Background Previous studies have suggested that moderate alcoholintake exerts a protective effect against coronary heart disease.Alterations in plasma lipoprotein levels represent one plausiblemechanism of this apparent protective effect.
Methods We therefore examined the interrelation among alcoholconsumption, plasma lipoprotein levels, and the risk of myocardialinfarction in 340 patients who had had myocardial infarctionsand an equal number of age- and sex-matched controls. The casepatients were men or women less than 76 years of age with nohistory of coronary disease who were discharged from one ofsix hospitals in the Boston area with a diagnosis of a confirmedmyocardial infarction. Alcohol consumption was estimated bymeans of a food-frequency questionnaire.
Results We observed a significant inverse association betweenalcohol consumption and the risk of myocardial infarction (Pfor trend, <0.001 after control for known coronary risk factors).In multivariate analyses, the relative risk for the highestintake category (subjects who consumed three or more drinksper day) as compared with the lowest (those who had less thanone drink a month) was 0.45 (95 percent confidence interval,0.26 to 0.80). The levels of total high-density lipoproteincholesterol (HDL) and its HDL2 and HDL3 subfractions were stronglyassociated with alcohol consumption (P for trend, <0.001for each). The addition of HDL or either of its subfractionsto the multivariate model substantially reduced the inverseassociation between alcohol intake and myocardial infarction,whereas the addition of the other plasma lipid measurementsdid not materially alter the relation.
Conclusions These data confirm the inverse association of moderatealcohol intake with the risk of myocardial infarction and supportthe view that the effect is mediated, in large part, by increasesin both HDL2 and HDL3.
The effects of alcohol consumption on cardiovascular diseaseare complex. Although heavy alcohol intake increases overallmortality1,2,3,4 and mortality due to cardiovascular diseases,3,4,5,6moderate intake appears to exert a protective effect againstcoronary heart disease, as compared with drinking no alcohol7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22.
The mechanisms by which moderate alcohol intake exerts thisprotective effect are not well understood. Alcohol intake raisesthe levels of high-density lipoprotein cholesterol (HDL),23,24,25,26,27,28,29a fact that may explain, at least in part, its apparent protectiveeffect against coronary heart disease30,31,32,33. However, previousstudies with small numbers of subjects have had apparently inconsistentfindings with respect to relations among alcohol, HDL levels,and myocardial infarction. Specifically, when subfractions ofHDL were examined, the inverse relation between the HDL2 subfractionand the risk of myocardial infarction was clearly demonstrated,whereas the data on the role of HDL3 were less consistent34,35,36.Moreover, evidence from small studies appeared to indicate thatmoderate alcohol consumption raised the level of HDL3 but notHDL237,38,39. More recently, in data from both the present case-controlstudy40 and a prospective cohort study,41 the levels of bothsubfractions have been shown to be independent predictors ofmyocardial infarction. In this case-control study, we examinedthe extent to which plasma lipoprotein levels, including thoseof HDL and its subfractions, mediate the relation between alcoholconsumption and the risk of myocardial infarction.
Methods
We reviewed all admissions between January 1, 1982, and December31, 1983, to the coronary care units and other intensive careunits of six suburban Boston hospitals (Emerson Hospital, FraminghamUnion Hospital, Leonard Morse Hospital, Mount Auburn Hospital,Newton-Wellesley Hospital, and Waltham-Weston Hospital) to identifyeligible patients. Those eligible for inclusion were white menor women less than 76 years of age who lived in the Boston areaand had no history of previous myocardial infarction or anginapectoris, in whom symptoms of myocardial infarction had begunduring the 24 hours before admission. Patients with a diagnosisof confirmed myocardial infarction, based on the clinical historyand an increased creatine kinase concentration, who were dischargedalive were enrolled in the study if they were willing and ableto participate and if informed consent could be obtained fromboth the patient and the admitting physician. The research protocolwas approved by the institutional human-subjects committeesof all the participating hospitals.
For each case patient, a control was chosen at random from thelist of residents of the town in which the patient lived. Morespecifically, the name of the case patient was located in theappropriate residence list of the town where the case patientlived, and the next resident of the same sex and age (withinfive years) who had a listed telephone number was selected asa control. Potentially eligible subjects were sent letters ofinvitation and then contacted by telephone. Of the eligiblesubjects contacted, 84 percent of the case patients and 60 percentof the controls were enrolled, yielding a total of 340 case-controlpairs.
All case patients and controls were interviewed in their homes.The patients were interviewed approximately eight weeks aftermyocardial infarction. Information was collected on a wide varietyof potential coronary risk factors during the period beforethe myocardial infarction (for the case patients) and beforethe interview (for the controls). This information covered age,sex, hypertension, cigarette smoking, body-mass index, familyhistory of premature myocardial infarction (at less than 60years of age), dietary intake, psychological variables, socioeconomicstatus, level of physical activity, and alcohol consumption.Information on diet and alcohol consumption was gathered bymeans of a semiquantitative food-frequency questionnaire42,43.Psychological variables were measured with the use of 18 questionsfrom the Framingham Heart Study (10 assessing type A behavior,7 assessing anger, and 1 regarding the number of promotionsover the past 10 years)44. Information on socioeconomic statusincluded the subject's usual occupation and his or her educationallevel. Fasting venous blood samples were obtained and analyzedfor lipids, including total HDL cholesterol and its HDL2 andHDL3 subfractions.
Total daily intake of alcohol was estimated on the basis ofinformation about the consumption of beer, wine, and liquorduring the year before the myocardial infarction, for the casepatients, and the year before the interview, for the controls.Daily intake was estimated in grams according to the averagenumber of grams of ethanol in a serving of each type of alcoholicbeverage (beer, 13.2 g; wine, 10.8 g; liquor, 15.1 g). Totaldaily intake was then converted into the number of drinks perday by dividing the total daily consumption in grams by 13.2g per drink (the ethanol content of one serving of beer). Fourcategories of alcohol intake were defined: less than one drinkper month, one or more drinks per month but less than one perday, one or more drinks per day but less than three per day,and three or more drinks per day. Although the fourth categoryincluded heavy drinkers (defined as those with an average dailyconsumption of five or more drinks per day), there were relativelyfew such subjects (n = 38).
Fasting venous blood was drawn into tubes containing 0.1 percentEDTA, and plasma was obtained by centrifugation at 3000 rpmfor 30 minutes at 4 °C. Fresh plasma was used to determinethe levels of total cholesterol, HDL, low-density lipoproteincholesterol (LDL), very-low-density lipoprotein cholesterol(VLDL), and triglycerides by the methods of the Lipid ResearchClinics45,46,47. Cholesterol determinations were standardizedwith the Lipid Standardization Program of the Centers for DiseaseControl and Prevention. HDL subfractions were measured in fresh,unfrozen plasma from a subgroup of 558 subjects (283 case patientsand 275 controls) by the dextran sulfate method of Gidez etal48. Apolipoproteins A-I, A-II, B, and E were measured withspecific radioimmunoassays in samples from a total of 346 subjects(206 case patients and 140 controls)49,50,51,52. Plasma samplesfor apolipoprotein analyses had been stored at -70 °C forless than one year, with virtually identical storage times forthose from case patients and controls.
Matched-pair and crude unmatched relative risks were calculated53.Since these were virtually identical, we judged that the matchingcould safely be disregarded and thereafter performed unmatchedanalyses. Although the results of our analyses with and withoutformer drinkers were not materially different, many subjectswho had recently stopped drinking may have been heavy consumersin the past, so the 19 subjects who reported ceasing alcoholconsumption within the past two years were excluded. Relativerisks were calculated for each of the three highest categoriesof alcohol consumption as compared with the lowest intake category.
Multiple logistic-regression analyses were used to estimaterelative risks, with simultaneous control for a number of coronaryrisk factors54. Logistic regression was used in tests for trend.To determine the degree to which the levels of various lipidsmediated any effect of alcohol, the levels of total cholesterol,LDL, triglycerides, VLDL, HDL, HDL2, HDL3, and the ratio ofHDL2 to HDL3 were added to the risk-factor model one at a time.Logistic-regression models were compared with the likelihood-ratiotest. Similarly, we added the levels of apolipoproteins A-I,A-II, B, and E sequentially to a model containing the coronaryrisk factors and total HDL in order to determine the degreeto which apolipoproteins mediate the effect of alcohol, beyondthe effect of HDL.
Results
Base-line characteristics of the case patients and controlsare shown in Table 1. The coronary risk factors for each drinkingcategory among the controls are shown in Table 2. The heavierdrinkers were more likely to be men, to smoke cigarettes, toengage in physical activity, and to have a higher total caloricintake and were less likely to have diabetes.
Table 2. Coronary Risk Factors among the Controls, According to Alcohol Consumption.
Adjusted relative risks for each intake category, as comparedwith the reference category, are shown in Table 3. The relativerisks of myocardial infarction, adjusted for age and sex, weresignificantly reduced in the two highest alcohol-consumptioncategories. Specifically, the relative risk was 0.50 (95 percentconfidence interval, 0.33 to 0.78) among those who consumedmore than one but fewer than three drinks per day and 0.49 (95percent confidence interval, 0.29 to 0.81) among those who consumedthree or more drinks per day. The test for trend across alcohol-consumptioncategories was highly significant (P for trend, <0.001).Controlling for coronary risk factors in the logistic-regressionanalyses did not materially alter the results. Lipoprotein levelsand complete data on risk factors were available for 541 subjects,after subjects who had recently stopped drinking were excluded.The results in this subgroup did not differ materially fromthose of the full model.
Table 3. Relative Risk of Myocardial Infarction, According to Alcohol Consumption.
The relations between alcohol consumption and lipoprotein levelsare shown in Table 4. Total HDL, as well as both HDL2 and HDL3,were strongly associated with alcohol consumption, whereas nosuch relation was apparent for total cholesterol, LDL, VLDL,or triglycerides. To determine the extent to which the reducedrisk of myocardial infarction was mediated by lipids, each lipoproteinmeasurement was added individually to the risk-factor model.The addition of the total cholesterol, LDL, VLDL, and triglyceridelevels did not substantially alter the relation between alcoholand myocardial infarction (Table 5). However, the apparent reductionsin risk in the two highest categories for alcohol intake weresubstantially attenuated by the addition of total HDL, HDL2,HDL3, or both HDL2 and HDL3 to the model. Each subfraction appearedto have an independent attenuating effect. Thus, the apparentprotective effect of moderate alcohol consumption appeared tobe mediated, in large part, by both the HDL2 and HDL3 subfractions.
Table 5. Adjusted Relative Risk of Myocardial Infarction among Subjects Whose Lipid Levels Were Measured, According to Alcohol Consumption.
Apolipoproteins A-I and A-II were also positively associatedwith alcohol consumption (P for trend, <0.001 for both A-Iand A-II), whereas there was no such relation for apolipoproteinsB and E. To determine whether the apparent risk reduction associatedwith moderate alcohol intake was further mediated by apolipoproteinlevels, we added each apolipoprotein to the risk-factor modelalong with total HDL; adding the HDL2 or HDL3 subfraction didnot significantly improve the model that included total HDL,according to the log-likelihood-ratio test (chi-square withone degree of freedom = 1.52, P = 0.22). The addition of apolipoproteinsA-I and A-II did significantly improve the model and appearedto further attenuate the effect of alcohol consumption in thehighest intake category. However, the sample size (n = 337)was relatively small, and the wide confidence intervals makethese findings difficult to interpret. Specifically, the relativerisk, adjusted for risk factors and the total HDL level, amongsubjects in the highest intake category as compared with thosein the lowest changed from 0.85 (95 percent confidence interval,0.35 to 2.05) to 0.94 (95 percent confidence interval, 0.38to 2.33) after the addition of apolipoprotein A-I and to 1.08(95 percent confidence interval, 0.42 to 2.77) after the additionof apolipoprotein A-II to the model. The addition of apolipoproteinB or apolipoprotein E did not materially alter the relation.
Discussion
These data indicate a significant inverse relation between alcoholconsumption and the risk of myocardial infarction, even afterthe effects of other coronary risk factors have been taken intoaccount. In addition, we found that alcohol consumption wasassociated with increased levels of HDL2 and HDL3, and thatboth subfractions were associated with decreased risks of myocardialinfarction40. Thus, these data suggest a beneficial effect ofalcohol consumption on the risk of myocardial infarction thatis mediated in large part by alterations in lipoprotein levels-- in particular, by increases in both HDL subfractions. Therewas also a suggestion that the beneficial effect might be furthermediated by increases in the levels of apolipoprotein A-I andA-II, but our data were insufficient to confirm this relation.Other potential contributing mechanisms, including alterationsin hemostasis, could not be evaluated in this study.
A consistent body of evidence now supports the hypothesis thatmoderate alcohol intake reduces the risk of coronary heart disease8,9,10,11,12,13,14,15,16,22.Shaper et al. have suggested that the inverse association isdue to the contamination of the nondrinking category with subjectswho have reduced their drinking because of existing coronaryheart disease55. However, this phenomenon would not explainthe apparent dose-response relation reported in most studies.In our study, none of the case patients or controls were knownto have preexisting coronary heart disease, and former drinkerswho had recently stopped drinking were excluded from the analyses,so it is unlikely that this potential source of bias had anyeffect on our results. A U-shaped relation between alcohol consumptionand coronary heart disease has been reported, with the lowestrisks observed among moderate drinkers and the highest risksamong heavy drinkers (defined as those consuming five or morealcoholic drinks per day)17,18,19,20. However, the current populationdid not include enough heavy drinkers for us to assess adequatelythe risk among heavy drinkers.
The evidence from both observational studies24,25,26,27,28,29,56and experimental trials28,29 suggests that alcohol raises thelevel of total HDL, and that approximately 50 percent of thereduction in risk attributable to alcohol consumption is explainedby the changes in total HDL26,27. The effect of alcohol consumptionon the HDL subfractions is far less consistent; short-term trials39and observational data37,38 among moderate drinkers supportan association only with HDL3, whereas studies among alcoholicsubjects have found evidence of increases in both subfractions57,58,59,60,61.Our study provides strong support for the hypothesis that levelsof both HDL2 and HDL3 are increased by alcohol consumption andthat increases in each subfraction decrease the risk of myocardialinfarction. The apparent discrepancies among the reported resultsmay reflect separate mechanisms for alcohol-induced alterationsin each subfraction, though speculation about the specific mechanismsare beyond the scope of our study. With regard to apolipoproteins,increases in both A-I and A-II have been consistently associatedwith moderate alcohol intake, as demonstrated in our study37,62,63,64.However, the degree to which the protective effect of alcoholis mediated by apolipoproteins A-I and A-II, beyond the effectof HDL, remains unclear.
Several limitations should be considered in interpreting theseresults. First, only survivors of myocardial infarction wereincluded in this study because of our need to obtain informationon a large number of lifestyle variables as well as to allowtransient alterations in lipoprotein levels to return to normalbefore plasma samples were obtained. As a result, we have probablyunderestimated the effect of many coronary risk factors becauseof our selection of the healthiest patients with myocardialinfarction.
Second, although the choice of neighborhood rather than hospitalcontrols had the advantage of providing a comparison group morelikely to have come from the same population as the case patients,there was, as expected, a higher response rate among case patientsthan among controls. Nonresponse could, in theory, have biasedour results, yet it seems unlikely that this occurred to anyappreciable degree. The response rate among the controls variedamong the neighborhoods of the six hospitals, and the observedassociations were not appreciably different between those withhigher response rates and those with lower rates. Furthermore,our results for other well-documented cardiovascular risk factorswere consistent with those observed in previous studies.
With respect to potential confounding, one of the strengthsof this study is that we were able to collect information ona wide variety of potential coronary risk factors, includingdemographic characteristics, medical history, and behavioralvariables. Although it is possible that residual confoundingby unmeasured factors could have affected the results, it isunlikely to have been extensive, since accounting for the largenumber of risk factors for which information was available didnot materially affect the results.
The timing of blood collection could have affected lipid levels,since myocardial infarction is known to affect lipid metabolismin the short term. For this reason, we used blood specimenscollected about eight weeks after hospital discharge, ratherthan samples drawn in the hospital. Several interventions aftermyocardial infarction may have altered lipid levels, includingdietary modifications, exercise, and treatment for elevatedcholesterol levels, as well as the use of beta-blockers or thiazidediuretics. Thus, confounding by the effects of interventionsafter myocardial infarction cannot be excluded. The overallresult of these interventions would probably have been onlyslight increases in HDL levels among the case patients. IncreasingHDL levels in the case patients would have caused us to underestimatethe true association between this lipoprotein and the risk ofmyocardial infarction and thus to minimize the attenuation ofthe alcohol effect by HDL levels. We could not control for drugtreatment or other interventions after myocardial infarctionsince the information collected from case patients covered theyear before the event, not the period after discharge. However,adjustment for previous treatment for elevated cholesterol levels,as well as for the use of beta-blocker and thiazide drugs, didnot materially alter the results.
The data on alcohol intake were collected for the year beforemyocardial infarction for the case patients, and changes inalcohol consumption after myocardial infarction could have affectedthe results. It is unlikely that subjects would have increasedtheir alcohol intake for health reasons in the early 1980s.Cessation of alcohol consumption after myocardial infarction,with a subsequent reduction in the HDL cholesterol level, wouldhave biased our results regarding the effect of HDL toward afinding of no effect. Furthermore, analyses were conducted inwhich subjects who reported stopping alcohol use within thepast two years were excluded; the results were not materiallydifferent.
In summary, this case-control study demonstrates a significantinverse association between alcohol consumption and the riskof myocardial infarction. Our results also strongly suggestthat the observed protective effect is mediated, in large part,by changes in HDL levels and more specifically by the levelsof both the HDL2 and HDL3 subfractions, although other contributingmechanisms of action have not been excluded. Although we judgethe association to be causal, any public health recommendationsor recommendations for individual patients must take into accountthe complexity of the metabolic, physiologic, and psychologicaleffects of alcohol. With alcohol, the differences between dailysmall-to-moderate amounts and large quantities may be the differencebetween preventing and causing disease. Finally, heavy alcoholconsumption is a leading avoidable cause of death in the UnitedStates. Thus, an important implication of these data, whichdemonstrate that the benefit of alcohol levels on myocardialinfarction is mediated in large part by increases in HDL, isthat further research should be directed to finding safer methodsof raising the level of this lipid.
Supported by research grants (HL-24423 and HL-21006) and aninstitutional training grant (HL-07575) from the National Heart,Lung, and Blood Institute.
We are indebted to the six hospitals in the Boston area thatparticipated in this study and to the respective collaborators:Emerson Hospital (Marvin H. Kendrick, M.D.), Framingham UnionHospital (Marvin Adner, M.D., and Gerald Evans, M.D.), LeonardMorse Hospital (L. Frederick Kaplan, M.D.), Mount Auburn Hospital(Leonard Zir, M.D.), Newton-Wellesley Hospital (James Sidd,M.D.), and Waltham-Weston Hospital (Solomon Gabbay, M.D.); weare also indebted to Peter Herbert and Conrad Blum for performingthe apolipoprotein analyses, and to Anne Cadigan for assistancein the preparation of the manuscript.
Source Information
From the Division of Preventive Medicine (J.M.G., J.E.B., M.V., C.H.H.), the Channing Laboratory (S.Z.G., B.R., W.W.), and the Cardiovascular Division (J.M.G., S.Z.G.), Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston; the Department of Ambulatory Care and Prevention, Harvard Medical School, Boston (J.E.B., C.H.H.); the Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston (W.W.); the Department of Medicine, Veterans Affairs Medical Center, West Roxbury, Mass. (J.M.G.); and the Laboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York (J.L.B.).
Address reprint requests to Dr. Gaziano at Brigham and Women's Hospital, 900 Commonwealth Ave. East, Boston, MA 02215-1204.
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