Triangulation of evidence from different study designs, including long-term RCTs, pragmatic trials and the evaluation of policy measures, combined will lead to the best available evidence. Because of space limitations, not all of the excellent scientific work on alcohol and the cardiovascular system could be assessed in this review. While some people develop a tolerance to alcohol over time, this isn’t true for everyone — and this ability doesn’t last forever, Dr. Cho notes. This article does not contain any studies with human or animal subjects performed by any of the authors. 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.
However, Dr. Cho points out that more recent data shows that there may be no amount of alcohol that is truly safe. 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. Alcohol-induced arrhythmias also may be caused by a reduction in the threshold for ventricular fibrillation.
Alcohol and Hypertension
Health experts may also advise individuals with cardiovascular disease or other chronic conditions to avoid alcohol if possible. One way alcohol raises blood pressure is by stimulating the sympathetic nervous system and the release of adrenaline. This is particularly true with excessive drinking behaviors, such as binge and heavy drinking. 3In this article, the term “moderate drinking” generally refers to the consumption of one or two drinks per day. 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.
Blocking the action of the enzyme known as hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase has been shown to suppress cell proliferation, among other effects (e.g., cholesterol reduction), and thus may provide another way to reduce plaque formation and slow atherosclerosis development. Certain cholesterol-lowering medications (e.g., lovastatin) block HMG-CoA reductase, but further research is needed to determine whether alcohol has a similar effect. Chylomicrons and very low density lipoproteins (VLDL) are two other major classes of lipoproteins in the body. Chylomicrons, the largest lipoprotein particles, carry triglycerides consumed in a complete guide to ketamine withdrawal & addiction food from the intestine to the blood, whereas the smaller VLDL particles are formed mainly in the liver and enter the blood circulation to transport cholesterol and triglycerides to peripheral tissues throughout the body. In the capillaries within fatty tissues and muscles, an enzyme known as lipoprotein lipase (LPL) breaks down triglycerides in both chylomicrons and VLDL to substances used in metabolism and energy storage (i.e., fatty acids and glycerol). Our review aims to summarize previous efforts to investigate the relationship of alcohol consumption with CVD risk using classic observational epidemiologic designs, RCTs and MR studies.
- Anticlotting therapies are therefore the cornerstone of managing acute coronary syndromes.
- The acute effects of alcohol on the myocardium include a weakening of the heart’s ability to contract (negative inotropic effect).
- This inflammatory process begins when LDL and immune cells (i.e., phagocytes) are trapped in the space beneath the interior lining of the artery walls (i.e., the subendothelial space).
- 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.
- Furthermore, a few additional limitations are of special importance when using MR to investigate the role of alcohol consumption.
It should also be noted that due to the limitations of alcohol-epidemiological studies, the beneficial associations tend to be overestimated. Furthermore, potential beneficial effects of non-heavy alcohol consumption on CVD endpoints, as described in this review, have already been observed at very low levels, such as 100 g pure alcohol per week, which, at the lower end, translates to about 1 drink every other day. Recommending drinking as a primary or secondary prevention measure for CVDs, which comes up occasionally in the literature, should be discouraged due to the substantial risks of any alcohol consumption for many health outcomes. With no current RCTs running, it is likely that some time will pass before gold standard evidence is obtained.
A Century of Research on the Relationship of Alcohol and Cardiovascular Disease and Still No Consensus: How Do We Move Forward?
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. The findings suggest a protective effect of overexpression of IGF-1 in the transgenic animals (Zhang et al. 2014).
Interestingly, the strength of this association was not consistent across different geographic regions. 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). 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). Despite the progress in standardizing measurement of alcohol, studies still vary in how they define the different levels of drinking, such as low-risk or moderate and heavy drinking. Most often, low-risk or moderate drinking has been defined as 1 to 2 standard drinks per day and heavy alcohol consumption as 4 or more standard drinks per day.
Smoking also is an important risk factor for subarachnoid hemorrhage (Juvela et al. 1993), and the combined effects of heavy drinking and smoking may be devastating. Epidemiological studies have reported a positive association between alcohol consumption and fibrinolytic activity in men and women. Iso and colleagues (1993) reported significant increases in plasma t-PA levels in heavy drinkers, and a recent study by Hendriks and colleagues (1994) also showed a sustained increase in t-PA following moderate consumption of alcohol with dinner. An increase in the plasma level of t-PA presumably would stimulate the conversion of plasminogen to its active form, plasmin; in turn, raising the level of plasmin would increase blood clot dissolution. 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.
Nonetheless, these studies too can be affected by confounding due to secular trends that co-occur with alcohol policy changes. Overall, we believe that the evidence from different approaches and study designs, with each their own strengths and limitations, when combined will result into the best available evidence [84, 85] (Fig. 1). Furthermore, to translate the research evidence to prevention in daily care, research on individual patient characteristics and absolute treatment effects is also needed. The design and initial conduct of the MACH15 trial show the feasibility of executing a large-scale trial. Sample size calculations show that 60,000 individuals are needed to detect the expected risk of any alcohol-related cancer, and when aiming to investigate specific forms of cancer, such as breast cancer, up to five times bigger samples are needed [7].
Ways alcohol can impact heart health
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. 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. Free cholesterol released from cells initially is incorporated into HDL by an enzyme called lecithin-cholesterol acyl transferase (LCAT), which changes the cholesterol to cholesteryl esters. 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.
Although results related to levels of alcohol consumption and stroke events are less clear, some conclusions can be drawn. Approximately 1 to 2 drinks per day may have no effect on or lead to a slight reduction in stroke events; however, greater daily alcohol levels increase the risk for all stroke events and incident stroke types. In terms of stroke subtypes, compared with nondrinkers, current alcohol drinkers have an increased risk (~14 percent) for hemorrhagic stroke (Ronksley et al. 2011). It is important to note that, unlike other studies with more discrete alcohol consumption categories, alcohol use was nonspecifically defined in INTERHEART as the consumption of at least 1 alcoholic beverage within the previous 12 months (Leong et al. 2014).
Ischaemic Heart Disease
We will elaborate on the strengths and weaknesses of the different designs and offer new directions for research for the future. 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). Whether it’s a glass alcoholic eyes of red wine with your turkey or toasting champagne for the new year, alcohol definitely becomes more present during the holiday season. And while enjoying celebratory spirits in moderation is alright for most people, it’s important to be aware you can fall victim to holiday heart syndrome if you overdo it. And sure, we’ve all had a night here or there where we’ve had one too many and we know it.
Although many behavioral, genetic, and biologic variants influence the interconnection between alcohol use and CV disease, dose and pattern of alcohol consumption seem to modulate this most. Low-to-moderate alcohol use may mitigate certain mechanisms such as risk and hemostatic factors affecting atherosclerosis and inflammation, pathophysiologic processes integral to most CV disease. But any positive aspects of drinking must be weighed against serious physiological effects, including mitochondrial dysfunction and changes in circulation, inflammatory barbiturate withdrawal symptoms response, oxidative stress, and programmed cell death, as well as anatomical damage to the CV system, especially the heart itself. Both the negative and positive effects of alcohol use on particular CV conditions are presented here. The review concludes by suggesting several promising avenues for future research related to alcohol use and CV disease. A lower risk of coronary heart disease and myocardial infarction among moderate drinkers compared to abstainers has been reported in observational studies and was confirmed in the latest meta-analyses.
Nevertheless, alcohol has numerous secrets that remain to be uncovered by ongoing research. Further investigations will clarify some of the effects of alcohol discussed in this article (e.g., its effects on fibrinolysis), including its mechanisms (e.g., alcohol’s possible role in the inhibition of the enzyme HMG-CoA reductase). In addition, other atherogenesis-related factors (e.g., the influence of hormones) that are not addressed in this article may be influenced by the use of alcohol, and research is needed to investigate these factors as well. Animal models do not replicate human cardiomyopathy exactly, but they can provide insight into the mechanisms of alcohol-induced damage.
Recent Comments