Published online before print April 24, 2006, doi: 10.1161/CIRCULATIONAHA.105.598664
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(Circulation. 2006;113:2045-2053.)
© 2006 American Heart Association, Inc.
Coronary Heart Disease |
Coffee Consumption and Coronary Heart Disease in Men and Women
A Prospective Cohort Study
From the Departments of Nutrition (E.L.-G., R.M.v.D., W.C.W., E.B.R., M.J.S., F.B.H.) and Epidemiology (W.C.W., E.B.R., J.E.M., M.J.S., F.B.H.), Harvard School of Public Health; the Channing Laboratory (W.C.W., E.B.R., J.E.M., M.J.S., F.B.H.) and Division of Preventive Medicine (J.E.M., M.J.S., K.M.R.), Harvard Medical School, Boston, Mass.
Reprint requests to Dr Frank B. Hu, Departments of Nutrition and Epidemiology, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115. E-mail nhbfh{at}channing.harvard.edu
Received October 31, 2005; revision received February 3, 2006; accepted February 24, 2006.
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Abstract |
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Background— We examined the association between long-term habitual coffee consumption and risk of coronary heart disease (CHD).
Methods and Results— We performed a prospective cohort study with 44 005 men and 84 488 women without history of cardiovascular disease or cancer. Coffee consumption was first assessed in 1986 for men and in 1980 for women and then repeatedly every 2 to 4 years; the follow-up continued through 2000. We documented 2173 incident cases of coronary heart disease (1449 nonfatal myocardial infarctions and 724 fatal cases of CHD) among men and 2254 cases (1561 nonfatal myocardial infarctions and 693 fatal cases of CHD) among women. Among men, after adjustment for age, smoking, and other CHD risk factors, the relative risks (RRs) of CHD across categories of cumulative coffee consumption (<1 cup/mo, 1 cup/mo to 4 cups/wk, 5 to 7 cups/wk, 2 to 3 cups/d, 4 to 5 cups/d, and 
6 cups/d) were 1.0, 1.04 (95% confidence interval 0.91 to 1.17), 1.02 (0.91 to 1.15), 0.97 (0.86 to 1.11), 1.07 (0.88 to 1.31), and 0.72 (0.49 to 1.07; P for trend=0.41); among women, the RRs were 1.0, 0.97 (0.83 to 1.14), 1.02 (0.90 to 1.17), 0.84 (0.74 to 0.97), 0.99 (0.83 to 1.17), and 0.87 (0.68 to 1.11; P for trend=0.08). Stratification by smoking status, alcohol consumption, history of type 2 diabetes mellitus, and body mass index gave similar results. Similarly, we found no effect when the most recent coffee consumption was examined. RRs for quintiles of caffeine intake varied from 0.97 (0.84 to 1.10) in the second quintile to 0.97 (0.84 to 1.11) in the highest quintile (P for trend=0.82) in men and from 1.02 (0.90 to 1.16) to 0.97 (0.85 to 1.11; P for trend=0.37) in women.
Conclusions— These data do not provide any evidence that coffee consumption increases the risk of CHD.
Key Words: diet • coronary disease • epidemiology • nutrition • risk factors
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Introduction |
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The relation between coffee consumption and cardiovascular disease has been studied extensively. Although many previous cohort studies found no significant association between coffee and coronary heart disease (CHD),1–4 more recent results have been inconsistent. Although case-control studies found a positive association between coffee consumption and risk of CHD,5,6 prospective cohort studies reported a lower risk among individuals with higher coffee consumption.7,8 In addition, other studies suggested that both high and low coffee intake were associated with an increase in the risk of CHD compared with moderate coffee consumption.9,10
Clinical Perspective p 2053
In view of these discrepancies and recent findings that coffee consumption may protect against diabetes mellitus,11–15 we extended our previous analysis4,16 and assessed the association between coffee consumption and risk of CHD in 2 ongoing large cohort studies of men and women. We also examined whether the association between coffee consumption and CHD was modified by the presence of type 2 diabetes mellitus, smoking, alcohol consumption, or obesity. The long duration of follow-up (14 years for men and 20 years for women) and the use of repeated measurements allowed us to assess both the short- and long-term effects of coffee.
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Methods |
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Study Population
The Health Professionals Follow-up Study (HPFS) was established in 1986 and the Nurses’ Health Study (NHS) in 1976. Information on the cohorts has been updated every 2 years. Further details have been published elsewhere.17 In the present study, after excluding participants with cardiovascular disease or cancer at baseline, we obtained 44 005 men and 84 488 women who were followed up until 2000. The Harvard School of Public Health and Brigham and Women’s Hospital Human Subjects Committee Review Board approved the study protocol.
Assessment of Coffee Consumption
Dietary questionnaires were sent to the HPFS participants in 1986, 1990, 1994, and 1998 and to the NHS participants in 1980, 1984, 1986, 1990, 1994, and 1998. On each questionnaire, participants were asked how often on average during the previous year they had consumed coffee and tea. The participants could choose from 9 responses. The method of coffee preparation was assessed only in 1990 in both studies. Decaffeinated coffee and different types of caffeinated soft drinks were first assessed in 1986 in the HPFS and in 1984 in the NHS. In addition, we also inquired in the NHS questionnaire of 1980 whether the participant’s consumption for each beverage had greatly increased or decreased over the past 10 years. Using the US Department of Agriculture food composition sources, supplemented with other sources, we estimated that the caffeine content was 137 mg per cup of coffee, 47 mg per cup of tea, 46 mg per can or bottle of cola beverage, and 7 mg per serving of chocolate candy. We assessed the total intake of caffeine by summing the caffeine content for a specific amount of each food during the previous year (1 cup for coffee or tea, one 12-ounce bottle or can for carbonated beverages, and 1 ounce for chocolate) multiplied by a weight proportional to the frequency of its use. In our validation study, we obtained high correlations between consumption of coffee and other caffeinated beverages estimated from the food frequency questionnaire and consumption estimated from repeated 1-week diet records (coffee, r=0.78; tea, r=0.93; and caffeinated sodas, r=0.85).18
Assessment of Nonfatal Myocardial Infarction and Fatal CHD
The primary end point for this analysis was CHD, which included symptomatic nonfatal myocardial infarction (MI) or fatal CHD that occurred after the return of the 1986 questionnaire in men and the 1980 questionnaire in women but before June 1, 2000. We requested permission to review medical records from subjects who reported having a nonfatal MI on a follow-up questionnaire. Physicians unaware of the self-reported risk factor status systematically reviewed the records. MI was classified as confirmed if the criteria of the World Health Organization were met, specifically, symptoms and either ECG changes or elevated cardiac enzyme levels.19 We included confirmed and probable cases for the analyses. Deaths were identified from state vital statistics records and the National Death Index or reported by the families and the postal system. Fatal CHD was considered to have occurred if fatal MI was confirmed by hospital records or an autopsy or if CHD was listed as the cause of death on the death certificate, if it was listed as an underlying and the most plausible cause of death, and if evidence of previous CHD was available.
Assessment of Medical History, Anthropometric Data, and Lifestyle Factors
On the baseline questionnaires, we requested information about age, weight, and height; smoking status; parental history of MI; use of hormone therapy in women; and personal history of MI and other diseases. This information, with the exception of height and parental history of MI, has been updated on the biennial follow-up questionnaires. Body mass index (BMI) was calculated as weight in kilograms divided by the square of height in meters. Physical activity was assessed biennially. In the HPFS, participants were queried about the average time spent per week during the preceding year in specific activities (eg, walking outdoors, jogging, and bicycling).20 The time spent in each activity in hours per week was multiplied by its typical energy expenditure, expressed in metabolic equivalent tasks (METs) and then summed over all activities to yield a METs/h score. In the NHS, physical activity was reported in hours per week of moderate (eg, brisk walking) and vigorous (eg, strenuous sports and jogging) exercise.21 Standard portion sizes for alcoholic drinks were specified as a can/bottle or glass for beer, 4-oz glass for wine, and 1 drink or shot for liquor. Detailed information on the validity and reproducibility of the questionnaire has been reported elsewhere.18,22–25
Statistical Analyses
Participants were classified according to levels of coffee consumption. Person-years of exposure were calculated from the date of return of the baseline questionnaire to the date of nonfatal MI, fatal CHD, or June 1, 2000, whichever came first. For individuals who developed a nonfatal MI and later died of fatal CHD during the follow-up, we only included follow-up time to the nonfatal event in the overall analysis to avoid double counting. Participants who had a nonfatal MI and later died of CHD within the same 2-year period were counted only for the fatal event.
Sex-specific Cox regression models were used to investigate the association between coffee consumption and incidence of CHD events. Hazard ratios were used to estimate relative risks (RRs). To reduce within-subject variation and best represent long-term diet, we used the cumulative average of dietary intakes from all available dietary questionnaires up to the start of each 2-year follow-up interval26; for example, the average of the 1986 and 1990 intake was used for the follow-up between 1990 and 1994, and the average of the 1986, 1990, and 1994 intake was used for the follow-up between 1994 and 1998. In alternative analyses, we also used simple updating (the most recent information on coffee consumption before the event) to study short-term effects of coffee on CHD.
Physical activity, alcohol intake, BMI, smoking status, and use of hormone therapy, aspirin, multivitamin supplements, and vitamin E supplements were also updated during follow-up with the most recent data for each 2-year interval. Models were first adjusted for age and smoking status. Furthermore, we adjusted for BMI, physical activity, alcohol intake, use of hormone therapy for women, parental history of MI, aspirin use, multivitamin use, vitamin E supplement use, and history of hypertension, hypercholesterolemia, and diabetes mellitus at baseline. To test for linear trends across categories, we modeled coffee consumption as a continuous variable in the models with the median value of each level of coffee consumption. Stratified analyses were conducted according to smoking status, alcohol consumption, history of diabetes mellitus, and BMI. We studied the association between caffeine intake, decaffeinated coffee and tea consumption, and CHD. We also examined separately the effect of filtered and non–paper-filtered (espresso/percolator) coffee on CHD.
As a complementary study, we examined the association of caffeinated and decaffeinated coffee and plasma levels of total, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol. We conducted these analyses in men and women who were selected as control subjects in 2 previous nested case-control studies of MI.27 Blood samples were collected in 1990 in women and 1994 in men; therefore, we used dietary information from the 1990 food frequency questionnaire for women and from the 1994 food frequency questionnaire for men. We calculated multivariable-adjusted means of plasma cholesterol levels across categories of consumption. All analyses were performed with SAS software, version 8.2 (SAS Institute Inc, Cary, NC).
The authors had full access to the data and take responsibility for its integrity. All authors have read and agree to the manuscript as written.
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Results |
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During 14 years of follow-up in the HPFS, we documented 2173 cases of CHD, including 1449 nonfatal MIs and 724 fatal CHD events. During 20 years of follow-up in the NHS, we documented 2254 cases of CHD (1561 nonfatal MIs and 693 fatal CHD events). Characteristics of the population are presented by levels of coffee consumption in Table 1. Frequent coffee consumption was strongly associated with smoking: 30% of the men and more than half of the women who drank
6 cups/d also smoked cigarettes. In addition, individuals who drank more coffee were more likely to drink alcohol and to use aspirin and less likely to drink tea, to exercise, and to use multivitamin and vitamin E supplements.
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In age-adjusted analyses, we found no significant association between long-term coffee consumption and risk of CHD for men but a positive association for women (Table 2). However, when we further adjusted for smoking status, the positive association in women disappeared, which suggests that the age-adjusted results were strongly confounded by smoking. After multivariable adjustment, the RRs were somewhat attenuated. Additional adjustment for total energy intake, glycemic load, cereal fiber, folate, and polyunsaturated, saturated, trans, and n-3 fatty acids did not appreciably alter the results. Interestingly, the consumption of 6 cups/d of coffee was associated with a slightly lower risk of fatal CHD in both men (RR 0.60, 95% confidence interval [CI] 0.26 to 1.36) and women (RR 0.61 95% CI 0.37 to 1.02); the pooled RRs across categories of coffee consumption were 1.0, 1.06 (95% CI 0.90 to 1.26), 1.04 (95% CI 0.89 to 1.21), 0.93 (95% CI 0.79 to 1.09), 1.01 (95% CI 0.81 to 1.28), and 0.61 (95% CI 0.39 to 0.93).
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The null association between coffee and CHD was independent of smoking status (Table 3; Figure; P for interaction=0.51 in men and P=0.96 in women) and alcohol consumption (P for interaction=0.32 in men and P=0.90 in women). The association was also similar for participants with and without type 2 diabetes mellitus and for obese (BMI 30 kg/m2) and nonobese participants (Table 3).
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Caffeine intake showed an apparent positive association with CHD in age-adjusted analyses, which again was attenuated after controlling for smoking (multivariable adjusted RRs for sex-specific quintiles of caffeine intake: 1.0, 0.97 [95% CI 0.84 to 1.10], 1.02 [95% CI 0.89 to 1.16], 1.03 [95% CI 0.90 to 1.18], and 0.97 [95% CI 0.84 to 1.11], P for trend=0.82 in men; and 1.0, 1.02 [95% CI 0.90 to 1.16], 0.97 [95% CI 0.85 to 1.11], 0.87 [95% CI 0.76 to 0.99], and 0.97 [95% CI 0.85 to 1.11], P for trend=0.37 in women). We also performed analyses for consumption of decaffeinated coffee, tea, and non–paper-filtered coffee without observing any significant association (Table 4).
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Alternative analyses with the most recent coffee consumption data showed no association between shorter-term intake (2- to 4-year interval) and CHD (multivariable RRs for men were 1.0, 0.88, 0.91, 0.93, 0.96, and 0.80 [P for trend=0.41]; the corresponding RRs for women were 1.0, 0.96, 1.09, 0.98, 0.96, and 0.98 [P for trend=0.72]). When we stopped updating coffee consumption after the person developed angina, hypertension, hypercholesterolemia, cancer, or type 2 diabetes mellitus, it did not change the results. We also tried excluding participants who reported a change in their coffee consumption during the 10 years before baseline and excluding the first 4 years of follow-up to avoid latent disease; these exclusions did not appreciably affect the association between coffee consumption and risk of CHD. Finally, we excluded from the analyses participants who reported hypertension, hypercholesterolemia, or diabetes mellitus at baseline, as well as those who developed these diseases during the follow-up, again obtaining similar results. The multivariable adjusted means of total, LDL, and HDL cholesterol across categories of caffeinated and decaffeinated coffee are presented in Table 5. No significant associations were observed between coffee consumption and blood lipids.
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Discussion |
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In this large prospective study, we did not find a detrimental effect of coffee consumption on risk of CHD in either men or women. No association was observed for total caffeine intake, decaffeinated coffee, or tea. These results provide strong evidence against the hypothesis that coffee consumption increases the risk of CHD.
Coffee is one of the most widely consumed beverages in the United States and worldwide.28 The health effects of coffee consumption have been studied and debated extensively. In an earlier meta-analysis,2 cohort studies did not support an association between coffee intake and risk of CHD (pooled RR=1.05, 95% CI 0.99 to 1.12 for drinking 5 or more cups/d versus none), whereas case-control studies tended to suggest a positive association (RR=1.63, 95% CI 1.50 to 1.78). Several biases could explain the difference. For instance, recall bias in case-control studies may explain a positive association if individuals who developed CHD were more likely to overreport coffee intake than healthy controls.
Results from recent epidemiological studies are mixed. Woodward and Tunstall-Pedoe7 followed a Scottish population for 8 years. Their results suggested that higher coffee consumption was associated with lower risk of cardiovascular disease among men but not among women. Kleemola et al8 assessed coffee consumption in a Finnish population 3 times during 10 years of follow-up and found a lower risk of nonfatal MI in men with high coffee consumption (>7 cups/d); however, they also observed a slightly increased CHD mortality in the same group. Additionally, in a case-control study, Hammar et al6 reported that daily consumption of 7 to 9 dL of filtered coffee was associated with an increased risk of CHD in men compared with a daily consumption of 3 dL or less; however, this association was not observed for women. Two other studies suggested a J-shaped relationship between coffee consumption and risk of CHD.9,10 The present analyses, which used repeated measures of coffee consumption over 14 to 20 years of follow-up, found no evidence of either short-term (2 to 4 years) or long-term effects. Likewise, we found no association with decaffeinated coffee or total caffeine intake. Repeated measurement of diet was a unique advantage in the present study because our analysis using a cumulative average of intake was able to best represent long-time diet and reduce within-subject variations.
Coffee is a major source of caffeine. Caffeine is an adenosine-receptor antagonist,29 and all tissues with adenosine receptors may be affected by caffeine exposure. Caffeine stimulates fat oxidation in muscle30 and increases basal energy expenditure.31 Also, caffeine stimulates free fatty acid release from peripheral tissues32 and decreases insulin sensitivity in skeletal muscle.33 In addition, caffeine might impair insulin action by stimulating the release of epinephrine, which is a potent inhibitor of insulin activity.34 Finally, caffeine increases blood pressure35 and homocysteine levels36 in short-term studies. However, the above effects of caffeine could be transient, because partial tolerance might develop after several days of use.37 Thus, some of these mechanisms cannot be extrapolated to long-term use,15 whereas others mechanisms could counterbalance the effects of caffeine. For instance, substances in coffee such as potassium, niacin, and magnesium have previously been shown to be beneficial for glucose and insulin metabolism.38 In addition, antioxidants in coffee such as chlorogenic acid and other phenolic compounds might improve insulin sensitivity.39 These mechanisms may explain the recent findings that habitual coffee intake is associated with a lower risk of developing type 2 diabetes mellitus.11–15 In the present study, coffee consumption had no adverse or beneficial effect on CHD in participants with or without diabetes mellitus. In both men and women, there was some suggestion that heavy consumption (6 cups or more per day) was associated with a lower risk of fatal CHD (Table 2); however, the number of fatal CHD cases was relatively small, and the results should be interpreted with caution.
Coffee consumption was strongly correlated with smoking; thus, it is not surprising that coffee intake was positively associated with CHD in age-adjusted analyses in the NHS cohort, in which smoking was more prevalent. However, this association disappeared after adjustment for smoking and in analyses stratified by smoking status. A recent study suggested a synergistic detrimental effect of acute smoking and caffeine (200 mg) on aortic stiffness.40 However, we did not find an interaction between smoking and coffee consumption in relation to CHD risk. Although smoking was strongly correlated with coffee consumption, the detrimental effects of smoking on CHD were the same among coffee drinkers and nondrinkers.
Finally, most participants in the present study consumed filtered coffee. Neither filtered caffeinated coffee nor filtered decaffeinated coffee was substantially associated with plasma levels of total, LDL, and HDL cholesterol. Among those who reported consuming non–paper-filtered coffee, we did not find an increased risk of CHD. Boiled coffee increases serum cholesterol,41,42 and some evidence suggests that high consumption of this beverage is related to CHD risk.6,43 The lack of association between non–paper-filtered coffee in the HPFS and the NHS I cohorts is likely to be due in part to (1) the inclusion of espresso in this category, which has lower concentrations of the cholesterol-increasing components kahweol and cafestol,44 and (2) the modest consumption even in the highest categories (2 cup/d), compared with intervention studies such as Bak and Grobbee’s work,45 which examined the effect of the consumption of 4 to 6 cups of boiled coffee per day. The results of the present study do not exclude a relation between high nonfiltered coffee consumption and CHD risk.
In conclusion, in these 2 large cohorts, after a follow-up of 14 years for men and 20 years for women, we found no evidence of an adverse association between coffee intake and the risk of developing CHD. Likewise, we found no association for consumption of total caffeine, decaffeinated coffee, or tea. These data do not provide any evidence that coffee consumption increases the risk of CHD.
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Acknowledgments |
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This study was supported by National Institutes of Health research grants CA87969, DK55523, DK58845, and HL34594. Dr Lopez-Garcia’s research is supported by a fellowship from the Secretaria de Estado de Educacion y Universidades (Ministerio de Educacion y Cultura de España) and Fondo Social Europeo. Dr Hu’s research is supported in part by an American Heart Association Established Investigator Award.
Disclosures
None.
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CLINICAL PERSPECTIVE
The association between coffee consumption and coronary heart disease has long been hypothesized under different premises. We followed a large population of US men and women during 20 years, assessing coffee intake repeatedly. For consumption of 6 or more cups of coffee per day, no increase in coronary heart disease risk was observed. Similar results were found for consumption of 2 cups per day of nonfiltered coffee, but the number of participants who drank this type of coffee was small. Decaffeinated coffee, tea, and caffeine intakes were also unrelated to coronary heart disease risk. Additional analyses testing the effect of short-term coffee consumption provided similar results as for long-term consumption. Finally, consumption of caffeinated and decaffeinated coffee was not significantly associated with blood lipid levels. Our results provide strong evidence against the hypothesis that coffee consumption increases the risk of coronary heart disease.
Circulation 2006 113: 2031.
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