29 October 2018 In Cancer

Epidemiological studies have been used to show associations between modifiable lifestyle habits and the incidence of breast cancer. Among such factors, a history of alcohol use has been reported in multiple studies and meta-analyses over the past decades. However, associative epidemiological studies that were interpreted as evidence that even moderate alcohol consumption increases breast cancer incidence have been controversial. In this review, we consider the literature on the relationship between moderate or heavy alcohol use, both in possible biological mechanisms and in variations in susceptibility due to genetic or epigenetic factors. We argue that there is a need to incorporate additional approaches to move beyond the associations that are reported in traditional epidemiological analyses and incorporate information on molecular pathologic signatures as a requirement to posit causal inferences. In particular, we point to the efforts of the transdisciplinary field of molecular pathological epidemiology (MPE) to evaluate possible causal relationships, if any, of alcohol consumption and breast cancer. A wider application of the principles of MPE to this field would constitute a giant step that could enhance our understanding of breast cancer and multiple modifiable risk factors, a step that would be particularly suited to the era of "personalized medicine".

27 September 2018 In General Health

OBJECTIVE: A systematic review and meta-analysis to estimate the magnitude of the association between alcohol consumption and the risk of community-acquired pneumonia (CAP) in adults was undertaken.

DESIGN: Systematic review and meta-analysis.

METHODS: Comprehensive searches of Medline, Embase and Web of Science were carried out to identify comparative studies of the association between alcohol intake and CAP between 1985 and 2017. Reference lists were also screened. A random-effects meta-analysis was used to estimate pooled effect sizes. A dose-response meta-analysis was also performed.

RESULTS: We found 17 papers eligible for inclusion in the review, of which 14 provided results which could be pooled. Meta-analysis of these 14 studies identified an 83% increased risk of CAP among people who consumed alcohol or in higher amounts, relative to those who consumed no or lower amounts of alcohol, respectively (relative risk=1.83, 95% CI 1.30 to 2.57). There was substantial between-study heterogeneity, which was attributable in part to differences in study continent, adjustment for confounders and pneumonia diagnosis (clinical vs death). Dose-response analysis found that for every 10-20 g higher alcohol intake per day, there was an 8% increase in the risk of CAP.

CONCLUSIONS: The findings suggest that alcohol consumption increases the risk of CAP. Therefore, strengthening policies to reduce alcohol intake would be likely to reduce the incidence of CAP.

27 September 2018 In Cardiovascular System

BACKGROUND/OBJECTIVES: Low/moderate alcohol consumption seems to be protective against cardiovascular disease (CVD). This study aimed to investigate the association of wine/beer consumption with the 10-year CVD incidence.

SUBJECTS/METHODS: During 2001-2002, 3042 CVD-free adults consented to participate in the ATTICA study; of them 2583 completed the 10-year follow-up (85% participation rate), but precise information about fatal/nonfatal CVD incidence (myocardial infarction, angina pectoris, cardiac ischemia, heart failure, chronic arrhythmias, and stroke) was available in 2020 participants (overall retention rate 66%). Alcohol/ethanol intake and the alcoholic beverages consumed were assessed; participants were categorized into three groups (no use; 1 glass/week).

RESULTS: Alcohol drinking was reported by 56% of the participants who did not develop a CVD event and 49% of those who had (p = 0.04); whereas ethanol intake was 14 +/- 16 g among those who did not had an event vs. 21 +/- 18 g among those who had a CVD event (p < 0.001). A strong inverse and similar association between low wine/beer intake (20 g/day had CVD-risk HRs (95% CI) of 0.60 (0.40-0.98), 1.22 (0.60-1.14), and 1.81 (0.70-4.61), respectively.

CONCLUSIONS: This study revealed similar results of low wine/beer consumption against CVD incidence, mainly due to its implication on low-grade chronic inflammation.

06 September 2018 In Cardiovascular System

BACKGROUND: Studies have shown that alcohol intake trajectories differ in their associations with biomarkers of cardiovascular functioning, but it remains unclear if they also differ in their relationship to actual coronary heart disease (CHD) incidence. Using multiple longitudinal cohort studies, we evaluated the association between long-term alcohol consumption trajectories and CHD.

METHODS: Data were drawn from six cohorts (five British and one French). The combined analytic sample comprised 35,132 individuals (62.1% male; individual cohorts ranging from 869 to 14,247 participants) of whom 4.9% experienced an incident (fatal or non-fatal) CHD event. Alcohol intake across three assessment periods of each cohort was used to determine participants' intake trajectories over approximately 10 years. Time to onset for (i) incident CHD and (ii) fatal CHD was established using surveys and linked medical record data. A meta-analysis of individual participant data was employed to estimate the intake trajectories' association with CHD onset, adjusting for demographic and clinical characteristics.

RESULTS: Compared to consistently moderate drinkers (males: 1-168 g ethanol/week; females: 1-112 g ethanol/week), inconsistently moderate drinkers had a significantly greater risk of incident CHD [hazard ratio (HR) = 1.18, 95% confidence interval (CI) = 1.02-1.37]. An elevated risk of incident CHD was also found for former drinkers (HR = 1.31, 95% CI = 1.13-1.52) and consistent non-drinkers (HR = 1.47, 95% CI = 1.21-1.78), although, after sex stratification, the latter effect was only evident for females. When examining fatal CHD outcomes alone, only former drinkers had a significantly elevated risk, though hazard ratios for consistent non-drinkers were near identical. No evidence of elevated CHD risk was found for consistently heavy drinkers, and a weak association with fatal CHD for inconsistently heavy drinkers was attenuated following adjustment for confounding factors.

CONCLUSIONS: Using prospectively recorded alcohol data, this study has shown how instability in drinking behaviours over time is associated with risk of CHD. As well as individuals who abstain from drinking (long term or more recently), those who are inconsistently moderate in their alcohol intake have a higher risk of experiencing CHD. This finding suggests that policies and interventions specifically encouraging consistency in adherence to lower-risk drinking guidelines could have public health benefits in reducing the population burden of CHD. The absence of an effect amongst heavy drinkers should be interpreted with caution given the known wider health risks associated with such intake.

TRIAL REGISTRATION: ClinicalTrials.gov, NCT03133689

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