RESULTS: A combination of 3 single nucleotide polymorphisms (SNPs) (PNPLA3:rs738409, SUGP1-TM6SF2:rs10401969, HSD17B13:rs6834314) and diabetes status best discriminated cirrhosis risk. The odds ratios (ORs) and (95% CIs) between the lowest (Q1) and highest (Q5) score quintiles of the 3-SNP score, based on independent allelic effect size estimates, were 5.99 (4.18-8.60) (GenomALC-1), 2.81 (2.03-3.89) (GenomALC-2), and 3.10 (2.32-4.14) (UK Biobank). Patients with diabetes and high risk scores had ORs of 14.7 (7.69-28.1) (GenomALC-1) and 17.1 (11.3-25.7) (UK Biobank) compared to those without diabetes and with low risk scores. Patients with cirrhosis and HCC had significantly higher mean risk scores than patients with cirrhosis alone (0.76 +/- 0.06 vs. 0.61 +/- 0.02, p = 0.007). Score performance was not significantly enhanced by information on additional genetic risk variants, body mass index or coffee consumption.
CONCLUSIONS: A risk score based on 3 genetic risk variants and diabetes status enables the stratification of heavy drinkers based on their risk of cirrhosis, allowing for the provision of earlier preventative interventions.
LAY SUMMARY: Excessive chronic drinking leads to cirrhosis in some people, but so far there is no way to identify those at high risk of developing this debilitating disease. We developed a genetic risk score that can identify patients at high risk. The risk of cirrhosis is increased >10-fold with just two risk factors - diabetes and a high genetic risk score. Risk assessment using this test could enable the early and personalised management of this disease in high-risk patients.
BACKGROUND: Both alcohol use and weight status have been linked to increased mortality risk, but evidence of their joint effect is limited. The goal of this study was to examine the combined effects of alcohol and weight status (BMI classes: underweight, normal, overweight, obesity) on mortality using nationally representative data.
METHODS: Using data from public-use National Health Interview Survey-Linked Mortality Files (NHIS-LMF), 2001-2011, linked to prospective mortality follow-up through December 2015, we used age-period-cohort Cox proportional hazards models to examine all-cause and cause-specific mortality associated with the joint effects of alcohol use and BMI on 209,317 individuals aged 35-85.
RESULTS: Individuals with an underweight BMI status had higher all-cause and cause-specific mortality risks than those with a normal BMI status and light/moderate alcohol intake. All-cause mortality risks were 148% (hazard ratio [HR] 2.48, 95% CI 1.60-3.83) higher in underweight heavy drinkers than light/moderate drinkers with normal BMI status. Obese heavy drinkers had a 16% higher chance of dying from all-cause mortality (HR 1.16, 95% CI 1.00-1.35). Individuals in the unknown alcohol and BMI category have a higher chance of death from all-cause (HR 1.35, 95% CI 1.14-1.59) or cause-specific (CVD HR 1.75, 95% CI 1.14-2.69 and Cancer HR 1.33, 95% CI 1.01-1.76).
CONCLUSIONS: Alcohol drinking levels result in heightened all-cause and cause-specific mortality risks; the risks are compounded among underweight, obese, and unknown BMI individuals across all or cause-specific mortality.