Certain cholesterol-lowering medications (e.g., lovastatin) block HMG-CoA reductase, but further research is needed to determine whether alcohol has a similar effect. Cells in the endothelium send out chemical signals that trigger an inflammatory process in response to the formation of fatty streaks in the arteries. 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).
- Of the numerous cellular and molecular mechanisms that are thought to explain the beneficial effects of moderate drinking, this article discusses four, involving (1) high density lipoproteins, (2) cellular signaling, (3) platelet function in blood clot formation, and (4) stimulation of blood clot dissolution.
- Several theories have been suggested to explain how alcohol possibly thwarts this inflammatory process and provides protection against atherogenesis.
- They described an increased risk for hypertension in lifetime abstainers and a reduced risk in the less-heavy consumption group; nonetheless, when adjusted by a propensity score method, these findings were not significant.
- 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.
- 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].
Can You Reverse Damage to the Cardiovascular System?
This article summarizes representative epidemiological and animal studies on these cardiovascular consequences of chronic heavy alcohol consumption and reviews mechanisms that have been suggested to explain alcohol’s effects. Many systematic reviews and meta-analyses [5,14,15,16,17,18,19,20] and numerous individual studies have been published in recent decades on the relationship between alcohol consumption and IHD, or myocardial infarction, the main subcategory of IHD. This relationship and its implications remain controversial due to a lack of long-term randomized controlled trials with CVD endpoints. Oftentimes, whether or not a J-curve or an inverse or U-shaped relationship is observed depends on the range of alcohol consumption reported in an individual study and the specific IHD endpoint considered (fatal or non-fatal). The factors responsible for the apparent cardiovascular benefits of how long does cymbalta withdrawal last light-to-moderate alcohol intake are uncertain.
The findings suggest a protective effect of overexpression of IGF-1 in the transgenic animals (Zhang et al. 2014). Data from transgenic animal models and pharmacologic approaches strongly support a role for ethanol-induced oxidative stress in CV disease. In addition, there was no evidence of nitrative damage in mice bred to disrupt (i.e., knock out) the gene for angiotensin I receptor (AT1-KO) that had been given ethanol for a similar length of time (Tan et al. 2012). 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). 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.
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. Chronic alcohol consumption has been verified as the cause of hypertension in two controlled trials.
Stroke
Nonetheless, the antioxidant effect of wine intake could be protective in oxidative stress situations [35]. Daily RW consumption for 21 consecutive days significantly enhanced vascular endothelial function in 20%. Although plasma stromal cell-derived factor-1 (SDF-1) concentrations remained unchanged, the endothelial progenitor cell (EPC) count and migration significantly increased after this period. RW increased the migration, proliferation, C-X-C chemokine receptor type 4 (CXCR-4) expression, and the activity of the Pi3K/Akt/eNOS signaling pathway and decreased the extent of apoptosis in glucose-stressed EPCs [36].
Alcohol’s Link to Coronary Artery Disease, Heart Attack, and Stroke
Large-scale longitudinal epidemiological studies with multiple detailed exposure and outcome measurements, and the extensive assessment of genetic and confounding variables, are necessary to elucidate these associations further. Conflicting associations depending on the exposure measurement and CVD outcome are hard to reconcile, and make clinical and public health recommendations difficult. The effect of the quantity of alcohol on hypertension according to the frequency of drinking is not yet clear, since studies remain contradictory.
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). Other studies have examined the effect of a single binge-drinking episode and found impairment in brachial artery endothelial-dependent and -independent vasodilation (Bau et al. central nervous system (cns) depressants 2005; Hashimoto et al. 2001; Hijmering et al. 2007). Therefore, as in animal studies, the effects of ethanol on endothelial function in humans likely depend on the dose and duration of ethanol consumption. Heavy drinking can make you more likely to get serious health problems like liver disease, cancer, and peptic ulcers, among others.
One study attributed 12 percent of subarachnoidal hemorrhage cases to recent heavy drinking (Juvela et al. 1993). Other research suggested that such cases could be precipitated by a transient increase in blood pressure. 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. The association between excessive alcohol consumption and enlargement of the heart and the occurrence of CHF in chronic alcoholics was first reported more than 100 years ago.
Who Shouldn’t Drink?
The associations between drinking and CV diseases such as hypertension, coronary heart disease, stroke, peripheral arterial disease, and cardiomyopathy have been studied extensively and are outlined in this review. Although many behavioral, how to ween off alcohol 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 response, oxidative stress, and programmed cell death, as well as anatomical damage to the CV system, especially the heart itself.
A study analyzing data of the 2005 US National Alcohol Survey, including 4083 individuals, evaluated the association between current drinking status and early life drinking patterns with three health conditions, including hypertension. They described an increased risk for hypertension in lifetime abstainers and a reduced risk in the less-heavy consumption group; nonetheless, when adjusted by a propensity score method, these findings were not significant. Current drinkers who drink 5 or more drinks/day at least monthly did show a significant risk of hypertension, meaning that consistent long-term heavy drinking is the real cause [60]. 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.
Studies using different methodologies have shown that low-to-moderate alcohol consumption decreases platelet activation and aggregation in certain cases—for example, in response to certain physiologic stimuli such as adenosine 5′-diphosphate (Salem and Laposata 2005). On the other hand, significant daily alcohol consumption increases platelet aggregation and reactivity. Infection or other stressful events also can lead to immune-triggered platelet production, a condition called rebound thrombocytosis, which may occur immediately after withdrawal from both heavy and one-time heavy (binge) drinking (Numminen et al. 1996).
A J-shaped relationship for females showed protective effects at or below consumption levels of 15 g/day (Taylor et al. 2009). These data highlight how gender may be an important modifier of the alcohol threshold level and can shape the alcohol benefit–risk relationship. Epidemiological studies indicate a complex relationship between various dimensions of alcohol consumption (i.e., life course drinking patterns) and CVD outcomes. Most epidemiological studies to date have relied on a single measurement of alcohol intake at baseline.
Evidence from epidemiological studies has been corroborated by intervention studies in humans. For example, Mori et al. carried out a randomized controlled trial evaluating BP changes in 24 premenopausal women at three drinking levels (alcohol free, low volume, and high volume) during a 4-week period each. SBP and DBP were higher in women who consumed greater amounts of alcohol (2–3 drinks per day) compared with the other two drinking levels. However, lower amounts of intake did not show the BP-lowering effects evidenced in other studies [62]. A meta-analysis by Roereck et al. evaluating 36 clinical trials including 2865 participants described that a reduction in alcohol consumption reduced BP in a dose-dependent manner, when intake was over 2 drinks per day in both healthy participants and people with risk factors for CVD [49].
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. However, modulatory influences related to drinking patterns, genetic susceptibility, nutritional factors, ethnicity, and gender also many play a role (Piano and Phillips 2014) (figure 4). Altered platelet responses (e.g., increased platelet activation/aggregation) leads to blood-clot formation (or thrombosis) in certain CV conditions.
