SciELO - Scientific Electronic Library Online

vol.76 issue2Correlação clínico-radiográfica author indexsubject indexarticles search
Home Pagealphabetic serial listing  

Services on Demand




Related links


Arquivos Brasileiros de Cardiologia

Print version ISSN 0066-782XOn-line version ISSN 1678-4170

Arq. Bras. Cardiol. vol.76 no.2 São Paulo Feb. 2001 



Alcohol and Atherosclerosis


Murilo Foppa, Flávio Danni Fuchs, Bruce B. Duncan

Porto Alegre, RS - Brazil



Observational studies have attributed a protective effect to alcohol consumption on the development of atherosclerosis and cardiovascular morbidity and mortality. Alcohol intake in the amount of one to two drinks per day results in an estimated 20-40% reduction in cardiovascular events. An additional protective effect, according to major cohort studies, has been attributed to wine, probably due to antioxidant effects and platelet antiaggregation agents. On the other hand, the influence of different patterns of alcohol consumption and environmental factors may explain a great part of the additional effect of wine. Protection may be mediated by modulation of other risk factors, because alcohol increases HDL-C, produces a biphasic response on blood pressure, and modulates the endothelial function, while it neither increases body weight nor impairs glucose-insulin homeostasis. Alcohol may also have a direct effect on atherogenesis. Despite these favorable effects, the current evidence is not enough to justify prescribing alcohol to prevent cardiovascular disease.



In recent years, the idea that regular alcoholic beverage consumption protects against cardiovascular diseases has been spread. Physicians, and more particularly cardiologists, are frequently asked about the veracity of this statement.

The cardiovascular diseases resulting from atherosclerosis are a challenge due to their epidemiological importance and the multifactorial features involved in their genesis. Many risk factors of atherosclerosis have been clearly identified, and some, such as hypertension 1, dyslipidemia 2, and diabetes mellitus 3, are amenable to effective interventions. The intensity of the association of other risk factors, however, has not been clearly established. The effect of alcoholic beverage consumption on the incidence of atherothrombotic diseases is a particular case among them. This is due not only to the intensity of the effect but also to the interaction with other risk factors making it difficult to grasp the real impact, be it beneficial or deleterious.

The habit of alcoholic beverage consumption is widespread and accepted in most countries. Ethanol available in different forms and its pattern of consumption is widely varied in population groups. Despite methodological difficulties in quantifying and classifying the amount of alcohol ingested and on the basis of a population study carried out in Porto Alegre 4, it is estimated that approximately 15% of the population have alcoholic beverage consumption above 30mg/day. In addition, it is suggested that the rate of abusers is proportional to the total consumption of the population 5. It is worth noting that abstainers and social consumers comprise three quarters of the population. In this latter group of individuals, understanding the interrelations between alcohol consumption and health may have a greater epidemiological impact.

Protection provided by alcohol consumption – Several population-based studies 6-8 suggest that moderate consumption of alcoholic beverages protects against coronary artery disease and cardiovascular disease.

In regard to cerebral strokes, a probably protective effect against ischemic events exists 9-11, but the effect on hemorrhagic events is inconsistent 9,11.

Despite the presumable benefit provided by alcoholic beverage consumption on the incidence of cardiovascular disease, the sequelae of alcohol intake are among the 20 major causes of loss of disability-adjusted life years 12. In addition, alcohol consumption increases mortality due to neoplastic diseases, diseases of the digestive tract, and external causes 13,14.

An overview assessment in most of the countries where the subject has been studied shows that mortality is still lower among those with moderate alcohol consumption, mainly in populations with a higher cardiovascular risk 14, (fig. 1) and in secondary prevention in patients suffering from myocardial infarction 15. On the other hand, heavy consumption of alcoholic beverages (more than 3 drinks a day) may be associated with an increase in mortality among men who have already experienced myocardial infarction 16.



Summarizing, evidence exists suggesting that consumption of 1-2 drinks of alcoholic beverages per day causes a 20-40% reduction in cardiovascular events as compared with that of abstainers, and a progressive increase in diseases attributed to consumption of higher levels of alcohol is observed.


Controversies about the benefits of alcohol consumption

Types of beverages – Some studies suggest a greater reduction in cardiovascular mortality among wine consumers, as well as fewer hospitalizations due to coronary artery disease 17 and a reduced incidence of cerebral strokes 10 among these individuals. In addition, moderate wine consumption seems not to be associated with an increase in the risk of cancer of the upper digestive tract, unlike beer and distilled spirits 18.

The hypothesis of the additional protective effect of wine is mainly based on two types of evidence. Studies where alcohol consumption and clinical events were measured as means or population ratios, usually called ecological studies 19-21, showed a reduced incidence of coronary events in populations with a relatively high consumption of saturated fat concomitantly with high alcohol intake, mainly in the form of wine. This phenomenon is known as the French paradox. This type of evidence, despite the consistent results in the mentioned studies, makes impossible the identification of the direct relation between exposure to factors of interest – consumption of alcohol and saturated fat – and occurrence of clinical events among the populations studied. The second type of evidence is the experiment showing the biological effects of flavonoids and polyphenols present in wine 22, which are mechanisms supposedly responsible for the reduction of thromboembolic events 23. Recently, a French cohort study 24 showed that the reduction of total and cardiovascular mortality was more pronounced (30-40% reduction in the risk) in those individuals with regular and exclusive wine consumption. This is consistent evidence even though it has not been corrected for the other potential factors present in wine consumers, who comprise most of the population.

Environmental factors – Rimm et al 8, reviewing ecological, cohort and case-control studies, reported that not only wine, but also beer and distilled spirits may have a more intense protective effect in certain populations. These effects are thought to be associated with the type of beverage most used in the regions. These findings suggest that maybe it is not the type of the beverage but the social and demographic, cultural, or even alimentary features 25 associated with alcohol consumption that are the real protectors against cardiovascular disease. Wannamethee and Shaper 26 compared the protective effect of different types of alcoholic beverages in a certain population and identified that a great part of the additional benefit attributed to wine could be explained by a lower prevalence of other risk factors, such as smoking, obesity, and sedentary lifestyle. The importance of the diet has also been shown in Lyon Diet Heart Study 27 of secondary prevention, where the use of a Mediterranean diet managed to reduce the incidence of new infarctions by approximately 70%. Therefore, the moderate consumption of alcoholic beverages typical of a certain society could be an indication of healthy behavior and not a real protective mechanism.

We may also consider that part of the increased risk in absteiners may correspond to individuals who stopped drinking because they were ill. This issue was assessed in several studies 6,9,14,28, which did not significantly change the original estimates. On the other hand, a reduction from an excessive alcoholic consumption to a moderate regular consumption, potentially associated with a healthier lifestyle, is more difficult to quantify.

Patterns of consumption – Even though laboratory evidence supports the protective effect of wine, other findings suggest that not the type of alcoholic beverage but its form of consumption modifies cardiovascular risk. Studies suggest that alcoholic beverage consumption in an excessive and sporadic manner is associated with cardiac arrhythmias 29 and with a higher incidence of cerebral strokes 30 and of acute coronary artery events 31, which are not supported by another study 32. However, in most studies, alcohol consumption is measured through questions about the mean consumption, limiting the recognition of the effects related to the forms of consumption on cardiovascular disease. On the other hand, the drinking pattern may vary with the type of alcoholic beverage, and a moderate and regular consumption is usually observed in wine consumers 26,33.

Another significant issue in regard to the pattern of consumption is that the usual consumption reported by European studies is substantially higher than that reported by American studies. One could speculate that the same mean alcoholic intake may correspond to a pattern of consumption considered moderate/regular in studies with greater consumptions, but may correspond to a pattern of occasional and isolated consumption of greater amounts in populations with a usually lower consumption.

Temporal bias – Recently, a new hypothesis has been formulated by Law and Wald 34 in an attempt to explain the French paradox. They showed that cholesterol levels and ischemic events correlate with the consumption of saturated fat from past decades (which corresponds to the time necessary for the development of atherosclerotic disease). They also showed that the disproportion between levels of cholesterol and ischemic events usually attributed to wine consumption is due to the recent increase in the saturated fat intake in Mediterranean countries.


Effects of alcohol on cardiovascular risk factors

Lipoproteins – Change in lipoproteins is the most often described mechanism mediating cardiovascular protection associated with alcohol intake. Population-based evidence shows higher levels of HDL-C in individuals drinking alcoholic beverages 35,36. However, only 50% of the protective effect may be explained by an increase in HDL-C 28.

Alcohol affects the metabolism of lipoproteins in different phases. Regular consumption may be associated with an increase in the synthesis of lipoproteins 37, a reduction in the degradation of HDL-C, and a higher hepatic metabolism of LDL-C36. In the postprandial period, alcohol accounts for an additional increase in the serum levels of triglycerides with inhibition of the oxidation of free fatty acids 38. It also modifies the dynamics and the metabolism of the lipoproteins of HDL-C 36. The higher amount of lipids aggregated to lipoproteins with alcohol consumption in the postprandial period may result in increased tissue removal through an increase in the mobilization of cholesterol esthers and triglycerides 37,39.

It is worth emphasizing that in individuals with coronary heart disease, postprandial increased serum levels of triglycerides are higher and more prolonged 40. An increase in serum levels of triglycerides and an increase in free fatty acids are associated with a reduction in endothelial vasodilation in healthy 41 and insulin-resistant 42 individuals.

Inflammation and endothelial dysfunction – An excessive consumption of alcoholic beverages has long been associated with a reduction in immunity probably because of a lower activity of leukocytes and cytokines. On the basis of laboratory experiments, alcohol has been shown to also affect vascular reactivity. Ethanol may reduce vasodilation mediated by endothelium in rat mesenteric capillaries 43. On the other hand, in humans the acute vasodilating effect of alcohol is associated with a reduction in peripheral resistance 44. The hemodynamic effects of wine may be secondary to antioxidant effects 45,46, induction of the sythesis of nitric oxide 47, and endothelium-mediated vasodilation 45, in addition to its effects on platelet aggregation 48, and plasminogen activation 49,50. Experimental models have shown an inhibition in formation of atherosclerotic plaques with administration of wine or its nonalcoholic components 51. Even though tempting, these clinical effects have only been demonstrated in small samples with no representation of its potential clinical relevance in population studies.

Hypertension – Excessive alcohol consumption has been associated with systemic hypertension. On the basis of prospective studies, a direct causal relation has been suggested, and a higher incidence of elevated blood pressure levels has been shown in individuals who drink excessively 52-54 and in alcoholic hypertensive patients, whose pressure levels decrease when they undergo reduction in alcohol intake 55.

Generally, the consumption of 1-2 drinks per day for men and half of this amount for women is not associated with a significant increase in blood pressure levels 52-54,56,57, and some studies even show lower pressure levels in these individuals 52,56,57.

Another not well understood phenomenon is the dissociation between acute vasodilating effects with isolated alcohol administration 58-61 and its chronic hemodynamic effects. Isolated alcohol consumption may cause an acute reduction in blood pressure with a possible dose-dependent rebounding aftereffect in healthy individuals 62 and reduction in the usual circadian variation in hypertensive obese individuals, when alcohol is ingested at lunch 63. This mechanism may help understanding the higher blood pressure levels between 13 and 24 hours after the last alcoholic intake observed in a population study 64. Sympathetic modulation, cortisol, the renin-angiotensin system, and endothelial activity are mechanisms potentially implicated in these effects. Changes in these different homeostatic mechanisms may be another link between alcohol effects and cardiovascular disease.

Smoking – Smoking is one of the changeable factors that most increase the absolute risk of cardiovascular events 65. A positive association between smoking and the amount of alcohol intake is also observed 66,67. Therefore, we can speculate that the protective effects of regular alcohol intake may be minimized by the risk associated with an increase in smoking.

However, in a Finnish study 35 with a limited number of cardiovascular events analyzed, the authors observed that the protective effect associated with alcohol consumption was limited to smokers. This may be explained by the highest absolute risk in smokers, which increases the potential benefits of protective factors.

Obesity – Moderate regular alcohol consumption is not associated with an increase in the incidence of obesity 66,68,69, and a specific protective effect against central obesity may exist in obese wine consumers 70.

In a crossover experiment 71, moderate wine consumption (270mL/day) changed neither the weight nor the metabolic substrate of individuals. Another study 72, using indirect calorimetry, showed an expenditure of approximately 20% of the energy present in alcohol in thermogenesis induced by alcohol, adding to the evidence that the caloric component of alcohol is not used in maintaining body weight 73,74.

Diabetes mellitus and insulin resistance – Moderate alcohol consumption is associated, in some studies, with a lower incidence of diabetes mellitus 67,75, hyperinsulinemia 76,77, and insulin resistance 78,79. Vasodilation caused by alcohol may provide an increase in peripheral glucose uptake in these states of reduction in peripheral homeostasis of glucose and insulin 80.

Just one single study 81 showed worsening in the metabolic control of diabetic patients, which was normalized in a short period of abstinence, but these individuals used a mean of 4 drinks of alcoholic beverages per day. However, acute moderate alcohol consumption does not cause a significant clinical worsening of the metabolic control 82,83.

Independently from the direct effect of alcohol consumption on the metabolism of glucose and insulin, the protective effect on coronary heart disease in type II diabetic patients is at least similar to that in nondiabetic individuals 84.

Atherogenesis – Even considering the individual effect on risk factors in a population with high alcohol consumption 85, an association between alcohol intake and the degree of carotid thickening has been observed. Considering that the results of this study were controlled as to weight, social activity, blood pressure, triglycerides, fibrinogen, glycemia, LDL-C, and HDL-C, it was suggested that alcohol might have a direct effect on the development of atherosclerotic disease, with a maximum protective effect when consumption was between 1 and 50g/day of alcohol. The risk was increased with a mean consumption above 200g/day (table I). Another study 86 on usually lower alcohol consumption (approximately one drink per day) has not shown the same protective association.




Comprehension of the innumerable effects of alcoholic beverage intake, a widespread habit among us, on risk factors and cardiovascular disease itself is fundamental for developing strategies and interventions aiming at reducing morbidity and mortality.

Regular alcohol intake is clearly associated with a reduction in cardiovascular events. The significance of this benefit, however, may have diverse clinical implications depending on other factors present, which may partially account for the effects attributed to alcohol. Regular alcoholic beverage consumers, mainly at middle age and with other risk factors for cardiovascular diseases, seem to be more protected against these diseases.

Even though the protective effects of alcohol consumption are potentially real and direct, recommendation for the regular use of alcohol should be based on clinical experiments we lack randomized clinical trials confirming the benefits shown in observational studies. We should also take into consideration potential individual and social risks secondary to the deleterious effects of widespread alcoholic beverage consumption. Decisions in individual cases should be based on reasoning and common sense, considering that we really do not know the actual effectiveness of alcohol consumption as a protective factor against cardiovascular diseases.



1. Collins R, Peto R, MacMahon S, et al. Blood pressure, stroke, and coronary heart disease: Part 2, short-term reductions in blood pressure: overview of randomised drug trials in their epidemiological context. Lancet 1990; 335: 827-38.        [ Links ]

2. Shepherd J. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. N Engl J Med 1995; 333: 1301         [ Links ]

3. UKPDS Group. Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). Lancet 1998; 352: 854-65.         [ Links ]

4. Moreira LB, Fuchs FD, Moraes RS, et al. Alcoholic beverage consumption and associated factors in Porto Alegre, a southern Brazilian city: a population-based survey. J Stud Alcohol 1996; 57: 253-9.         [ Links ]

5. Rose G, Day S. The population mean predicts the number of deviant individuals. Br Med J 1990; 301: 1031-4.         [ Links ]

6. Marmot M, Brunner E. Alcohol and cardiovascular disease: the status of the U shaped curve. Br Med J 1991; 303: 565-8.         [ Links ]

7. McClure M. Demonstration of deductive meta-analysis: ethanol intake and risk of myocardial infarction. Epidemiol Review 1993; 15: 328-51.         [ Links ]

8. Rimm EB, Klatsky A, Grobbe DG, Stampfer MJ. Review of moderate alcohol consumption and reduced risk of coronary heart disease: Is the effect due to beer, wine, or spirits? Br Med J 1996; 312: 731-6.         [ Links ]

9. Stampfer MJ, Colditz GA, Willet WC, Speizer FE, Hennekens CH. A prospective study of moderate alcohol consumption and the risk of coronary disease and stroke in women. N Engl J Med 1988; 319: 267-73.         [ Links ]

10. Truelsen T, Gronbaek M, Schnohr P, Boysen G. Intake of beer, wine, and spirits and risk of stroke: The Copenhagen City Heart Study. Stroke 1998; 12: 2467-72.         [ Links ]

11. Berger K, Ajani UA, Kase CS, et al. Light-to-moderate alcohol consumption and the risk of stroke among U.S. male physicians. N Engl J Med 1999; 341: 1557-64.         [ Links ]

12. Murray CJL, Lopez AD. Global mortality, disability, and the contribution of risk factors: Global Burden of Disease Study. Lancet 1997; 349: 1436-42.         [ Links ]

13. Gordon T, Doyle JT. Drinking and mortality. The Albany Study. Am J Epidemiol 1987; 125: 263-70.         [ Links ]

14. Thun MJ, Peto R, Lopez AD, et al. Alcohol consumption and mortality among middle-aged and elderly U.S. adults. N Engl J Med 1997; 337: 1705-14.         [ Links ]

15. Muntwyler J, Hennekens CH, Buring JE, Gaziano JM. Mortality and light to moderate alcohol consumption after myocardial infarction. Lancet 1998; 352: 1882-5.         [ Links ]

16. Shaper AG, Wannamethee SG. Alcohol intake and mortality in middle aged men with diagnosed coronary heart disease. Heart 2000; 83: 394-9.         [ Links ]

17. Klatsky AL, Armstrong MA, Friedman GD. Red wine, white wine, liquor, beer, and the risk for coronary artery disease hospitalization. Am J Cardiol 1997; 80: 416-20.         [ Links ]

18. Gronbaek M, Becker U, Johansen D, Tonnesen H, Jensen G, Sorensen TIA. Population based cohort study of the association between alcohol intake and cancer of the upper digestive tract. Br Med J 1998; 317: 844-7.         [ Links ]

19. Nanji AA. Alcohol and ischemic hearth disease: wine, beer or both? Int J Cardiol 1985; 8: 487-9.         [ Links ]

20. Renaud S, Lorgeril M. Wine, alcohol, platelets, and the French paradox for coronary heart disease. Lancet 1992; 339: 1523-6.         [ Links ]

21. Criqui MH, Ringel BL. Does diet or alcohol explain The French Paradox? Lancet 1994; 344: 1719-23.         [ Links ]

22. Nigdikar SV, Williams NR, Griffin BA, Howard AN. Consumption of red wine polyphenols reduces the suscebility of low-density lipoprotein oxidation in vivo. Am J Clin Nutr 1998; 68: 258-65.         [ Links ]

23. Hertog MGL, Feskens EJM, Hollman PCH, Katan MB, Kromhout D. Dietary antioxidant flavonoids and risk of coronary heart disease: the Zutphen Elderly Study. Lancet 1993; 342: 1007-11.         [ Links ]

24. Renaud S, Gueguen R, Siest G, et al. Wine, beer, and mortality in middle-aged men from Eastern France. Arch Intern Med 1999; 159: 1865-70.         [ Links ]

25. Evans AE, Ruidavets J, McCrum EE, et al. Autres pays, autres coeurs? Dietary patterns, risk factors and ischaemic heart disease in Belfast and Toulouse. Q J Med 1995; 88: 469-77.         [ Links ]

26. Wannamethee SG, Shaper AG. Type of alcoholic drink and risk of major heart disease events and all-cause-mortality. Am J Public Health 1999; 89: 685-90.         [ Links ]

27. de Lorgeril M, Salen P, Martin JL, Monjaud I, Delaye J, Mamelle N. Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: final report of the Lyon Diet Heart Study. Circulation 1999; 99: 779-85.         [ Links ]

28. Langer RD, Criqui MH, Reed DM. Lipoproteins and blood pressure as biological pathways for effect of moderate alcohol consumption on coronary heart disease. Circulation 1992; 85: 910-5.         [ Links ]

29. Ettinger PO, Wu CF, De La Cruz C. Arrhytmias and the holiday heart: Alcohol associated cardiac rhythm disorders. Am Heart J 1978; 95: 555-62.         [ Links ]

30. Hillbom M, Numminen H. Alcohol and stroke: pathophysiologic mechanisms. Neuroepidemiology 1998; 17: 281-7.         [ Links ]

31. Kauhanen J, Kaplan GA, Goldberg DE, Salonen JT. Beer binging and mortality: results from the Kuopio ischaemic heart disease risk factor study, a prospective population based study. Br Med J 1997; 315: 846-51.         [ Links ]

32. Hammar N, Romelsjö A, Alfredsson L. Alcohol consumption, drinking pattern and acute myocardial infarction. A case referent study based on the Swedish Twin Register. J Intern Med 1997; 241: 125-31.         [ Links ]

33. Hoidrup S, Gronbaek M, Gottschau A, Lauritzen JB, Schroll M. Alcohol intake, beverage preference, and risk of hip fracture in men and women. Am J Epidemiol 1999; 149: 993-1001.         [ Links ]

34. Law M, Wald M. Why heart disease mortality is low in France: the time lag explanation. Br Med J 1999; 318: 1471-80.         [ Links ]

35. Mänttäri M, Tenkanen L, Alikoski T, Manninen V. Alcohol and coronary heart disease: the roles o HDL-cholesterol and smoking. J Intern Med 1997; 241: 157-63.         [ Links ]

36. Savolainen MJ, Kesäniemi YA. Effects of alcohol on lipoproteins in relation to coronary heart disease. Curr Opin Lipidol 1995; 6: 243-50.         [ Links ]

37. Nishiwaki M, Ishikawa T, Ito T, et al. Effects of alcohol on lipoprotein lipase, hepatic lipase, cholesteryl ester transfer protein, and lecithin: cholesterol acyltranferase in high-density lipoprotein elevation. Atherosclerosis 1994; 111: 99-109.         [ Links ]

38. Brewster AC, Lankford HG, Schwartz MG, Sullivan JF. Ethanol and alimentary lipemia. Am J Clin Nutr 1966; 19: 255-9.         [ Links ]

39. Franceschini G, Moreno Y, Apebe L, et al. Alterations in high-density lipoprotein subfractions during postprandial lipidaemia induced by fat with and without ethanol. Clin Sci 1988; 75: 135-42.         [ Links ]

40. Patsch JR, Miesenböck G, Hopperwieser T, et al. Relation of triglyceride metabolism and coronary artery disease. Studies in the postprandial state. Arterioscl Thromb 1992; 12: 1336-45.         [ Links ]

41. Vogel RA, Corretti MC, Plotnick GD. Effect of a single high-fat meal on endothelial function in healthy subjects. Am J Cardiol 1997; 79: 350-4.         [ Links ]

42. Steinberg HO, Tarshoby M, Monestel R, et al. Elevated circulating free fatty acid levels impair endothelium-dependent vasodilation. J Clin Invest 1997; 100: 1230-9.         [ Links ]

43. Criscione L, Powell JR, Burdet R, Engesser S, Schlager F, Schoepfer A. Alcohol supresses endothelium-dependent relaxation in rat mesenteric vascular beds. Hypertension 1989; 13: 964-7.         [ Links ]

44. Iwase S, Matsukawa T, Ishihara S, et al. Effect of oral ethanol intake on muscle sympathetic nerve activity and cardiovascular functions in humans. J Autonom Nerv Syst 1995; 54: 206-14.         [ Links ]

45. Stein JH, Keevil JG, Wiebe DA, et al. Purple grape juice improves endothelial function and reduces the susceptibility of LDL cholesterol to oxidation in patients with coronary artery disease. Circulation 1999; 100: 1050-5.         [ Links ]

46. Flesch M, Schwarz A, Bohm M. Effects of red and white wine on endothelium-dependent vasorelaxation of rat aorta and human coronary arteries. Am J Physiol 1998; 275: H1183-90.         [ Links ]

47. Venkov CD, Myers PR, Tanner MA, Su M, Vaughan DE. Ethanol increases endothelial nitric oxide production through modulation of nitric oxide synthase expression. Thromb Haemost 1999; 81: 638-42.         [ Links ]

48. Renaud S, Beswick AD, Fehily AM, Sharp DS, Elwood PC. Alcohol and platelet aggregation: the Caerphilly Prospective Heart Study. Am J Clin Nutr 1992; 55: 1012-7.         [ Links ]

49. Ruf JC. Wine and polyphenols related to platelet aggregation and atherothrombosis. Drugs Exp Clin Res 1999; 25: 125-31.         [ Links ]

50. Laug WE. Ethyl alcohol enhances plasminogen activator secretion by endothelial cells. JAMA 1983; 250: 772-6.         [ Links ]

51. da Luz PL, Serrano Junior CV, Chacra AP, et al. The effect of red wine on experimental atherosclerosis: lipid-independent protection. Exp Mol Pathol 1999; 65: 150-9.         [ Links ]

52. Dyer AR, Cutter GR, Armstrong MA, et al. Alcohol intake and blood pressure in young adults: The Cardia Study. J Clin Epidemiol 1990; 43: 1-13.         [ Links ]

53. Witteman JC, Willet WC, Stampfer MJ, et al. Relation to moderate alcohol consuption and risk of systemic hypertension in women. Am J Cardiol 1990; 65: 633-7.         [ Links ]

54. Klatsky AL, Friedman GD, Siegelaub MS, Gérard MJ. Alcohol consumption and blood pressure. Kaiser-Permanente Multiphasic Health Examination Data. N Engl J Med 1977; 296: 1194-200.         [ Links ]

55. Maheswaran R, Gill JS, Davies P, Beevers DG. High blood pressure due to alcohol. A rapidly reversible effect. Hypertension 1991; 17: 787-92.         [ Links ]

56. Harburg E, Ozgoren F, Hawthorne VM, Schork MA. Community norms of alcohol usage and blood pressure: Tecumseh, Michigan. Am J Public Health 1980; 70: 813-20.         [ Links ]

57. Gordon T, Kannel WB. Drinking and its relation to smoking, BP, blood lipids, and uric acid. The Framinghan Study. Arch Intern Med 1983; 143: 1366-74.         [ Links ]

58. Riff DP, Jain AC, Doyle JT. Acute hemodynamic effects of ethanol on normal human volunteers. Am Heart J 1969; 78: 592-7.         [ Links ]

59. Pirwitz MJ, Lange RA, Willard JE, et al. Effects of intravenous ethanol on diameter of epicardial coronary arteries. Am J Cardiol 1995; 75: 77-9.         [ Links ]

60. Kawano Y, Abe H, Imanishi M, et al. Pressor and depressor hormones during alcohol-induced blood pressure reduction in hypertensive patients. J Hum Hypert 1996; 10: 595-9.         [ Links ]

61. Kawano Y, Abe H, Kojima S, et al. Acute depressor effect of alcohol in patients with essential hypertension. Hypertension 1992; 20: 219-26.         [ Links ]

62. Rosito GA, Fuchs FD, Duncan BB. Dose-dependent biphasic effect of ethanol on 24 hour blood pressure in normotensive subjects. Am J Hypertens 1998; 12: 236-41.         [ Links ]

63. Foppa M. Vinho com o almoço reduz a pressão arterial no período pós-prandial: Ensaio clínico randomizado em indivíduos obesos hipertensos. (Mestrado) Curso de Pós-Graduação em Medicina: Cardiologia UFRGS, 1998: 61p.         [ Links ]

64. Moreira LB, Fuchs FD, Moraes RS, Bredemeier M, Duncan BB. Alcohol intake and blood pressure: The importance of the time elapsed since the last drink. J Hyperten 1998; 16: 175-80.         [ Links ]

65. McGinnis J, Foege W. Actual causes of death in the United States. JAMA 1993; 270: 2207-12.         [ Links ]

66. Gordon T, Doyle JT. Alcohol consuption and its relationship to smoking, weight, blood pressure, and blood lipids. The Albany study. Arch Intern Med 1986; 146: 262-5.         [ Links ]

67. Rimm EB, Chan J, Stampfer MJ, Colditz GA, Willett WC. Prospective study of cigarette smoking, alcohol use, and the risk of diabetes in men. Lancet 1995; 310: 555-9.         [ Links ]

68. Istvan J, Murray R, Voelker H. The relationship between patterns of alcohol consumption and body weight. Int J Epidemiol 1995; 24: 543-6.         [ Links ]

69. Liu S, Serdula MK, Williamson DF, Mokdad AH, Byers T. A prospective study of alcohol intake and change in body weight among US adults. Am J Epidemiol 1994; 140: 912-20.         [ Links ]

70. Duncan BB, Chambless LE, Schmidt MI, et al. Association of the waist-to-hip ratio is different with wine than with beer or hard liquor consumption. Am J Epidemiol 1995; 142: 1-6.         [ Links ]

71. Cordain L, Bryan ED, Melby CL, Smith MJ. Influence of moderate daily wine comsuption on body weight regulation and metabolism in healthy free-living males. J Am Coll Nutr 1997; 16: 134-9.         [ Links ]

72. Suter PM, Jequier E, Schutz Y. Effect of ethanol on energy expenditure. Am J Physiol 1994; 266: R1204-12.         [ Links ]

73. Clevidence BA, Taylor PR, Campbell WS, Judd JT. Lean and heavy women may not use energy from alcohol with equal efficiency. J Nutr 1995; 125: 2536-40.         [ Links ]

74. Lands WEM. Alcohol and energy intake. Am J Clin Nutr 1995; 62: 1101 S-6 S.         [ Links ]

75. Stampfer MJ, Colditz GA, Willet WC, et al. A prospective study of moderate alcohol drinking and risk of diabetes in women. Am J Epidemiol 1988; 128: 549-58.         [ Links ]

76. Mayer EJ, Newman B, Quesenberry CP Jr, Friedman GD, Selby JV. Alcohol consuption and insulin concentrations. Role of insulin in associations of alcohol intake with high-density lipoprotein cholesterol and triglycerides. Circulation 1993; 88: 2190-7.         [ Links ]

77. Kiechl S, Willeit J, Poewe W, et al. Insulin sensitivity and regular alcohol consumption: large, prospective, cross sectional population study (Bruneck study). Br Med J 1996; 313: 1040-4.         [ Links ]

78. Lazarus R, Sparrow D, Weiss ST. Alcohol intake and insulin levels. The Normative Aging Study. Am J Epidemiol 1997; 145: 909-16.         [ Links ]

79. Facchini F, Ida Chen Y, Reaven GM. Light-to-moderate alcohol intake is associated with enhanced insulin sensitivity. Diabetes Care 1994; 17: 115-9.         [ Links ]

80. Baron AD. Insulin and vasculature-old actors, new roles. J Investig Med 1996; 44: 406-12.         [ Links ]

81. Ben G, Gnudi L, Maran A, et al. Effects of chronic alcohol intake on carbohydrate and lipid metabolism in subjects with type II (non-insulin-dependent) diabetes. Am J Med 1996; 90: 70-6.         [ Links ]

82. Singh SP, Kumar Y, Snyder AK, Ellyin FE, Gilden JL. Effect of alcohol on glucose tolerance in normal and noninsulin-dependent diabetic subjects. Alcoholism 1988; 12: 727-30.         [ Links ]

83. Koivisto VA, Tulokas S, Toivonem M, Haapa E, Pelkonen R. Alcohol with a meal has no adverse effects on postprandial glucose homeostasis in diabetic patients. Diabetes Care 1993; 16: 1612-4.         [ Links ]

84. Valmadrid CT, Klein R, Moss SE, Klein BEK, Cruickshanks KJ. Alcohol intake and the risk of coronary heart disease mortality in persons with older-onset Diabetes Mellitus. JAMA 1999; 282: 239-46.         [ Links ]

85. Kiechl S, Willeit J, Egger G, Oberhollenzer M, Aichner F. Alcohol consumption and carotid atherosclerosis: Evidence of dose-dependent atherogenic and antiatherogenic effects. Results from the Bruneck Study. Stroke 1994; 25: 1593-8.         [ Links ]

86. Demirovic J, Nabulsi A, Folsom AR, et al. Alcohol consumption and ultrasonographically assessed carotid artery wall thickness and distensibility. The Atherosclerosis Risk in Communities (ARIC) Study Investigators. Circulation 1993; 88:2787-93.         [ Links ]



Hospital de Clínicas de Porto Alegre and Universidade Federal do Rio Grande do Sul
Mailing address: Murilo Foppa - Rua Ramiro Barcelos, 2600/414 - 90035-003 - Porto Alegre, RS, Brazil
English version by Stela Maris C. Gandour

Creative Commons License All the contents of this journal, except where otherwise noted, is licensed under a Creative Commons Attribution License