A closer look at alcohol’s effect on heart health

But like many people, I enjoy the occasional glass of wine with dinner, and nothing tastes better than an ice-cold beer on a sweaty summer day. When it comes to alcohol and heart health, the existing research is quite conflicting — some studies say alcohol improves heart health, while others imply the opposite. In some studies, the BP did not change after the chronic administration of alcohol to animals. Abdel-Rahman85 reported that the BP increase was not different between ethanol-fed (5–20% in drinking water) spontaneously hypertensive (SH) rats and control SH rats during a 13-week observation period.

Finally, there is also evidence to suggest that traits that predispose individuals to binge drinking may also predispose to binge eating 66. The reasons for the inconsistent results in experimental studies are not clear, but cannot be explained by differences in daily doses of alcohol administration. The periods of alcohol administration, however, are generally longer in studies showing BP reduction than those showing BP elevation. Crandall et al.90 administered 30% alcohol twice daily (7–8 g kg−1) for 10 weeks to rats and examined the levels of BP and blood alcohol. In their study, BP was normal at the time of the peak blood alcohol level but was elevated at 24 h after alcohol consumption, when alcohol was not detected in the plasma. Their results suggest that alcohol-induced hypertension is not because of its direct action but to alcohol withdrawal.

Controlling Your Blood Pressure

Methamphetamine is better known by the colloquial terms “ice” or what percentage of violent crimes involve alcohol “crystal meth.” Misuse occurs by oral, intravenous, and intranasal use, as well as by inhalation when smoking. Its deleterious effects on the cardiovascular system include hypertension, accelerated atherosclerosis, vasospasm-induced acute coronary syndromes, sudden cardiac death, and dilated cardiomyopathy with congestive heart failure. A massive methamphetamine exposure causes vasoconstriction and vasospasm, which may ultimately lead to hypertension, tachycardia, endothelial dysfunction, and cardiotoxicity. Some adverse BP-related mechanisms that may be triggered by alcohol include changes in intracellular calcium levels, baroreflex control, and heart rate and activation of other neurohormonal systems besides the RAAS, such as the sympathetic nervous system (Marchi et al. 2014).

“Excessive alcohol consumption can cause nerve damage and irreversible forms of dementia,” Dr. Sengupta warns. Your body breaks alcohol down into a chemical called acetaldehyde, which damages your DNA. Damaged DNA can cause a cell to grow out of control, which results in cancerous tumors. But prolonged alcohol abuse can lead to chronic (long-term) pancreatitis, which can be severe. That’s because your body already has processes in place that allow it to store excess proteins, carbohydrates and fats.

Heavy drinking can make you more likely to get serious health problems like liver disease, cancer, and peptic ulcers, among others. Regular or high alcohol use can hurt your heart and lead to diseases of the heart muscle, called cardiomyopathy. However, Yost did add that one day of irregularly eating can impact people with chronic health conditions.

Alcohol and PAD

However, evidence suggests an association between consuming alcohol and problems with the cardiovascular system. Whether it’s a glass 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. This is when overeating and overindulging in alcohol lead to an irregular heartbeat.

Alcohol Consumption and Obesity: An Update

While cross-sectional and longitudinal studies have controlled for a number of important lifestyle factors, there are many to consider when examining body weight regulation. It is highly likely that the paradoxical results seen in studies examining the effect of alcohol on weight gain and obesity are also the product of a multitude of factors beyond the individual’s ingestion habits. Future research must consider the other important factors that may influence the link between alcohol and obesity, some of which are discussed below. 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.

Such an analysis allows for a more complete description of participants’ drinking patterns, and is important as cross-sectional studies suggest that drinking frequency and intensity influence weight differently 14–16. 3 Greenfield and colleagues (2005) studied the effects of alcohol at meal time in a group of nonsmoking, healthy postmenopausal women. 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. Several reports indicate that alcohol first exerts a seemingly positive effect, followed by a more negative impact (i.e., it is biphasic) on the endothelial−nitric oxide–generating system.

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. Data from transgenic animal models and pharmacologic approaches strongly support a role for ethanol-induced oxidative stress in CV disease.

1. However, the preponderance of the evidence taken as a whole suggests that alcohol may be a risk factor for obesity in some individuals, especially when consumed in large quantities.
2. In their study, the plasma level of norepinephrine was decreased in ethanol-fed animals.
3. 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.
4. 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.
5. Different levels of daily wine consumption (i.e., sometimes, 1 to 2 glasses/day, and ≥3 glasses/day) had no effect on fatal or nonfatal outcomes (e.g., hospitalization for a CV event).

This suggests a direct or indirect role for ethanol-mediated oxidative stress in the heart (Jiang et al. 2012; Tan et al. 2012). Howe et al.86 reported that BP values in alcohol-fed (5–20% in drinking water) Wister Kyoto, SH and stroke-prone SH rats were lower than those of respective control rats during a 6-month observation period. Hatton et al.87 observed a BP decrease during chronic ethanol administration (36% in a liquid diet) for 18 weeks in Wistar rats. The vasoconstrictor response of resistant arteries to norepinephrine was enhanced and the vasodilator response to alcohol was attenuated in their study.

Stroke

This supports the findings from other studies that the alcohol-induced changes in HDL-c do not fully account for the lower risk of CHD in moderate alcohol drinkers (Mukamal 2012). High triglyceride levels in the blood stream have been linked to atherosclerosis and, by extension, increased risk of CHD and stroke. 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.