For example, how to force yourself to pee for a drug test some people who are on cholesterol-lowering medicines may experience muscle aches when they drink alcohol. Because alcohol and cholesterol medicine both are processed through your liver, they are, in a sense, competing for clearance. So, it’s important to think about your overall health and talk to a healthcare provider about your personal risk factors. Significant progress has been made in the last decade in understanding both the beneficial and harmful effects of alcohol on the cardiovascular system. 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 terms of stroke subtypes, compared with nondrinkers, current alcohol drinkers have an increased risk (~14 percent) for hemorrhagic stroke (Ronksley et al. 2011). 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. However, ascertaining the exact alcohol consumption threshold for determining both the benefit and risk has been challenging, and threshold levels continue to differ across studies. It should also be noted that due to the limitations of alcohol-epidemiological studies, the beneficial associations tend to be overestimated.
Is some level of alcohol safe or beneficial?
The higher the alcohol consumption within 24 h or one week, the higher the risk for IS or HS [53,80]. In addition to epidemiological studies, in vitro studies have investigated the effects of alcohol on fibrinolysis. Laug (1983) reported alcohol-induced increases in t-PA secretion in cultured endothelial cells, and Kjaeldgaard and colleagues (1988) observed similar effects with a human melanoma cell line. Reeder and colleagues (1996) suggested that the interaction between alcohol consumption and fibrinolysis may involve the influence of rhythmic daily fluctuations in the levels of fibrinolytic proteins, but the exact mechanisms remain to be elucidated.
Alcoholic Cardiomyopathy
Although cardiomyopathy is more common in men than women, a recent study showed that women are actually more susceptible to alcohol-induced cardiomyopathy than men (Urbano-Marquez et al. 1995). In that study, the prevalence of cardiomyopathy in men and women was comparable, even though the total lifetime alcohol consumption by women was only 60 percent that of men. 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. The biochemical mechanisms for alcohol-induced increases in HDL levels are largely unknown, however.
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. However, the heterogeneity found in epidemiological studies points to more than just biological differences.
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. 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.
Alcohol Consumption: Categories, Measurement, and Patterns
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.
These data suggest that antioxidant defense mechanisms that attempt to protect the heart against oxidative damage appear to be initiated soon after drinking alcohol. Also, as noted below, data from other studies demonstrate the protective role of administered antioxidants, such as a synthetic compound that mimics the native superoxide dismutase enzyme, called a superoxide dismutase mimetic. This suggests a direct or indirect role for ethanol-mediated oxidative stress in the heart (Jiang et al. 2012; Tan et al. 2012).
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 all of these processes, which would help explain the antithrombotic effects of alcohol reported by several researchers. 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.
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. In addition, a newly discovered species of HDL called pre-high density lipoprotein binds with free cholesterol in a process known as reverse cholesterol transport, in which excess cholesterol is removed from body tissues, transported to the liver, and excreted in bile. On the contrary, a prospective randomized trial evaluated the effect of 90 days of moderate RW intake (150 mL/day for women, 300 mL/day for men) in 44 healthy subjects.
The evidence suggests that the type of alcoholic beverage does not play a role in the shape of the relationship. A meta-analysis [22] of fatal or non-fatal CVD events showed that a J-shaped association was observed for the consumption of wine, an inverse relationship for beer consumption, and a negative association for spirits. Moreover, excessive alcohol consumption is related to a higher risk of injuries and deaths by traffic accidents, suicide, marital violence, or child abuse, among others [12]. In contrast, light-to-moderate alcohol drinking has been linked with beneficial effect such as a reduction of risk of mortality by CVD, coronary heart disease (CHD), and stroke [12]. For example, several studies have reported that people with a higher SES may consume similar or higher amounts of alcohol than those in the lower category. Nevertheless, groups with the lowest SES seem to present higher negative alcohol-related consequences [12].
- Several reports suggest that ethanol-induced decreases in myocardial protein synthesis may be mediated in part by decreased activity of an enzyme called mammalian (or mechanistic) target of rapamycin (mTOR) (Lang and Korzick 2014; Vary and Deiter 2005; Vary et al. 2008).
- As noted above, chronic alcohol exposure leads to a decrease in mTOR activity, which corresponds to increased markers of autophagy (Lang and Korzick 2014).
- Epidemiological studies indicate a complex relationship between various dimensions of alcohol consumption (i.e., life course drinking patterns) and CVD outcomes.
- 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.
- When alcohol consumption is chronic, platelet function is significantly reduced, and clotting time increases.
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 what is mary jane drug 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).
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). The J-shaped risk relationship has been found in both sexes and for IHD morbidity and mortality [16,21]. In a meta-analysis comprising 957,684 participants and 38,627 events, a J-shaped curve in relation to lifetime abstainers was observed in women for both fatal and non-fatal IHD outcomes, and an inverse relationship was observed in men with non-fatal IHD events [16]. Using only studies fully stratified by sex and endpoint, the nadir was found at 32 g per day for IHD mortality in men, 69 g per day for IHD morbidity in men, 11 g per day for IHD mortality in women, and 14 g per day for IHD morbidity in women.
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 how do you know you got roofied during ATP depletion, mitochondrial dysfunction, and oxidative stress.
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