Author: John Carter

Alcohols Effects on the Cardiovascular System PMC

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. 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).

As reviewed in the text, data from pharmacologic and transgenic approaches revealed an important role for oxidative stress and the hormone angiotensin II. In humans, endothelial function is assessed by measuring the widening (i.e., dilation) of the brachial artery under different conditions. Some research noted that endothelial function is impaired in abstinent individuals with a long-term history of alcohol abuse or alcoholism(Di Gennaro et al. 2007, 2012; Maiorano et al. 1999).

One study showed that the risk increased with a higher frequency of heavy episodic drinking [78]. The higher the alcohol consumption within 24 h or one week, the higher the risk for IS or HS [53,80]. 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.

Consequently, this increases blood pressure and the amount of blood pumped out of the heart. Let’s face it, a hangover in your mid-40s doesn’t feel the same as one in your early 20s. 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. 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.

How much alcohol is safe to drink?

Furthermore this design lends itself perfectly for stratification of the results in categories of alcohol consumption at baseline, which is insightful given the debate surrounding the possible J-shaped curve in the relationship of alcohol consumption on CVD outcomes. An alternative path to explore is the evaluation of the impact of alcohol consumption policy measures, in which pre- and post-intervention data in an interrupted time series analysis can be compared without using randomization [80, 81]. Alcohol consumption might lend itself particularly well for this kind of research, since the ambiguity on the relationship between limited alcohol consumption on health outcomes resulted in a large variety and frequent changes of alcohol consumption guidelines worldwide [82, 83]. Nonetheless, these studies too can be affected by confounding due to secular trends that co-occur with alcohol policy changes.

1. 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).
2. 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.
3. Figure 3 summarizes the potential mechanisms underlying the cardioprotective and adverse effects of alcohol consumption.
4. Quite a bit of attention has been given to the fact that red wine seems to be particularly beneficial.
5. Short-term randomized controlled trials (RCT) have identified potentially beneficial effects of alcohol consumption on cardiovascular risk factors, but studies investigating genetic polymorphisms that influence alcohol consumption (i.e., Mendelian randomization) have yielded inconclusive results.

As such, evidence instead suggests that drinking alcohol in any amount can be harmful. Historically, some studies suggested that when people drank alcohol moderately, they experienced protective cardiovascular benefits. However, researchers now argue that scientists misinterpreted these perceived benefits. Some of the potential cellular changes related to ethanol consumption reviewed above are illustrated in figure 5. More than one cellular event may be happening at the same time, and, as with other chronic health conditions, the relevant mechanisms may be synergistic and interrelated. 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.

Impact of Drinking Patterns and Types of Alcoholic Beverages on Risk

Each woman was given either no alcohol or 15 g of alcohol (1 standard drink) with either a low-carbohydrate or a high-carbohydrate, high-fat meal. The researchers found that the alcohol-drinking subjects (particularly those who were insulin sensitive) had higher insulin levels and a slower rise in glucose levels after a low-carb meal. They recommended confirming these results in younger women and in men, particularly since their subjects had been older women, who have more significant cardiovascular risk. In various biologic systems, oxidative stress can be measured or inferred by several biologic indexes.

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. One of the long-term effects of alcohol on your heart is alcoholic cardiomyopathy. 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.

Alcohol Consumption and Cardiovascular Disease Risk: Placing New Data in Context

Dynastic effects are similar and occur when the expression of the parental genotype in the parental phenotype has a direct effect on their offspring’s phenotype. These are environmental and social factors that have the potential to affect the distribution of genetic variants for specific traits within the population. Studies of other exposures (e.g., BMI or education) have indeed shown that this leads to bias by inducing an association between the instrumental variable and the outcome [74, 75]. Although this has not been investigated for alcohol consumption, an earlier study provided evidence for presence of assortative mating for alcohol consumption [75], and parental substance use disorder is known to influence adult chronic diseases [76], suggesting dynastic effects. Finally, no evidence currently exists that genetic variants can separate the various domains of alcohol consumption (e.g., quantity versus frequency), despite their vastly different associations with CVD. Altogether, MR studies provide evidence from a different angle, but can by themselves not solve the debate on the role of limited drinking on cardiovascular health.

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For example, a J-shaped relationship emerges for average alcohol consumption and IHD and IS. On the other hand, the relationship with incident hypertension, which is a potent risk factor for most if not all CVDs, is quite different between men and women, with an increased risk for any amount of alcohol consumption in men. 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.

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. Alcohol is one of the most important risk factors for disease and mortality globally [1]. The relationship between alcohol consumption and cardiovascular diseases (CVDs) is complex, and hundreds if not thousands of individual research reports have been published.

Holiday heart syndrome can happen if you don’t typically 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. Newer research indicates that drinking alcohol, even within the recommended limits, could increase the risk of several types of cancer and even cardiovascular disease. This is why the Dietary Guidelines for Americans suggests that adults who do not drink alcohol should avoid starting, if possible. Ethanol-induced changes may be related to oxidative or nonoxidative pathways of ethanol metabolism. More than one mechanism may be activated and may lead to the multitude of ethanol-induced changes in cellular proteins and cell function.

Since in observational studies, limited alcohol consumption has no beneficial association with most cancers, a RCT specifically to prove alcohol causes cancer is ethically dubious. Secondly, the fear of falsely extrapolating results from a specific and high-risk study population to a more general public has been expressed. However, we argue that if a protective effect is observed in a high-risk population, these effects are likely to be physiologically generalizable to a lower risk population, albeit with a smaller absolute risk reduction. Ultimately, we emphasize that alcohol is consumed by half of the world’s population, and to date, there is a nearly complete lack of causal evidence on its long-term effects. Therefore, obtaining highest level of evidence—in an appropriate way—is in everyone’s benefit. To argue otherwise is to leave patients, physicians and public health professionals in a state of artificially engineered ignorance.

However, the heterogeneity found in epidemiological studies points to more than just biological differences. Socioeconomic status, for example, might influence the impact of alcohol on CVD [83]. 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.