More recently, Cosmi and colleagues (2015) examined the effects of daily wine consumption in subjects enrolled in an Italian trial of heart failure patients (mean age ~67), most of whom had reduced ejection-fraction heart failure. Different levels of daily wine consumption (i.e., sometimes, 1 to 2 glasses/day, and ≥3 glasses/day) had no effect on fatal or nonfatal outcomes (e.g., hospitalization for a CV event). Subjects who drank wine more often, however, were less likely to have symptoms of depression and more likely to have a better perception of health status. They also had lower levels of circulating inflammatory markers, such as C-terminal proendothelin-1 and pentraxin-3 (Cosmi et al. 2015).
Instead, factors that coincided with moderate drinking, such as favorable lifestyle choices and, in some cases, the socioeconomic environment, were responsible. Previous research indicated a potential link between moderate drinking and certain heart benefits. Significant progress has been made in the last decade in understanding both the beneficial and harmful effects of alcohol on the cardiovascular system.
However, some reports indicate that alcohol-dependent women develop ACM after consuming less alcohol over a shorter period than do age-matched alcohol-dependent men (Fernández-Solà et al. 1997; Urbano-Marquez et al. 1989). The acute effects of alcohol on the myocardium include a weakening of the heart’s ability to contract (negative inotropic effect). Data from isolated papillary and heart muscle cell (myocyte) experiments demonstrate that acute physiologic intoxicating doses of alcohol (80 mg% to 250 mg%) can have a negative inotropic effect (Danziger et al. 1991; Guarnieri and Lakatta 1990). These effects also may involve an irregular and often very fast heart rate (arrhythmia) during which the heart’s upper chambers (atria) contract chaotically out of coordination with its lower chambers (ventricles), known as atrial fibrillation, or (rarely) sudden cardiac death. 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).
Alcohol’s Effects on Blood Clot Dissolution
While potential sources of bias, such as the reference group, i.e., separating lifetime abstainers, former drinkers, and heavy episodic drinkers, have been systematically investigated for the relationship between alcohol and IHD, their impact on other CVD outcomes remains less clear. While there is a lack of large-scale randomized studies on the long-term effect of alcohol consumption on various CVD endpoints, short-term clinical trial data indicate a sizable effect of alcohol consumption on HDL-C and fibrinogen. However, the heterogeneity found in epidemiological studies points to more than just biological differences.
- However, modulatory influences related to drinking patterns, genetic susceptibility, nutritional factors, ethnicity, and gender also many play a role (Piano and Phillips 2014) (figure 4).
- One study attributed 12 percent of subarachnoidal hemorrhage cases to recent heavy drinking (Juvela et al. 1993).
- 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.
- Infection or other stressful events also can lead to immune-triggered platelet production, a condition called rebound thrombocytosis, which may occur immediately after withdrawal from both heavy and one-time heavy (binge) drinking (Numminen et al. 1996).
In addition, a newly discovered species of HDL called pre-high density lipoprotein binds with free cholesterol in a process known as reverse cholesterol transport, in which excess cholesterol is removed from body tissues, transported to the liver, and excreted in bile. Although these forms of bias are inherent to observational studies, they do not diminish the importance of such studies to identify potential associations and they remain the only available approach to date to directly link alcohol consumption with long-term outcomes. They do not pass readily through cell membranes, and they are major components of very-low-density lipoproteins (VLDLs), which are converted in the blood to LDLs.
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It is best for people with heart conditions to avoid alcohol or, at the very least, reduce their consumption if they drink excessively. It is important to note that there is no causal link to suggest that drinking, even moderately, contributes to better heart health. Alcohol, in particular, can increase the risk of several conditions that fall under the term CVD. 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.
Since RCTs require strict inclusion and exclusion criteria, the results are by definition definitively applicable only to a selected part of the population. Because alcoholic beverages are widely consumed worldwide, the danger is that results of an RCT executed in a specific population could be wrongfully be applied to excluded individuals in whom the results would have differed [65]. Furthermore, several potentially adverse but rare outcomes, such as the risk of developing specific types of cancer, are impossible to investigate in an RCT due to the alcohol use disorder symptoms and causes unrealistically large sample sizes needed. To date, all attempts to execute a large-scale RCT with sufficient follow-up time have stranded and currently no large RCTs are running to our knowledge. However, none of these studies has been able to resolve the pressing question of whether there is a true protective effect of moderate alcohol consumption. In addition, while such studies are innovative and potentially informative, they are not free of their own limitations and caution is equally required when interpreting the results of these new studies.
This results in an artificial elevation of the health risk among abstainers, in which it is not the absence of alcohol but impaired health status that increases the observed elevated risk [25, 41–50]. Evidence of oxidative stress is found after short periods of alcohol consumption (2 to 18 weeks), at least in animal models. These data suggest that antioxidant defense mechanisms that attempt to protect the heart against oxidative damage appear to be initiated soon after drinking alcohol. Also, as noted below, data from other studies demonstrate the protective role of administered antioxidants, such as a synthetic compound that mimics the native superoxide dismutase enzyme, called a superoxide dismutase mimetic.
How Alcohol Affects Your Heart
Some investigators have suggested that drinking wine may offer more protection against CV disease because it contains polyphenols, such as resveratrol and flavonoids, which are micronutrients with antioxidant activity (Tangney and Rasmussen 2013). However, among studies designed to examine the influence of beverage type, no differences have been found in CV disease outcomes or biologic markers, such as HDL-c (Mukamal et al. 2003a; Volcik et al. 2008). Differential associations of CV risk with certain beverage types such as wine instead have been attributable to other lifestyle factors (e.g., increased physical activity) or drinking with meals (Malarcher et al. 2001). Several studies and meta-analyses have been conducted to determine the relationship between alcohol consumption and the risk of developing heart failure in healthy subjects, as well as in those with a history of MI or CHD.
RCTs are not influenced by these forms of bias and are often regarded as the gold standard to prove causality in the relations between a risk factor and outcome. Due to the difficulty and costs of performing a long-term RCT of limited alcohol consumption on hard outcomes such as CVD, the main body of evidence comes from short-term RCTs on cardiovascular risk factors. Several meta-analyses show that moderate alcohol consumption increased high-density lipoprotein (HDL) cholesterol, apolipoprotein A1 and adiponectin [59•, 60, 61].
Potential Biologic MechanismsUnderlying Alcohol-Induced BP Effects
Further epidemiological studies show an association between alcohol consumption and increased plasma HDL levels.6 A study by Linn and colleagues (1993) reported an increase of about 5 mg/dL in plasma HDL cholesterol levels after daily consumption of moderate amounts of alcohol. Heavy drinking, on the other hand, is linked to a number of poor health outcomes, including heart conditions. Excessive drinking can also contribute to cardiomyopathy, a disorder that affects the heart muscle. In contrast to the methodological problems faced when conducting and interpreting results from observational studies, important practical and ethical concerns face large-scale, long-term RCTs [7, 65]. Besides the question whether it is justifiable to impose alcohol consumption on individuals—although MACH15 was designed to exclude abstainers and heavy drinkers—one of the major concerns is on how the general public will conceive possible outcomes of RCTs.
However, evidence suggests an association between consuming alcohol and problems with the cardiovascular system. 1The term “heavy drinking” is not used consistently in the alcohol literature; therefore, this article generally refers to “heavy drinking” and “heavy drinkers” based on the terms used in the reference cited. Another possible mechanism for CAD risk reduction relates to the inhibition of cell proliferation that results from cellular signaling.
What’s more, alcohol can contribute to obesity and the long list of health problems that can go along with it. Alcohol is a source of excess calories and a cause of weight gain that can be harmful in the long term. Exercise can also boost HDL cholesterol levels, and antioxidants can be found in other foods, such as fruits, vegetables and grape juice.
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.
In addition to epidemiological studies, in vitro studies have investigated the effects of alcohol on fibrinolysis. Laug (1983) reported alcohol-induced increases in t-PA secretion in cultured endothelial cells, and Kjaeldgaard and colleagues (1988) observed similar effects with a global news: busting myths on alcohol and covid-19 human melanoma cell line. Reeder and colleagues (1996) suggested that the interaction between alcohol consumption and fibrinolysis may involve the influence of rhythmic daily fluctuations in the levels of fibrinolytic proteins, but the exact mechanisms remain to be elucidated.
The way in which alcohol consumption has been measured and categorized varies, sometimes making it challenging to compare data among studies. More studies today report alcohol consumption in terms of either “drinks” or grams/units of ethanol per day or week, and alcohol consumption is measured by self-report. Most investigators also define the amount of alcohol that constitutes a “standard” alcohol poisoning symptoms and treatment drink as 12 to 15 g (with only slight variation). The short-term effects of alcohol (headache, nausea, you know the rest) are easy to pinpoint. But there are ways that alcohol affects your body over time that are important to understand. This is when your heart-pumping function gets weaker and your heart gets larger due to changes from heavy alcohol use over a long period of time.