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. Other researchers have used genetic approaches (i.e., transgenic animals) to prevent ethanol-induced oxidative stress. One approach included overexpression of proteins such as insulin-like growth factor (IGF-1), which stimulates growth and cell proliferation and has antiapoptotic effects (see Zhang et al. 2014). In contrast to control mice, the IGF-1–expressing animals exhibited no evidence of changes in expression of antioxidant enzymes (i.e., superoxide dismutase-1) or any decreases in contractile function after 16 weeks of ethanol consumption.

Staying Healthy

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). Findings have been equivocal for other lipids, such as low-density lipoprotein cholesterol (LDL-c) (the estimated amount of cholesterol within LDL particles, or “bad cholesterol”) and triglyceride levels (Rimm et al. 1999; Volcik et al. 2008; Waskiewicz and Sygnowska 2013). High triglyceride levels in the blood stream have been linked to atherosclerosis and, by extension, increased risk of CHD and stroke.

How Much Alcohol Is Too Much?

Increased autophagy as a possible mechanism underlying the adverse myocardial effects of ethanol is intriguing. This is especially true in light of the relationship between a sensor of stress (mTOR) and nutrient deprivation and how essential autophagy is to cell survival. As noted above, chronic alcohol exposure leads to a decrease in mTOR activity, which corresponds to increased markers of autophagy (Lang and Korzick 2014). The autophagy pathway also is rapidly upregulated during ATP depletion, mitochondrial dysfunction, and oxidative stress.

The effects of alcohol on health are various and heterogeneous and vary depending on the dose and pattern of consumption [1,2] (Figure 1). Heavy use of alcohol is one of the leading global risk factors for poor health outcomes, having a direct impact on a variety of diseases. It has been described that up to 19% of alcohol-attributable deaths were due to cardiovascular diseases (CVD) in 2016, after cancer and liver disease [1].

I want to get healthier

When a rupture occurs, platelets coming in contact with collagen and other exposed subendothelial compounds become activated and operate in conjunction with other clotting (i.e., coagulation) factors to form a blood clot and seal off damage. Researchers have found evidence of mitochondrial dysfunction or impaired bioenergetics related to alcohol consumption. Dysfunctional mitochondria are less efficient, can become a source of ROS, and are more likely to initiate apoptosis (Marzetti et al. 2013). Some people should avoid even that much and not drink at all if they have certain heart rhythm abnormalities or have heart failure. But it may be worthwhile learning about what counts as binge drinking and whether or not you may be drinking too much and don’t even know it. And if you have a history of high blood pressure, it’s best to avoid alcohol completely or drink only occasionally, and in moderation.

However, the negative associations between alcohol consumption and CV outcomes in these countries also may relate to pervasive patterns of binge drinking (Leon et al. 2009). 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. Studies also have examined the “safety” of alcoholic beverage consumption in subjects with heart failure. Results from another meta-analysis of 12 cohort studies found a similar dose–response relationship between alcohol consumption and HTN for males.

Because of space limitations, not all of the excellent scientific work on alcohol and the cardiovascular system could be assessed in this review. If you or a loved one is struggling whippets balloons with alcohol misuse and/or you’re concerned about the possible effects alcohol can have on cardiovascular health, help is available. American Addiction Centers offers multiple treatment centers throughout the U.S., providing everything from alcohol detox and inpatient treatment to outpatient care, telehealth treatment, and aftercare. Additionally, some people  may experience arrhythmias such as AFib during alcohol withdrawal as the body adjusts to the absence of the substance.12 Thus, it’s important to seek professional help to detox from alcohol and to monitor for heart safety during alcohol withdrawal. Hypertension (aka high blood pressure) is a serious medical condition characterized by persistent elevations in blood pressure. The pressure that’s measured when the heart contracts to pump blood is systolic blood pressure, which is the top number in a blood-pressure reading.

Changes in mitochondrial function have been reported from a number of animal studies in different species, under various alcohol consumption paradigms (ethanol in water or liquid diet), and after variable durations of chronic ethanol consumption (6 weeks to 6 months). Through the process of oxidative phosphorylation, the mitochondria generate ~90 percent of cellular ATP. Common findings in alcohol studies from the 1970s and early 1980s included decreases in mitochondrial indices that reflected mitochondrial state III respiration, or ADP-stimulated respiration (Pachinger et al. 1973; Segel et al. 1981; Williams and Li 1977).

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. Due to the limitations of typical epidemiological studies, other types of study design, such as Mendelian randomization studies using an instrumental variable approach, sought to answer questions about the causality of the lower risk of low-level alcohol drinkers. However, the use of such an approach [45,46], which depends on several assumptions that are not easily met in a complex relationship, such as between alcohol consumption patterns and CVD risk, is highly debated [47,48,49,50]. An important aspect of the alcohol-hypertension association—and a fertile area for future studies—concerns alcohol’s interactions with antihypertensive medications such as propranolol and clonidine. Alcohol enhances the elimination of propranolol and opposes five rules of recovery the effect of clonidine, resulting in a decrease in the blood pressure-lowering properties of these medications. Also, because chronic alcohol consumption decreases the concentration of magnesium ions in the blood, the use of medications that increase kidney excretion of electrolytes and water (i.e., diuretics) to control blood pressure may be contraindicated, because their use can exacerbate magnesium loss.

The cardiovascular health effects of alcohol have classically been described as having a J-shaped curve, in which low-to-moderate consumers present less risk than lifetime abstainers, and heavy drinkers show the highest risk [5,19,20,22,23,24,25]. Alcohol intake benefits not only healthy individuals, but also patients with established CVD [3,5]. This review will focus on the association between cardiovascular risk factors (i.e., hypertension, diabetes mellitus type 2, and dyslipidemia) and alcohol consumption and its underlying mechanisms of damage, with review of the literature from the last 10 years.

There also is desensitization of the mitochondrial permeability transition pore, which can mitigate ischemia–reperfusion injury (Walker et al. 2013). In addition, alcohol may attenuate ischemia–reperfusion injury by activating protein kinase C epsilon (PKCɛ) (Walker et al. 2013). Activation of PKCɛ may protect the myocardium against ischemia–reperfusion injury by stimulating the opening of mitochondrial ATP-sensitive potassium channels. This in turn prevents the opening of the mitochondrial permeability transition pore (Walker et al. 2013).

1. Although highly individualized and dose dependent, alcohol use also can increase bleeding time (i.e., taking longer to develop a clot)(Salem and Laposata 2005).
2. Similarly, the observed increase in the activity of the enzyme LCAT may not play an important role in the alcohol-induced HDL increase (Nishiwaki et al. 1994).
3. 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).
4. For example, dogs fed alcohol for 1 year and rats fed alcohol for 8 months showed significant decreases in left ventricular function (Capasso et al. 1991).
5. Alcohol use was protective against CHD for subjects in most countries, except for people of South Asian ethnicity living in South Asia (India, Bangladesh, Nepal, Pakistan, and Sri Lanka).

Moderate drinking cannot be achieved by simply averaging the number of drinks consumed, however. For example, consuming seven drinks on a Saturday night will not have the same effects as consuming one drink each day of the week. Alcohol-induced damage to the cardiovascular system may result from either excessive prenatal alcohol exposure or from excessive alcohol use later in life. This article, however, focuses on four specific cardiovascular consequences (i.e., cardiomyopathy, cardiac arrhythmia, hypertension, and stroke) that result from heavy drinking later in life. Clinical studies have shown, however, that every 1-percent reduction in plasma cholesterol levels decreases the risk for CAD by 2 percent.

Alcohol’s Link to Coronary Artery Disease, Heart Attack, and Stroke

Holiday heart syndrome can happen if you don’t typically how long does molly stay in your hair drink alcohol, but then have a few at a holiday party or if you binge drink. This can cause you to develop an irregular heartbeat, called atrial fibrillation, which can increase your risk of stroke, heart attack and heart failure. BP, blood pressure; HDL-c, high-density lipoprotein cholesterol; HTA, hypertension; TG, triglycerides; T2D, type 2 diabetes. 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. High levels of triglycerides in the blood have therefore been linked to atherosclerosis, heart disease, and stroke.