He described that there was no significant correlation between these two variables and concluded that further studies are needed to evaluate this association in heavier drinkers [40]. Some adverse BP-related mechanisms that may be triggered by alcohol include changes in intracellular calcium levels, baroreflex control, and heart rate and activation of other neurohormonal systems besides the RAAS, such as the sympathetic nervous system (Marchi et al. 2014). As with most forms of disease, a healthy lifestyle—including a proper diet, exercise, minimal stress, and low or moderate levels of alcohol consumption or abstinence—can work to promote healing. There is some evidence that moderate amounts of alcohol might help to slightly raise levels of “good” HDL cholesterol. Researchers have also suggested that red wine, in particular, might protect the heart, thanks to the antioxidants it contains.
As with isolated animal heart experiments, some investigators have found that acute alcohol exposure (blood alcohol levels 40 to 110 mg%) depresses myocardial systolic function in humans (Delgado et al. 1975; Lang et al. 1985; Timmis et al. 1975). For example, in one study, the ejection fraction decreased by 4 percent after alcohol consumption (Delgado can alcohol affect the gallbladder et al. 1975). Most likely, the decrease in contractility was offset by corresponding decreases in afterload (end-systolic wall stress), systemic vascular resistance, and aortic peak pressure, which maintained cardiac output. An additional factor in alcohol’s perturbing effect on fibrinolytic proteins may involve its effects on modifiers that influence fibrinolytic activity, such as the serum level of triglycerides. An increase in triglyceride level is positively correlated with PAI-1 plasma levels, indicating a predisposition to thrombosis and atherogenesis (Reeder et al. 1996). Moderate alcohol consumption decreases fasting plasma concentrations of triglycerides, however, and a concomitant reduction in the level of PAI-1 could allow fibrinolytic activity to increase.
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. Finally, in studies of people from certain Eastern European countries, investigators have failed to find a cardioprotective effect with any level of ethanol consumption (Britton and McKee 2000). This suggests that alcoholic beverage type may be an important mediator, because in countries such as Russia, spirits are the alcoholic beverage of choice.
Regular or high alcohol use can hurt your heart and lead to diseases of the heart muscle, called cardiomyopathy. The last thing you want is for that casual drink after work or glass of wine at dinner to negatively impact your heart health. There’s a way to have a healthy, balanced relationship with alcohol that lets you enjoy a drink occasionally and celebrate with friends and family. But your heart is an important organ that should also be cared for, so be sure to drink in moderation, learn about binge drinking and know what your body can (and can’t) tolerate before opening that tab. 3In this article, the term “moderate drinking” generally refers to the consumption of one or two drinks per day.
However, Dr. Cho points out that more recent data shows that there may be no amount of alcohol that is truly safe. Heavy alcohol consumption, on the other hand, has precipitated ischemic strokes caused by blood clots (i.e., non-atherosclerotic, or emoblic, ischemic strokes) (Hillbom 1995). For instance, increased thickening and scarring of connective tissue (the tissue between cardiac cells) in heart muscle, which has been observed in alcoholic cardiomyopathy, could provide the anatomical source of the disturbance in ventricular rhythm by impeding electrical conduction.
Pathophysiology and Oxidative Stress
Some studies have shown an association between moderate alcohol intake and a lower risk of dying from heart disease. 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.
- INTERHEART results also suggested that the protective effect of any alcohol use against MI was greater in women and those over age 45.
- A study by Ridker and colleagues (1994) provided further evidence that alcohol induces the secretion of t-PA.
- Epidemiological studies have reported a positive association between alcohol consumption and fibrinolytic activity in men and women.
- The factors responsible for the apparent cardiovascular benefits of light-to-moderate alcohol intake are uncertain.
- 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.
Dilated cardiomyopathy is characterized by low cardiac output and enlargement of the heart (i.e., hypertrophy) and its chambers (i.e., dilatation) (see figure) and eventually leads to congestive heart failure (CHF). A variety of factors can cause dilated cardiomyopathy, including prolonged heavy drinking (i.e., alcoholic cardiomyopathy) as well as the late effects of viral infections and toxic substances. Although alcoholic cardiomyopathy may be reversible after abstention, severe cases still may progress into CHF despite a cessation of alcohol use.
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). Several reports indicate that alcohol first exerts a seemingly positive effect, followed by a more negative impact (i.e., it is biphasic) on the endothelial–nitric oxide–generating system.
The importance the type of alcoholic beverage has on its health effects has been a subject of discussion. Studies examining the influence of beverage type have shown that there is no difference in CVD outcomes, and that the benefit comes from alcohol itself [6,18,19,20]. Thus, it appears that components other than ethanol could also exert beneficial effects [21]. It has been suggested that wine could provide greater protection because of its polyphenol content, but it is argued that lifestyle and time of day can play a more significant role in the wine-drinking population [5,18,19]. 3Greenfield and colleagues (2005) studied the effects of alcohol at meal time in a group of nonsmoking, healthy postmenopausal women.
Biochemical studies examining alcohol’s effects on HDL are rooted in epidemiological studies that show an inverse relationship between plasma HDL cholesterol levels and CAD. 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. Another cohort study following 1471 black South African individuals over a period of 5 years evaluated the association between alcohol intake, mortality, and the development of hypertension. They described that participants self-reporting alcohol intake had a 30% increased risk for developing hypertension (hazard ratio (HR) 1.30, 1.07–1.59) [16]. Evidence suggests that moderate alcohol consumption—i.e., less than 30 g of alcohol per day-may have beneficial effects on inflammation, diminishing pro-inflammatory markers (e.g., IL-6, CRP) and raising anti-inflammatory markers (e.g., IL-10). The protective effect of alcoholic beverages could be related to the type of drink and the amount of alcohol ingested, as well as their polyphenol content [6,42].
How Much Alcohol Is Too Much?
INTERHEART results also suggested that the protective effect of any alcohol use against MI was greater in women and those over age 45. Finally, data from INTERHEART support the finding that the risk of MI is increased in the 24 hours after consumption of 6 or more drinks, suggesting that binge drinking increases MI risk (table 1). In heavy drinkers, researchers have observed reduced activity of CETP, which also plays a role in regulating HDL cholesterol levels. Hannuksela and colleagues (1996) attributed this reduction to increased clearance of CETP from the blood rather than to a decrease in its cellular secretion. Such diminished CETP activity may maintain HDL levels by limiting the transfer of cholesteryl ester from HDL to LDL (Dreon and Krauss 1996).
Executive Editor, Harvard Men’s Health Watch
6Alcohol also may affect LDL and triglyceride levels, but its influences on these substances are beyond the scope of this article demi moore sober (for more information, see the exhaustive review by Dreon and Krauss 1996). In many ways, your medical history (and present) can tell you a lot about your future with alcohol. That means, if you’re living with other medical conditions and/or taking certain medications, this will all have an impact on how alcohol affects you. Several theories have been suggested to explain how alcohol possibly thwarts this inflammatory process and provides protection against atherogenesis.
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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 enabling vs supporting day and 10 who reported consuming 2 to 6 drinks per day) showed significant blood pressure reductions after abstinence (Malhotra et al. 1985). As mentioned earlier, it has been suggested that the modulation of oxidative biomarkers could depend on the type of beverage consumed (Table 1). The evidence available at the time of a review by Covas et al. could not suggest that sustained wine consumption provided further antioxidant benefits in healthy individuals, but rather counteracted its own possible pro-oxidative effect.
Cardiovascular Consequences of Heavy Alcohol Consumption
NIAAA defines binge drinking as a pattern of drinking alcohol that brings the blood alcohol concentration to 0.08 percent or above. A typical adult consuming the defined number of standard drinks for binge drinking would reach a blood alcohol concentration of 0.08 in about 2 hours (NIAAA 2015b). Several mechanisms have been identified to explain alcohol’s negative effects on cardiac muscles. For example, when an electrical current spreads to the interior of cardiac muscle fibers, it causes the release of large quantities of calcium ions from a network of tubules (i.e., the sarcoplasmic reticulum), which in turn trigger the chemical events that produce muscular contractions.
The latter changes in these indices could be brought about by ethanol-induced imbalances in the reducing equivalents nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide hydrogen (NADH), an important chemical pathway involved in oxidative stress. In cardiomyocyte mitochondria as well as other mitochondrial types, such imbalances could lead to further decreases in cellular respiration and oxidative phosphorylation. Evidence of oxidative stress is found after short periods of alcohol consumption (2 to 18 weeks), at least in animal models.
