27 February 2017 In Cardiovascular System

BACKGROUND: Emerging evidence suggests that arterial stiffness, an important marker of cardiovascular health, is associated with alcohol consumption. However, the role of longer-term consumption patterns in the progression of arterial stiffness over time remains unclear. A longitudinal cohort design was used to evaluate the association between alcohol consumption over 25 years and subsequent changes in arterial stiffness.

METHODS AND RESULTS: Data (N=3869; 73% male) were drawn from the Whitehall II cohort study of British civil servants, in which participants completed repeat pulse wave velocity assessments of arterial stiffness across a 4- to 5-year interval. Repeated alcohol intake measurements were used to categorize participants into alcohol consumer types, accounting for longitudinal variability in consumption. Sex-stratified linear mixed-effects modeling was used to investigate whether drinker types differed in their relationship to pulse wave velocity and its progression over time. Males with consistent long-term heavy intake >112 g of ethanol/week had significantly higher baseline pulse wave velocity (b=0.26 m/s; P=0.045) than those who drank consistently moderately (1-112 g of ethanol/week). Male former drinkers showed significantly greater increases in arterial stiffness longitudinally compared to consistently moderate drinkers (b=0.11 m/s; P=0.009). All associations were nonsignificant for females after adjustment for body mass index, heart rate, mean arterial pressure, diabetes mellitus, high-density lipoprotein, and triglycerides.

CONCLUSIONS: This work demonstrates that consistently heavy alcohol consumption is associated with higher cardiovascular risk, especially among males, and also provides new insights into the potential impact of changes in drinking levels over time. It discusses the additional insights possible when capturing longitudinal consumption patterns in lieu of reliance on recent intake alone.

CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT02663791

01 February 2017 In Liver Disease

BACKGROUND: Liver damage is a serious and sometimes fatal consequence of long-term alcohol intake, which progresses from early-stage fatty liver (steatosis) to later-stage steatohepatitis with inflammation and fibrosis/necrosis. However, very little is known about earlier stages of liver disruption that may occur in problem drinkers, those who drink excessively but are not dependent on alcohol.

METHODS: We examined how repeated binge-like alcohol drinking in C57BL/6 mice altered liver function, as compared with a single binge-intake session and with repeated moderate alcohol consumption. We measured a number of markers associated with early- and later-stage liver disruption, including liver steatosis, measures of liver cytochrome P4502E1 (CYP2E1) and alcohol dehydrogenase (ADH), alcohol metabolism, expression of cytokine mRNA, accumulation of 4-hydroxynonenal (4-HNE) as an indicator of oxidative stress, and alanine transaminase/aspartate transaminase as a measure of hepatocyte injury.

RESULTS: Importantly, repeated binge-like alcohol drinking increased triglyceride levels in the liver and plasma, and increased lipid droplets in the liver, indicators of steatosis. In contrast, a single binge-intake session or repeated moderate alcohol consumption did not alter triglyceride levels. In addition, alcohol exposure can increase rates of alcohol metabolism through CYP2E1 and ADH, which can potentially increase oxidative stress and liver dysfunction. Intermittent, excessive alcohol intake increased liver CYP2E1 mRNA, protein, and activity, as well as ADH mRNA and activity. Furthermore, repeated, binge-like drinking, but not a single binge or moderate drinking, increased alcohol metabolism. Finally, repeated, excessive intake transiently elevated mRNA for the proinflammatory cytokine IL-1B and 4-HNE levels, but did not alter markers of later-stage liver hepatocyte injury.

CONCLUSIONS: Together, we provide data suggesting that even relatively limited binge-like alcohol drinking can lead to disruptions in liver function, which might facilitate the transition to more severe forms of liver damage.

15 December 2016 In Diabetes
Background Although alcohol consumption is commonly encountered in clinical practice, few studies have investigated the clinical significance of alcohol intake on the use of the hemoglobin A1c (HbA1c) level. Objectives This study was performed to investigate the association between alcohol intake and HbA1c level in the general population. Methods Among the 24,594 participants who participated in the 2011-2013 Korea National Health and Nutrition Examination Survey (KNHANES), 12,923 participants were analyzed in this study. We excluded diabetic patients currently taking antidiabetes medication. We compared the HbA1c level and proportions of patients with an HbA1c level of =5.7%, =6.1%, and =6.5% according to the fasting plasma glucose (FPG) concentration range and the amount of alcohol intake. The average amounts of daily alcohol intake were categorized into three groups: 0 g/day, <30 g/day, =30 g/day. Results The mean HbA1c level was 5.65%, and the mean FPG concentration was 95.3 mg/dl. The percentages of patients with an HbA1c level of =5.7%, =6.1%, and =6.5% were 42.6%, 13.4%, and 4.5%, respectively. The average amount of alcohol intake was 12.3 g/day. The percentages of subjects with alcohol intake 0, <30, and = 30 g/day were 16.5%, 69.7%, and 13.8%, respectively.There was a significant positive relationship between alcohol intake and FPG concentration (P < 0.001), the prevalence of impaired fasting glucose (P < 0.001), and the prevalence of diabetes (P < 0.001). However, there was no significant relationship between the alcohol intake and HbA1c level.Overall, the adjusted HbA1c levels decreased across alcohol intake (5.70% ± 0.01%, 5.66% ± 0.01%, and 5.55% ± 0.01%) after adjustment for confounding factors such as age, sex, FPG concentration, college graduation, smoking history, presence of hypertension, waist circumference, serum total cholesterol concentration, serum high-density lipoprotein cholesterol concentration, serum triglyceride concentration, presence of anemia, serum white blood cell count, and serum alanine aminotransferase concentration (P < 0.001). The adjusted proportions (%) of patients with an HbA1c level of =5.7% (P < 0.001), =6.1% (P < 0.001), and =6.5% (P < 0.001) showed significant negative trends across alcohol intake after adjustment for confounders. Logistic regression analyses showed that, when using the group that abstained as the control, the group that consumed = 30g/day was negatively associated with the risk of an HbA1c level of =5.7% (P < 0.001), =6.1% (P < 0.001), and =6.5% (P < 0.001), using the above-mentioned variables as covariates. Conclusions Higher alcohol intake was associated with lower HbA1c levels, even after adjusting for confounding factors, including the FPG concentration, in this nationally representative sample of Korean adults. These results suggest that excessive drinking shifts the HbA1c level downward, which might complicate use of the HbA1c level for the diagnosis of diabetes or prediabetes.
15 December 2016 In Cardiovascular System

Alcohol is popular in Western culture, supported by a perception that modest intake is cardioprotective. However, excessive drinking has detrimental implications for cardiovascular disease. Atrial fibrillation (AF) following an alcohol binge or the "holiday heart syndrome" is well characterized. However, more modest levels of alcohol intake on a regular basis may also increase the risk of AF. The pathophysiological mechanisms responsible for the relationship between alcohol and AF may include direct toxicity and alcohol's contribution to obesity, sleep-disordered breathing, and hypertension. We aim to provide a comprehensive review of the epidemiology and pathophysiology by which alcohol may be responsible for AF and determine whether alcohol abstinence is required for patients with AF.

Page 8 of 81

Contact us

We love your feedback. Get in touch with us.

  • Tel: +32 (0)2 230 99 70
  • Email: This email address is being protected from spambots. You need JavaScript enabled to view it.


The authors have taken reasonable care in ensuring the accuracy of the information herein at the time of publication and are not responsible for any errors or omissions. Read more on our disclaimer and Privacy Policy.