Behavioral risk factors such as overweight and obesity, poor diet, sedentarism or low physical activity, excessive alcohol consumption, and smoking have been correlated with a higher incidence and prevalence of CVD, diabetes, and dementia [8,14,15]. A recent systematic review reported that non-smoker individuals, with a moderate alcohol consumption, who were physically active and followed a healthy diet showed a lower risk of all-cause mortality (66%) than those that had none or only one of these healthy behaviors [15]. Ford et al. [8] reported similar results, showing that non-smoker individuals following a healthy diet and who were physically active presented a lower risk of mortality by CVD (65%) than those that have none of these healthy behaviors.
However, in a recently conducted Mendelian randomization study, Vu and colleagues (2016) reported that low-to-moderate alcohol consumption reduced triglyceride and LDL-c and increased HDL-c, in particular the HDL2-c subfraction. Interestingly, the researchers found a nonlinear effect of alcohol consumption on HDL2-c levels. This supports the findings from other studies that the alcohol-induced changes in HDL-c do not fully account for the lower risk of CHD in moderate alcohol drinkers (Mukamal 2012). Alcohol can be beneficial or harmful to the cardiovascular system, depending on the amount consumed and the characteristics of the consumer. Of the numerous cellular and molecular mechanisms that are thought to explain the beneficial effects of moderate drinking, this article discusses four, involving (1) high density lipoproteins, (2) cellular signaling, (3) platelet function in blood clot formation, and (4) stimulation of blood clot dissolution. Although light-to-moderate drinking can protect against coronary artery disease, heavy alcohol consumption can damage the cardiovascular system, resulting in maladies such as heart muscle disorders, irregular heart rhythms, high blood pressure, and strokes.
- Excessive drinking can also contribute to cardiomyopathy, a disorder that affects the heart muscle.
- Most cases of atrial fibrillation are caused by factors other than alcohol, but one study reported that the majority of emergency room patients with atrial fibrillation had a history of alcohol abuse (Rich et al. 1985).
- Decreases in mTOR activation may play a role in reduced myocardial protein synthesis, ventricular wall thinning, and dilation.
- Elevated triglyceride levels resulting from heavy alcohol consumption may further stimulate PAI-1 gene expression—especially in people with a genetic makeup particularly sensitive to PAI-1—resulting in the inhibition of fibrinolysis and thus increasing the risk for acute cardiac events.
- To remove cholesterol from the circulation, the cholesteryl esters then are transported to LDL by cholesteryl ester transfer protein (CETP) for recapture by the LDL receptors in the liver.
It is important to acknowledge the detrimental health effects of alcohol and its public health implications. Ethanol-induced changes may be related to oxidative or nonoxidative pathways of ethanol metabolism. More than one mechanism may be activated and may lead to the multitude of ethanol-induced changes in cellular proteins and cell function. As reviewed in the text, data from pharmacologic and transgenic approaches revealed an important role for oxidative stress and the hormone angiotensin II. In various biologic systems, oxidative stress can be measured or inferred by several biologic indexes. In humans, endothelial function is assessed by measuring the widening (i.e., dilation) of the brachial artery under different conditions.
Each woman was given either no alcohol or 15 g of alcohol (1 standard drink) with either a low-carbohydrate or a high-carbohydrate, high-fat meal. The researchers found that the alcohol-drinking subjects (particularly those who were insulin sensitive) had higher insulin levels and a slower rise in glucose levels after a low-carb meal. They recommended confirming these results in younger women and in men, particularly since their subjects had been older women, who have more significant cardiovascular risk.
If you’re not sure, make a note to tune into how much you’re having over the course of the next month or so. If it’s more than recommended, try to consciously pace your drinking to help reduce the spike in your blood pressure that excessive alcohol liberty bells mushrooms causes. As plaque builds up within the wall of an artery, the deposit begins to bulge into the vessel’s interior, obstructing blood flow, and eventually may rupture into the vessel.
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The fun substance abuse group activities inverse association between red wine consumption and mortality by CVD was initially published in 1979 [26]. Later on, in 1992, the concept of the “French Paradox” was introduced to describe an epidemiological observation in which the French show a relatively low incidence of CHD, despite the consumption of a diet rich in saturated fat and the presence of risk factors similar to those of other populations [27,28]. The relationship between alcohol consumption and cardiovascular events or all-cause mortality in apparently healthy people or patients with CVD has been depicted as a J-shaped curve attributed to a dose-related combination of beneficial and harmful effects [29,30]. Does some alcohol consumption protect some people against ischaemic diseases to some degree? For example, a J-shaped relationship emerges for average alcohol consumption and IHD and IS.
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Building on this foundation, the article next examines several specific consequences of long-term heavy alcohol consumption on the cardiovascular system. In this article, a bibliographic review was carried out through PubMed, ScienceDirect, and Google Scholar from October 2019 to February 2020. This review is based on the most relevant articles and studies performed in human subjects published no longer than 10 years ago.
Does Excessive Drinking Contribute to Heart Disease?
It is assumed that the self-reported drinking levels, preferably including drinking patterns, remains the same before and after the baseline measurement. For many people this is clearly not the case, and even lifetime abstainers are hard to identify [82]. A condition known as dilated cardiomyopathy constitutes a major subset of the disorders grouped under the umbrella term “cardiomyopathy,” which encompasses any chronic disorder affecting the heart muscle.
Alcohol abuse also can cause rapid and chaotic heartbeats to occur in the upper chambers of the heart (i.e., atrial fibrillation), although numerous other risk factors (e.g., age, hypertension, CAD, and diseases of the heart valves) can precipitate this condition as well. Most cases of atrial fibrillation are caused by factors other than alcohol, but one study reported that the majority of emergency room patients with atrial fibrillation had a history of alcohol abuse (Rich et al. 1985). Finally, Baliunas et al. published a meta-analysis of 20 cohort studies evaluating the relationship between alcohol consumption and T2D. They concluded that moderate alcohol consumption is protective for T2D in men and women [80].
Endothelial dysfunction is an early indicator of blood vessel damage and atherosclerosis, as well as a strong prognostic factor for future CV events (Deanfield et al. 2007; Ras et al. 2013). Low-to-moderate levels of alcohol consumption may initially improve endothelial function, whereas high daily levels and binge drinking may impair it. Several studies have reported an elevated risk for both IS and HS from heavy episodic drinking [77,78,79]. One study showed that the risk increased with a higher frequency of heavy episodic drinking [78].
Ethanol-mediated increases in autophagy therefore may be an important mechanism underlying the adverse myocardial effects of ethanol. Mechanisms related to the positive and adverse effects of alcohol on cardiovascular conditions, such as coronary heart disease and stroke as well as cardiomyopathy. Different mechanisms may be in effect depending on the dose, duration, and pattern of alcohol consumption. You should never consider wine or any other alcohol as a staying motivated in recovery way to lower your heart disease risk. And, in fact, the study also showed that drinking one or fewer drinks per day was related to the lowest likelihood of dying from a stroke.
For example, alcohol may disrupt the NF-κB function, thereby reducing the expression of NF-κB–regulated adhesion molecules and ultimately decreasing the inflammatory process of atherosclerotic lesions. These usually come with a warning sticker from your pharmacy that tells you not to drink while you take them. One drink is 12 ounces of beer or wine cooler, 5 ounces of wine, or 1.5 ounces of 80-proof liquor.
Figure 3 summarizes the potential mechanisms underlying the cardioprotective and adverse effects of alcohol consumption. This area of research was briefly outlined here; more comprehensive reviews on these mechanisms are available (Krenz and Korthuis 2012; Mathews et al. 2015). The biochemical basis of alcohol-induced cardiomyopathy also involves disturbances in cardiac energy metabolism. For example, high blood concentrations of alcohol reduce the oxygen supply to the cardiac muscle and interfere with oxygen-requiring (i.e., aerobic) metabolism in the heart. This effect decreases the level of the high-energy molecules that power the contraction process (i.e., adenosine triphosphate [ATP]) as well as the level of another energy source, phosphocreatine.