Cardiovascular System

Is the “J-Curve” Real?

  

1. J-curve - Lower risk for light to moderate drinkers compared to abstainers

For many decades, epidemiological studies have consistently shown that light-to-moderate  consumers of alcoholic beverages have a lower risk of cardiovascular disease (CVD) and a lower risk of death from all causes (including total cancer) compared with non-drinkers or those who drink heavily. It is not limited to alcohol-related causes of death, but instead captures all deaths combined (Brien et al 2011, Ronksley et al 2011, di Castelnuovo et al 2006, Roerecke et al 2012, Ferrari et al 2014, Jayasekara et al 2014, Xi et al 2017, Wood et al 2018, Colpani et al 2018).

  • Such a J-shaped relationship (J-curve) has been shown in many different populations and dozens of observational studies. In different degrees, it is also seen in men and women and with other types of alcoholic beverages.
  • Observational studies cannot prove causality but the observed association is considered biologically plausible (see below). However, there is a scientific debate at which level of consumption the nadir of this curve lies.

 

  • Such a J-shaped relationship (J-curve) has been shown in many different populations and dozens of observational studies. In different degrees, it is also seen in men and women and with other types of alcoholic beverages.
  • Observational studies cannot prove causality but the observed association is considered biologically plausible (see below). However, there is a scientific debate at which level of consumption the nadir of this curve lies.

 

2. Comparison to Smoking

WHO and other institutions have repeatedly declared the risks of alcohol consumption equivalent to smoking. However, no benefit of “moderate smoking” has ever been found.

WHO and other institutions have repeatedly declared the risks of alcohol consumption equivalent to smoking. However, no benefit of “moderate smoking” has ever been found.

 

De Gaetano et al, 2017, Alcohol and health – praise of the J-curve, J Am Coll Cardiology, vol 70, no 8

 

3. J-shape also for other diseases

In addition to CVD and total mortality, a J-shaped curve exists for the risk of other diseases, for example for type-2 diabetes and dementia. 

 

4. Correlation or cause?

Observational studies can only provide statistical associations and present absolute or relative risks of developing certain diseases and cannot be interpreted as a proof of a causal relationship. However, the associations described are biologically plausible: controlled experiments have proven the beneficial physiological effects of light to moderate drinking of wine/alcoholic beverages.

 

Biologically plausible: How does it work?

Effect of alcohol:

  • Improvement of cholesterol levels: „good“ HDL increases, „bad“ LDL decreases
  • Lowering of blood viscosity (blood becomes „thinner“)

Effect of phenolic, non-alcoholic compounds of wine:

  • Improvement of endothelial function
  • Antioxidant effect/scavenger of free radicals

 

5. Wine versus other alcoholic beverages

Light to moderate wine consumption may be more beneficial than consuming other alcoholic beverages. An increasing number of both animal experiments and human trials demonstrate that non-alcoholic substances (polyphenols) in wine provide additional protective effects against risk factors and diseases.

 

6. Influencing factors

Most epidemiological studies have only used the average amount of alcohol consumed (over a week or month) as the measure of exposure, however, other factors play an important role in the health outcome. i.e. Regular moderate consumers of alcoholic beverages had considerable health advantages compared to binge drinkers, even though they consumed on average the same amount.

  • Drinking pattern (moderate, regular vs. binge drinking)
  • Drinking with the meals
  • Alternate wine with water
  • The famous advice of Serge Renaud is: “You drink water, but you sip wine”.

 

7. Underreporting

An important problem of observational studies is “under-reporting” of alcohol intake. This subsequently affects the J-curve. When “under-reporters” are removed from the study analysis, the curve shifts to the right, which means that the lowest risk of moderate drinkers is actually related to a higher amount of alcohol intake and the increased risk starts at a higher dosage.

 

8. Moderate wine consumption within a healthy lifestyle

Light to moderate consumption of wine/alcoholic beverages should be considered only one component of lifestyle factors related to health. The most important aspects are:

  • Don’t smoke
  • Maintain a normal body weight (avoid becoming obese)
  • Exercise regularly
  • Eat a healthy diet (e.g., a Mediterranean-type diet)
  • Consume alcoholic beverages moderately and regularly with food, unless contraindicated

These lifestyle factors contribute not only to a longer life expectancy but also a longer life free of chronic diseases.

 

9. Sick-quitters

Earlier studies included ex-drinkers in the non-drinking reference/control group that may have artificially increased the risk of disease for “current abstainers”, thus, confounding the J-shaped curve and negating a protective relationship with moderate drinking. However, more recent studies have corrected this flaw and when including only lifetime abstainers in the non-drinking category, a similar J-shaped curve was found and disproved the so called “sick-quitters” hypothesis.

Alcoholic-dilated Cardiomyopathy (ACM) is the most prevalent form of ethanol-induced heart damage. Ethanol induces ACM in a dose-dependent manner, independently of nutrition, vitamin, or electrolyte disturbances. It has synergistic effects with other heart risk factors. ACM produces a progressive reduction in myocardial contractility and heart chamber dilatation, leading to heart failure episodes and arrhythmias. Pathologically, ethanol induces myocytolysis, apoptosis, and necrosis of myocytes, with repair mechanisms causing hypertrophy and interstitial fibrosis. Myocyte ethanol targets include changes in membrane composition, receptors, ion channels, intracellular [Ca(2+)] transients, and structural proteins, and disrupt sarcomere contractility. Cardiac remodeling tries to compensate for this damage, establishing a balance between aggression and defense mechanisms. The final process of ACM is the result of dosage and individual…
Cardiovascular disease (CVD) is a leading cause of morbidity and mortality for women. This review summarizes the relationship between alcohol consumption and common CVDs in women and highlights potential differences from men. Except for risk of hypertension, no sex-related effects of alcohol consumption on the risk for coronary heart disease and stroke have been reported, and data on the sex-related effects on risk for peripheral arterial disease are limited. For women, alcohol consumption has a J-shaped relationship with hypertension. About 1 to 2 standard drinks per day is associated with lower risk for the development of hypertension, whereas for men, the relationship is relatively linear. In the area of alcoholic cardiomyopathy, the prevalence is greater for men, but women may…
BACKGROUND AND AIMS: The alcohol-hypertension relation has been well documented, but whether women have protective effect or race and type of beverage consumed affect the association remain unclear. To quantify the relation between total or beverage-specific alcohol consumption and incident hypertension by considering the effect of sex and race. METHODS AND RESULTS: Articles were identified in PubMed and Embase databases with no restriction on publication date. Pooled relative risks (RRs) and 95% confidence intervals (CIs) were calculated by random effects models. Restricted cubic splines were used to model the dose-response association. This study involved 22 articles (31 studies) and included 414,477 participants. The hypertension risk was different among liquor, wine, and beer at 5.1-10 g/d of ethanol consumption (P-across subgroups…
There is a paucity of studies on the influence of alcohol intake among non-drinkers. We evaluated the association between an increase in alcohol consumption and primary prevention of major adverse cardiovascular events (MACE) among non-drinkers. Data collected by the National Health Insurance Service in the Korea between 2007 and 2013 were analysed. A total of 112,403 subjects were included and followed up from 1 January 2011 to 31 December 2013. Increases in alcohol consumption, measured as glasses per day, at the second medical check-up, were categorized into maintenance of nondrinking (0), > 0- 1- 2- 4. Hazard ratios (HRs) for MACE and all-cause mortality on increase in alcohol consumption were calculated. Compared to that in non-drinkers at the second check-up,…
BACKGROUND: The causal role of alcohol consumption for cardiovascular disease remains unclear. We used Mendelian randomization (MR) to predict the effect of alcohol consumption on 8 cardiovascular diseases. METHODS: Up to 94 single-nucleotide polymorphisms were used as instrumental variables for alcohol consumption. Genetic association estimates for cardiovascular diseases were obtained from large-scale consortia and UK Biobank. Analyses were conducted using the inverse variance-weighted, weighted median, MR-PRESSO, MR-Egger, and multivariable MR methods. RESULTS: Genetically predicted alcohol consumption was consistently associated with stroke and peripheral artery disease across the different analyses. The odds ratios (ORs) per 1-SD increase of log-transformed alcoholic drinks per week were 1.27 ([95% CI, 1.12-1.45] P=2.87x10(-4)) for stroke and 3.05 ([95% CI, 1.92-4.85] P=2.30x10(-6)) for peripheral artery disease…
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