Alcohols Impact on the Cardiovascular System PMC

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. This article first focuses on advances from biochemical research that have improved our understanding of alcohol’s beneficial effects on the cardiovascular system. Building on this foundation, the article next examines several specific consequences of long-term heavy alcohol consumption on the cardiovascular system.

Methodological shortcomings, such as exposure classification and measurement, reference groups, and confounding variables (measured or unmeasured) are discussed. Based on systematic reviews and meta-analyses, the evidence seems to indicate non-linear relationships with many CVDs. Large-scale longitudinal epidemiological studies with multiple 11 famous heavy drinkers in history and their favorite drinks detailed exposure and outcome measurements, and the extensive assessment of genetic and confounding variables, are necessary to elucidate these associations further. Conflicting associations depending on the exposure measurement and CVD outcome are hard to reconcile, and make clinical and public health recommendations difficult.

Alcohol alters the permeability of the sarcoplasmic reticulum to calcium ions, however, and thus reduces the efficiency by which calcium activates muscle contraction (Thomas et al. 1996). In addition, alcohol has a negative effect on the integrity and function of the contractile proteins known as actin and myosin (Preedy et al. 1996). Alcohol reduces the synthesis of cardiac proteins in both the contractile apparatus (i.e., the actinmyosin complex) and in the cell’s “powerhouses” (i.e., mitochondria), especially in alcoholics with high blood pressure (Preedy et al. 1996). Similarly, acetaldehyde (a metabolite of alcohol) and free radicals may contribute to decreased protein synthesis as well. Another way that alcohol can induce cardiac muscle damage is by increasing the expression of a certain gene (i.e., c-myc), which can promote programmed cell death, resulting in muscle cell loss (Paice et al. 1996).

Are there benefits to drinking alcohol?

The meta-analysis of RCTs on reduction of alcohol consumption on blood pressure included four trials with a duration of 1 year or longer, and these results were in line with the overall meta-analysis [62]. These longer trials suggest feasibility of a longer term RCT on hard outcomes to resolve the ongoing debate about effects of light to moderate alcohol consumption on CVD. Despite this, a recent effort to conduct such a long-term trial—the Moderate Alcohol and Cardiovascular Health trial (MACH15)—seemed feasible, but was terminated prematurely by the US National Institutes of Health, which funded the trial [7, 65].

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, 11 natural remedies for erectile dysfunction ed duration, and pattern of alcohol consumption. Oxidative stress is an imbalance between production of free radicals and the body’s ability to detoxify or fight off their harmful effects through neutralization by antioxidants.

Alcohol’s Impact on the Cardiovascular System

Furthermore, the impact of alcohol on other health outcomes needs to be taken into account. One common risk factor for CV disease is the composition of the lipids found in the blood, and the effects of alcohol consumption on lipid profiles have been extensively studied. Many researchers have found that alcohol intake increases HDL cholesterol (HDL-c) levels, HDL (“good cholesterol”) particle concentration, apolipoprotein A-I, and HDL-c subfractions (Gardner et al. 2000; Muth et al. 2010; Vu et al. 2016).

A recent large-scale study from the UK reported a J-curve for most CVD outcomes in patients with CVD [43]. Numerous epidemiological studies have established an association between chronic alcohol consumption and hypertension independent of other risk factors such as obesity and smoking, and their results have been summarized previously (Beilin and Puddey 1992; Klatsky 1995; Camargo and Rimm 1996). This association has been observed with alcohol consumption in excess of two drinks per day and described in white, black, and Asian men and women who reported daily intake of three or more drinks (see, for example, Klatsky 1995).

1. Studies also have examined the “safety” of alcoholic beverage consumption in subjects with heart failure.
2. Many short-term RCTs and a few longer term trials have shown potentially beneficial effects of alcohol consumption on cardiovascular risk factors.
3. 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.
4. INTERHEART results also suggested that the protective effect of any alcohol use against MI was greater in women and those over age 45.

Chronic alcohol consumption has been verified as the cause of hypertension in two controlled trials. In the first study, the blood pressure of 16 hypertensive men, who drank 4 pints of beer on average, dropped significantly when alcohol was withdrawn for 4 days (Potter and Beevers 1984). In the second study, 20 hypertensive subjects (10 who reported consuming less than 2 drinks per day and 10 who reported consuming 2 to 6 drinks per day) showed significant blood pressure reductions after abstinence (Malhotra et al. 1985). Long-term heavy alcohol consumption induces adverse histological, cellular, and structural changes within the myocardium. These mechanisms contribute to the myocyte cellular changes that lead to intrinsic cell dysfunction, such as sarcoplasmic reticular dysfunction and changes in intracellular calcium handling and myocyte loss.

Acute and Long-term Effects of Alcohol on the Myocardium

In addition, there was no evidence of nitrative damage in mice bred to disrupt (i.e., knock out) the gene for angiotensin I receptor (AT1-KO) that had been given ethanol for a similar length of time (Tan et al. 2012). Both experimental approaches also prevented accumulation of ethanol-induced scarring (collagen and fibronectin); apoptotic cell death; and changes in the size, shape, and function of the heart after injury to heart muscle (ventricular remodeling). Thus, low levels of alcohol consumption (1 to 2 drinks, but not every day) in patients with heart failure may not exacerbate the condition, especially in those with heart failure attributable to ischemic CHD. Because heart failure patients usually are older (over age 65) and often are prescribed numerous medications, both the effects of age and of medication use should be carefully considered by patients, clinicians, and researchers.

Moderate alcohol consumption has also shown to reduce low-density lipoprotein cholesterol, fibrinogen levels, Interleukin-6, HbA1c and fasting insulin concentrations in various studies [59•, 61]. A meta-analysis of RCTs up to 2017 performed in people with diabetes showed no effect of moderate alcohol consumption during 4 to 104 weeks on HbA1c or blood glucose [63], although the longest such study to date identified a benefit specifically among those with slow ethanol metabolism [8]. Altogether, these studies provide plausible underlying mechanisms not only for the observed risk reduction of myocardial infarction with moderate alcohol consumption, but also for increased risks of other cardiovascular outcomes such as heart failure or stroke. The associations between drinking and CV diseases such as hypertension, coronary heart disease, stroke, peripheral arterial disease, and cardiomyopathy have been studied extensively and are outlined in this review.

Alcohol and Heart Failure

Various studies with animals and humans indicate that ethanol can increase the development of reactive oxygen species (ROS), leading to increases in redox-signaling pathways and decreases in protective antioxidant levels. Alcohol also can increase levels of co-enzymes or reducing equivalents (e.g., reduced nicotinamide adenine dinucleotide phosphate [NADPH]), which lead to increases in ROS formation and decreases in eNOS activity (Ceron et al. 2014). Several excellent reviews offer more detailed assessments of vascular cellular mechanisms (Cahill and Redmond 2012; Husain et al. 2014; Marchi et al. 2014; Toda and Ayajiki 2010). Another trend in recent studies of alcohol and CV risk and disease is to include a measurement for binge drinking. In most investigations, this means consuming more than 5 standard drinks on a single occasion for men and more than 4 standard drinks for women.

For example, a thrombus or embolus interrupting the blood supply to the heart could produce a heart attack (i.e., myocardial infarction), whereas a blood clot impairing the blood supply to the brain could cause a stroke. Thus, any factor that reduces platelet aggregation, inhibits blood clot formation, or promotes blood clot dissolution (discussed in the next section) could attenuate the thrombotic complications of atherosclerosis. Moderate alcohol consumption may ameliorate i drink every night am i an alcoholic all of these processes, which would help explain the antithrombotic effects of alcohol reported by several researchers. After nearly a century of research on the effects of alcohol consumption on cardiovascular health, we find ourselves running in circles, asking the same questions and reporting the same limitations. To move forward and gain greater insight into the health effects of limited alcohol consumption, a reconsideration of the standard of evidence is needed.

More contemporary studies have not found evidence of mitochondrial injury in biopsy samples from long-term alcohol drinkers (Miró et al. 2000). Differences among results from human studies may relate to small sample sizes, duration of drinking, and degree of myocardial dysfunction. In the Miró study, alcohol drinkers also had been receiving pharmacologic treatments such as beta-adrenergic blocking agents that reduce blood pressure and also may have antioxidant effects. Data from transgenic animal models and pharmacologic approaches strongly support a role for ethanol-induced oxidative stress in CV 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]. Both chronic heavy drinkers and binge drinkers are at an increased risk for subarachnoid hemorrhage. One study attributed 12 percent of subarachnoidal hemorrhage cases to recent heavy drinking (Juvela et al. 1993). Other research suggested that such cases could be precipitated by a transient increase in blood pressure.