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Drinking is part of human society worldwide. However, alcohol consumption has been strongly linked to human diseases, including dementia, liver cirrhosis, and neurological conditions. A recent research paper examined whether drinking was related to hypertension, the root factor in morbidity and mortality caused by cardiovascular disease (CVD).
Review: Alcohol Intake and Arterial Hypertension: Retelling of a Multifaceted Story. Image Credit: Adheamir / Shutterstock
Introduction
Alcohol consumption appears to be a widespread human practice. Over two billion people drink, with the highest per capita consumption in the European Union (EU). People who drink regularly consume a mean of 33 g of anhydrous alcohol per day, with beer being the most common alcoholic beverage.
The link between excessive alcohol consumption with CVD, hepatic, neurological, metabolic, and neoplastic conditions is well known. The world over, CVD is a major killer as well as being responsible for significant morbidity rates. For this reason, many guidelines suggest that no alcohol is the safe threshold for alcohol consumption but that among drinkers, “daily intake should be limited to one drink or less for women or two drinks or less for men.”
These include the International Society of Hypertension, European Society of Cardiology/European Society of Hypertension, and American Heart Association/American College of Cardiology.
Nevertheless, there is much evidence that the moderate consumption of alcohol is beneficial for cardiovascular health, beginning from the “French Paradox” – the finding of reduced ischemic heart disease (IHD) among those who regularly drink red wine. While this may be partly attributable to the multitude of antioxidants, anti-inflammatory, and cytoprotective bioactive compounds in red wine, such as quercetin and resveratrol, the pro-inflammatory effect of ethanol metabolites could be more than sufficient to overcome this potential benefit.
Notably, studies have shown that alcohol dehydrogenase variants occur in different individuals and that categorization according to variant nullifies the protective effect of moderate alcohol intake.
Hypertension is rising in prevalence due to the rising mean age of the population as well as due to the increased prevalence of poor dietary patterns and other lifestyle factors. Therefore, potential interventions could target weight loss, a sedentary lifestyle, appropriate sodium/potassium intake changes, smoking, and excessive alcohol intake.
The current paper, which appears in the journal Nutrients, aimed to review all current studies dealing with the association between alcohol and blood pressure.
What does the study show?
The review showed indications that over the short term, high or sustained alcohol consumption, including drinking more than 30 g of alcohol per day over a long period, caused a higher risk of hypertension, which was associated with the dosage.
With moderate doses of alcohol, blood pressure (BP) went up for up to seven hours but normalized after that. A biphasic response was observed with high doses of alcohol, with an initial decrease in both systolic and diastolic blood pressure (SBP and DBP, respectively) for up to 12 hours, increasing at more than 13 hours from consumption. The heart rate increased at all doses, from low to high.
“Despite absolute short-term changes of blood pressure appearing to be quite small after alcohol ingestion, these changes could be sustained over time in chronic alcohol consumers and become relevant for chronic blood pressure control.”
In fact, over the long term, Blacks appear more prone to BP elevations than Whites or Asians. In one study, the risk for high BP among men increased by a fifth with 1-2 drinks but by half and three-fourths with 3-4 and 5 or more drinks a day. Women failed to show an increased risk at low dosages, but above two drinks a day, they had a 42% increase in risk. However, this finding remains to be validated and has been contradicted by other research.
Neurohormones and alcohol
Neurohormonal disruptions may mediate the mechanisms of harm in alcohol consumption. For example, sympathetic activation could underlie the observed BP elevation, as could the disruption of carotid baroreceptor responses that regulate BP. This disruption might be due to higher amounts of endorphins and histamine released by alcohol.
Cortisol, plasma renin activity (causing vasoconstriction and sodium and water retention), and impaired endothelial function (inhibiting vasodilatory responses and promoting oxidative stress) have also been reported in heavy drinkers.
Alcohol and organ damage/CVD
Moreover, not only does drinking cause elevated blood pressure, but in excess, it can directly enhance the damage caused to cardiac and renal tissues by hypertension. Some scientists suggest a J-shaped curve between alcohol and CVD, but this remains a hypothesis.
A recent study shows the least mortality at 100 g/week or less of alcohol, with a dose-dependent relationship between alcohol and stroke, IHD, fatal hypertensive disease, heart failure, and fatal aortic aneurysm. Notably, the heart attack risk was in inverse relation to alcohol consumption levels.
The type of alcoholic beverage also determines the impact on health, with red wine being considered healthy, for instance, due to the high polyphenol content. Most importantly, masked hypertension, where patients are hypertensive at home but not in the doctor’s office, is as serious a health risk as sustained hypertension.
“Alcohol consumption might affect left ventricular diastolic properties, even in nonalcoholic patients,” say the researchers.
Above 14 drinks a week, heart failure risk is higher, with hypertensive patients who drink more being more likely to show subclinical features of heart damage affecting the heart’s diastolic function. This is a dose-dependent association, as is that with left ventricular hypertrophy. Elevated uric acid levels could mediate this due to alcohol consumption.
Since the kidneys excrete a tenth of ingested alcohol, toxicity in these organs is expected, which could enhance inflammation and renal damage in hypertensive patients. However, chronic kidney disease appears to be less common among drinkers.
Conversely, moderate drinking has been repeatedly demonstrated to have potential benefits for patients with diabetes and abnormal lipoprotein profiles. At the same time, some studies suggest that stopping or reducing alcohol intake produces better outcomes for those with high blood pressure or CVD. Alcohol withdrawal reverses the adverse impact of alcohol on endothelial function, with rapid normalization of the BP.
Some evidence suggests that reducing alcohol intake in heavy drinkers could help reduce BP, but much more research is required to validate these observations.
What are the implications?
The findings of this review support the current recommendations to avoid alcohol. The regular consumption of over 30 g/day of alcohol increases hypertension risk in linear proportion to the dosage and may independently cause cardiac damage in hypertensive patients. Alcohol may also increase the CVD risk in such patients.
Despite this, “the evidence currently available in support of the possible benefits of the restriction of alcohol consumption on hypertension, and its complications, is all but conclusive and deserves further investigation.”
