Meta-analyses of alcohol use, alcohol dosage and alcohol-related problems as risk factors for tuberculosis incidence were undertaken. The global alcohol-attributable tuberculosis burden of disease was also re-estimated.Systematic searches were conducted, reference lists were reviewed and expert consultations were held to identify studies. Cohort and case-control studies were included if there were no temporal violations of exposure and outcome. Risk relations (RRs) were pooled by using categorical and dose-response meta-analyses. The alcohol-attributable tuberculosis burden of disease was estimated by using alcohol-attributable fractions.36 of 1108 studies were included. RRs for alcohol use and alcohol-related problems were 1.35 (95% CI 1.09-1.68; I2: 83%) and 3.33 (95% CI 2.14-5.19; 87%), respectively. Concerning alcohol dosage, tuberculosis risk rose as ethanol intake increased, with evidence of a threshold effect. Alcohol consumption caused 22.02 incident cases (95% CI 19.70-40.77) and 2.35 deaths (95% CI 2.05-4.79) per 100 000 people from tuberculosis in 2014. Alcohol-attributable tuberculosis incidence increased between 2000 and 2014 in most high tuberculosis burden countries, whereas mortality decreased.Alcohol consumption was associated with an increased risk of tuberculosis in all meta-analyses. It was consequently a major contributor to the tuberculosis burden of disease.

Published in General Health

BACKGROUND & AIMS: The ingestion of small to moderate alcohol consumption amounts has been associated to cardiovascular protection. This study aimed to evaluate the association between alcohol consumption and coronary artery disease severity.

MATERIAL AND METHODS: Cross-sectional Study with patients undergoing coronary angiography. Age, cardiovascular risk factors (smoking, systemic arterial hypertension, dyslipidemia and diabetes) and alcohol drinking habit were investigated. Alcohol consumption was divided in three categories: nondrinker, moderate alcohol consumption (less than 15 g ethanol/day for women or 30 g ethanol/day for men) and heavy alcohol consumption. Coronary artery disease severity was assessed through the Friesinger Score (FS) in the coronary angiography, by interventional cardiologists blinded to alcohol consumption.

RESULTS: The final sample included 363 adults; of those, 228 were men (62.81%). Mean age was 60.5 +/- 10.9 y. Unadjusted analyses identified sex, age, hypertension, diabetes, dyslipidemia and alcohol consumption as the main covariates associated with the Friesinger score. Lower Friesinger scores were also observed in moderate alcohol consumption when comparing to those who do not drink (RR 0.86; 95% CI 0.79-0.95).

CONCLUSION: Among patients with suspected coronary artery disease undergoing coronary angiography, moderate alcohol consumption is associated to a lower coronary artery disease severity than heavy drinking.

Published in Cardiovascular System

PURPOSE: To estimate the Australian cancer burden attributable to lifestyle-related risk factors and their combinations using a novel population attributable fraction (PAF) method that accounts for competing risk of death, risk factor interdependence and statistical uncertainty.

PARTICIPANTS: 365 173 adults from seven Australian cohort studies. We linked pooled harmonised individual participant cohort data with population-based cancer and death registries to estimate exposure-cancer and exposure-death associations. Current Australian exposure prevalence was estimated from representative external sources. To illustrate the utility of the new PAF method, we calculated fractions of cancers causally related to body fatness or both tobacco and alcohol consumption avoidable in the next 10 years by risk factor modifications, comparing them with fractions produced by traditional PAF methods.

FINDINGS TO DATE: Over 10 years of follow-up, we observed 27 483 incident cancers and 22 078 deaths. Of cancers related to body fatness (n=9258), 13% (95% CI 11% to 16%) could be avoided if those currently overweight or obese had body mass index of 18.5-24.9 kg/m2. Of cancers causally related to both tobacco and alcohol (n=4283), current or former smoking explains 13% (11% to 16%) and consuming more than two alcoholic drinks per day explains 6% (5% to 8%). The two factors combined explain 16% (13% to 19%): 26% (21% to 30%) in men and 8% (4% to 11%) in women. Corresponding estimates using the traditional PAF method were 20%, 31% and 10%. Our PAF estimates translate to 74 000 avoidable body fatness-related cancers and 40 000 avoidable tobacco- and alcohol-related cancers in Australia over the next 10 years (2017-2026). Traditional PAF methods not accounting for competing risk of death and interdependence of risk factors may overestimate PAFs and avoidable cancers.

FUTURE PLANS: We will rank the most important causal factors and their combinations for a spectrum of cancers and inform cancer control activities.

Published in Cancer

BACKGROUND: Alcohol-related mortality and morbidity are high in socioeconomically disadvantaged populations compared with individuals from advantaged areas. It is unclear if this increased harm reflects differences in alcohol consumption between these socioeconomic groups, reverse causation (ie, downward social selection for high-risk drinkers), or a greater risk of harm in individuals of low socioeconomic status compared with those of higher status after similar consumption. We aimed to investigate whether the harmful effects of alcohol differ by socioeconomic status, accounting for alcohol consumption and other health-related factors.

METHODS: The Scottish Health Surveys are record-linked cross-sectional surveys representative of the adult population of Scotland. We obtained baseline demographics and data for alcohol consumption (units per week and binge drinking) from Scottish Health Surveys done in 1995, 1998, 2003, 2008, 2009, 2010, 2011, and 2012. We matched these data to records for deaths, admissions, and prescriptions. The primary outcome was alcohol-attributable admission or death. The relation between alcohol-attributable harm and socioeconomic status was investigated for four measures (education level, social class, household income, and area-based deprivation) using Cox proportional hazards models. The potential for alcohol consumption and other risk factors (including smoking and body-mass index [BMI]) mediating social patterning was explored in separate regression models. Reverse causation was tested by comparing change in area deprivation over time.

FINDINGS: 50 236 participants (21 777 men and 28 459 women) were included in the analytical sample, with 429 986 person-years of follow-up. Low socioeconomic status was associated consistently with strikingly raised alcohol-attributable harms, including after adjustment for weekly consumption, binge drinking, BMI, and smoking. Evidence was noted of effect modification; for example, relative to light drinkers living in advantaged areas, the risk of alcohol-attributable admission or death for excessive drinkers was increased (hazard ratio 6.12, 95% CI 4.45-8.41 in advantaged areas; and 10.22, 7.73-13.53 in deprived areas). We found little support for reverse causation.

INTERPRETATION: Disadvantaged social groups have greater alcohol-attributable harms compared with individuals from advantaged areas for given levels of alcohol consumption, even after accounting for different drinking patterns, obesity, and smoking status at the individual level.

FUNDING: Medical Research Council, NHS Research Scotland, Scottish Government Chief Scientist Office

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