Produção Nacional
Revisado por pares
Vascular Effects of Alcoholic Beverages
2005; Lippincott Williams & Wilkins; Volume: 45; Issue: 5 Linguagem: Inglês
10.1161/01.hyp.0000164627.01274.ec
ISSN1524-4563
Autores Tópico(s)Fatty Acid Research and Health
ResumoHomeHypertensionVol. 45, No. 5Vascular Effects of Alcoholic Beverages Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBVascular Effects of Alcoholic BeveragesIs It Only Alcohol That Matters? Flávio D. Fuchs Flávio D. FuchsFlávio D. Fuchs From the Division of Cardiology, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil. Originally published18 Apr 2005https://doi.org/10.1161/01.HYP.0000164627.01274.ecHypertension. 2005;45:851–852Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: April 18, 2005: Previous Version 1 The relationship between alcoholic beverage consumption and cardiovascular disease is complex and not fully elucidated. The idea that drinking moderately protects against coronary heart disease prevails among physicians and the public at large. There are 218 reviews in MedLine under the search terms "coronary heart disease alcohol," limited to title and abstract, almost all asserting that the consumption of moderate amounts of alcoholic beverages is beneficial for cardiovascular health. Wine is the beverage typically associated with cardioprotection, being presumably a determinant of the low incidence of CHD in France, the French paradox. The epidemiological evidence comes along with the demonstration of beneficial effects of alcohol or other wine products on some mediators of cardiovascular disease, such as blood lipoproteins, clotting and fibrinolytic factors, insulin sensitivity, endothelin, NO, and LDL susceptibility to oxidation. However, not all epidemiological studies have shown a cardiovascular protection derived from the moderate consumption of alcoholic beverages. In blacks, this amount of consumption was associated with an increased risk for coronary heart disease incidence.1 The observational design of studies that have demonstrated the beneficial effect of alcoholic beverages precluded the full control of confounding by a healthier lifestyle of moderate drinkers. In addition, other negative cardiovascular effects of alcohol could nullify its beneficial effects. Among the harmful effects of alcoholic beverages is their blood pressure–raising effect. Drinkers of alcoholic beverages have higher blood pressure2 or are at higher risk for developing hypertension.3 A J-shaped relationship between blood pressure and ingestion of alcoholic beverages has been described by some studies, with lower blood pressure at moderate levels of consumption.4 However, the habit of drinking 2 to 3 drinks per day is an unequivocal threshold dose for increasing of blood pressure. The evidence from epidemiological studies was corroborated by human experimental studies, which have shown that alcohol ingestion increases blood pressure,5 and withdrawing of alcoholic beverages lowers blood pressure.6Contrasting effects of alcohol and of some components of alcoholic beverages, such as antioxidant polyphenols, could eventually explain the paradoxical effects of alcohol and alcoholic beverages, particularly wine, on cardiovascular regulation. In this issue of Hypertension, Zilkens et al present the results of an experiment addressing this possibility.7 Twenty-eight healthy male individuals, regular daily drinkers, were assigned to 4 periods of a 4-week open-label crossover study. The 4 interventions included abstention from all alcohol and grape products (control period), 375 mL daily of red wine (39 g alcohol), 375 mL of the same red wine dealcoholized, and 1125 mL daily (41 g alcohol) of beer. Ambulatory daily systolic blood pressure was 1.9 and 2.9 mm Hg higher at the end of the beer and wine periods, respectively, compared with the abstinence period. Blood pressure at the end of the dealcoholized red wine period did not differ from the abstinence period. None of the interventions had an effect on flow and glyceryl trinitrate mediated dilatation of the brachial artery. Urinary endothelin-1 (ET-1) excretion was higher in the alcohol (beer or wine) periods than in the nonalcohol (abstinence or dealcoholized wine) periods.The results of this experiment add 2 more pieces to the whole picture of effects of alcohol and alcoholic beverages on the cardiovascular system. First, it confirms that the most active component of alcoholic beverages is alcohol itself. Blood pressure increased with the intake of 39 g daily of ethanol carried on indistinctly by beer or wine. Second, it shows that other components of red wine have negligible, if any, sustained effect on cardiovascular parameters of human beings. Four weeks of daily intake of 375 mL of wine without alcohol, with ≈700 mg of polyphenols, did not produce any detectable effect on blood pressure, heart rate, endothelial function, or endothelin secretion. In this respect, these findings contradict the results of other experiments, which have shown that grape juice or dealcoholized wine improved endothelium-dependent vasodilation.8–10 Zilkens et al attributed these contradictory results to the noncontrolled design of 2 experiments8,9 but did offer an explanation for the differences with the results of the experiment of Agewall et al.10 These differences may be attributable to chance or the evaluation of endothelial function just after the ingestion of wine or dealcoholized wine by Agewall et al. The results of the experiment of Zilkens et al, with a controlled design and adequate statistical power, suggest that the effects of alcohol or other components of wine on potential mediators of their beneficial effects on cardiovascular system may in fact be null or pharmacologically irrelevant. In this regard, these findings strengthen the interpretation that drinking moderately may be a surrogate marker of a healthier behavior responsible for the lower incidence of coronary artery disease.1Zilkens et al suggested that the vasopressor effect of alcohol was caused, at least in part, via an alcohol-induced increase in ET-1, which was higher in the 24-hour urine collections at the end of wine and beer ingestion periods. Corder et al showed that polyphenols from red wine decreased ET-1 synthesis in cultured bovine aortic endothelial cells.11 If this effect happens in vivo, it may be overridden by a subsequent increase in endothelin synthesis, secondary to a dual effect of ethanol on blood pressure regulation. Epidemiological12 and experimental13,14 studies have demonstrated that the ingestion of alcohol is associated with an immediate decreasing of blood pressure (an effect typical of vasodilators), which is followed by a rebounding elevation of blood pressure. Heart rate increases in response to vasodilation and decreases thereafter. The rebound effects of acute alcohol ingestion on blood pressure and heart rate may be mediated by sympathetic modulation. Structural adaptation of the resistance vessels exposed to the recurrent cardiovascular effects of ethanol would lead to chronic hypertension.Regardless of source, alcohol consumption, above a certain threshold level, raises blood pressure, and this effect does not appear to be counteracted by other components of wine. In view of the large risk for cardiovascular disease attributable to blood pressure >115/75 mm Hg,15 physicians should caution their patients against excess alcohol consumption.The opinions expressed in this editorial commentary are not necessarily those of the editors or of the American Heart Association.FootnotesCorrespondence to Flávio Danni Fuchs, Serviço de Cardiologia, Sala 2061, Hospital de Clínicas de Porto Alegre, Ramiro Barcelos, 2350, 90.035-903, Porto Alegre, RS, Brazil. E-mail [email protected] References 1 Fuchs FD, Chambless LE, Folsom AR, Eigenbrodt ML, Duncan BB, Gilbert A, Szklo M. Association between alcoholic beverage consumption and incidence of coronary heart disease in whites and blacks: the Atherosclerosis Risk in Communities Study. Am J Epidemiol. 2004; 160: 466–474.CrossrefMedlineGoogle Scholar2 Klatsky AL, Friedman GD, Siegelaub AB, Gérard MJ. Alcohol consumption and blood pressure: Kaiser-Permanent Multiphasic Health Examination Data. N Engl J Med. 1977; 296: 1194–2000.CrossrefMedlineGoogle Scholar3 Fuchs FD, Chambless LE, Whelton PK, Nieto FJ, Heiss G. Alcohol consumption and the incidence of hypertension: the Atherosclerosis Risk in Communities Study. Hypertension. 2001; 37: 1242–1250.CrossrefMedlineGoogle Scholar4 Kaplan NM. Primary hypertension: pathogenesis. In: Kaplan NM, ed. Kaplan's Clinical Hypertension. Philadelphia, Pa: Lippincott Williams & Wilkins; 2002: 56–135.Google Scholar5 Puddey IB, Beilin LJ, Vandongen R, Rouse IL, Rogers P. Evidence for a direct effect of alcohol consumption on blood pressure in normotensive men. A randomized controlled trial. Hypertension. 1985; 7: 707–713.LinkGoogle Scholar6 Xin X, He J, Frontini MG, Ogden LG, Motsamai OI, Whelton PK. Effects of alcohol reduction on blood pressure: a meta-analysis of randomized controlled trials. Hypertension. 2001; 38: 1112–1117.CrossrefMedlineGoogle Scholar7 Zilkens RR, Burke V, Hodgson JM, Barden A, Beilin LJ, Puddey IB. Both red wine and beer elevate blood pressure in normotensive men. Hypertension. 2005; 45: 874–879.LinkGoogle Scholar8 Stein JH, Keevil JG, Wiebe DA, Aeschlimann S, Folts JD. Purple grape juice improves endothelial function and reduces the susceptibility of LDL cholesterol to oxidation in patients with coronary artery disease. Circulation. 1999; 100: 1050–1055.CrossrefMedlineGoogle Scholar9 Chou EJ, Keevil JG, Aeschlimann S, Wiebe DA, Folts JD, Stein JH. Effect of ingestion of purple grape juice on endothelial function in patients with coronary heart disease. Am J Cardiol. 2001; 88: 553–555.CrossrefMedlineGoogle Scholar10 Agewall S, Wright S, Doughty RN, Whalley GA, Duxbury M, Sharpe N. Does a glass of red wine improve endothelial function? Eur Heart J. 2000; 21: 74–78.CrossrefMedlineGoogle Scholar11 Corder R, Douthwaite JA, Lees DM, Khan NQ, Viseu Dos Santos AC, Wood EG, Carrier MJ. Endothelin-1 synthesis reduced by red wine. Nature. 2001; 414: 863–864.CrossrefMedlineGoogle Scholar12 Moreira LB, Fuchs FD, Moraes RS, Bredemeier M, Duncan BB. Alcohol intake and blood pressure: the importance of time elapsed since last drink. J Hypertens. 1998; 16: 175–180.CrossrefMedlineGoogle Scholar13 Abe H, Kawano Y, Kojima S, Ashida T, Kuramochi M, Matsuoka H, Omae T. Biphasic effects of repeated alcohol intake on 24-hour blood pressure in hypertensive patients. Circulation. 1994; 89: 2626–2633.CrossrefMedlineGoogle Scholar14 Rosito GA, Fuchs FD, Duncan BB. Dose-dependent biphasic effect of ethanol on 24-h blood pressure in normotensive subjects. Am J Hypertens. 1999; 12: 236–240.CrossrefMedlineGoogle Scholar15 World Health Report 2002: Reducing risks, promoting healthy life. Geneva, Switzerland: World Health Organization; 2002. Available at http://www.who.int/whr/2002. Accessed April 1, 2005.Google Scholar eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetailsCited By Hernández-Hernández A, Oliver D, Martínez-González M, Ruiz-Canela M, Eguaras S, Toledo E, de la Rosa P, Bes-Rastrollo M and Gea A (2023) Mediterranean Alcohol-Drinking Pattern and Arterial Hypertension in the "Seguimiento Universidad de Navarra" (SUN) Prospective Cohort Study, Nutrients, 10.3390/nu15020307, 15:2, (307) Whayne T (2019) Alcohol Excess Is an Insufficiently Considered Cause of Malignant Refractory Hypertension, Angiology, 10.1177/0003319719888101, 71:4, (297-300), Online publication date: 1-Apr-2020. 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