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Hypertension. 1999;33:647-652

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(Hypertension. 1999;33:647-652.)
© 1999 American Heart Association, Inc.

Scientific Contributions

The Effect of Chronic Coffee Drinking on Blood Pressure

A Meta-Analysis of Controlled Clinical Trials

Sun Ha Jee; Jiang He; Paul K. Whelton; Il Suh; Michael J. Klag

From the Department of Epidemiology and Disease Control, Yonsei University Graduate School of Health Science and Management, Seoul, Korea (S.H.J.); Welch Center for Prevention, Epidemiology, and Clinical Research (S.H.J., J.H., M.J.K.) and Department of Medicine (M.J.K.), The Johns Hopkins University School of Medicine, Baltimore, Md; Departments of Epidemiology (S.H.J., J.H., M.J.K.) and Health Policy and Management (M.J.K.), The Johns Hopkins University School of Hygiene and Public Health, Baltimore, Md; School of Public Health and Tropical Medicine, Tulane University, New Orleans, La (P.K.W.); and Department of Preventive Medicine and Public Health, Yonsei University College of Medicine, Seoul, Korea (I.S.).


*    Abstract
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 *Abstract
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Abstract—We sought to assess the effect of coffee consumption on blood pressure in humans. Our data sources included a MEDLINE search of the literature published before December 1997, bibliography review, and expert consultation. We selected controlled trials in which coffee consumption was the only difference between the intervention and control groups, mean blood pressure change was reported for each group or period, and treatment lasted for >24 hours. Of 36 studies initially identified, 11 (522 participants) met these inclusion criteria. Information on sample size, study design, participant characteristics (gender, race, age, baseline blood pressure, and antihypertensive medications), and treatment results were abstracted by 3 reviewers using a standardized protocol. Treatment effect of coffee consumption on blood pressure was estimated with the use of a random-effects model. In the 11 trials, median duration was 56 days (range, 14 to 79 days), and median dose of coffee was 5 cups/d. Systolic and diastolic blood pressure increased by 2.4 (range, 1.0 to 3.7) mm Hg and 1.2 (range, 0.4 to 2.1) mm Hg, respectively, with coffee treatment compared with control. Multiple linear regression analysis identified an independent, positive relationship between cups of coffee consumed and subsequent change in systolic blood pressure, independent of age of study participants and study design characteristics. The effect of coffee drinking on systolic and diastolic blood pressure was greater in trials with younger participants. Our findings provide support for a relationship between coffee consumption and higher blood pressure. Trials of coffee cessation of longer duration and in persons with hypertension should be performed.


Key Words: blood pressure • coffee • meta-analysis • clinical trials


*    Introduction
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It has long been suspected that coffee consumption may have adverse effects on the cardiovascular system. Some1 2 3 4 5 but not all6 7 8 9 10 cross-sectional studies have identified a positive association between coffee drinking and blood pressure. At least one prospective study11 has shown that coffee drinking is associated with an increase in blood pressure. Inferences regarding causality, however, must be made with caution from observational studies because other characteristics associated with coffee drinking may underlie the observed relationships.

Experimental studies provide the best opportunity to determine whether a relationship is causal and whether an intervention, such as coffee cessation, has therapeutic relevance. In 1934, Horst et al12 reported on a clinical trial of coffee drinking in hypertensive patients. Since then, >36 experimental investigations of the effects of coffee consumption on blood pressure in humans have been published. However, most of these trials have been small and cannot provide definitive results. The effects of coffee drinking on heart rate and the question of whether the health effects of coffee drinking differ according to the method used for brewing have also been controversial.13 14

Pooling the results of clinical trials provides a means to obtain more precise estimates of intervention effect as well as an opportunity to explore the basis for any heterogeneity in trial outcomes. With this in mind, we present the results of a meta-analysis of 11 clinical trials in which the effect of long-term coffee drinking on blood pressure was assessed.


*    Methods
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Study Selection
The medical literature was searched for all reports on the effect of coffee supplementation in humans published before December 1997. This included the following: (1) a MEDLINE computer database search using the medical subject headings blood pressure and caffeine and the text word coffee; (2) a review of reference lists from original research articles and several review articles15 16 17 18 ; and (3) a review of the authors' reference files. Thirty-six studies were identified, all of which were published in English.12 13 14 16 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 These articles were reviewed by 3 of the authors (S.H.J., J.H., and M.J.K) to determine whether they met a series of predetermined criteria for inclusion in our subsequent analysis. Areas of disagreement or uncertainty were adjudicated by consensus. To be included, a study had to have (1) been based on results from human experimentation; (2) included an active treatment (coffee) intervention; (3) included no intervention difference between the active treatment and control groups or periods other than coffee consumption (ie, concurrent treatment with antihypertensive medications, stressful challenges, and smoking had to have been applied equally to the active treatment and control groups or periods); (4) reported the mean blood pressure changes for systolic and/or diastolic blood pressure after both the active and control treatments, and (5) have been of >=24 hours' duration.

Eleven trials met the criteria for inclusion in our analysis. The major reasons for exclusion were as follows: (1) active treatments were applied to the coffee group but not to the control group16 23 40 ; (2) decaffeinated coffee was compared with caffeine tablets41 42 43 44 45 46 47 48 49 50 ; (3) insufficient data were provided to calculate the net change in blood pressure and its variance from baseline to the end of follow-up12 16 ; and (4) duration of <24 hours.19 20 21 24 25 26 27 28 29 35

Data Abstraction
Information on sample size, age, gender, hypertensive status, antihypertensive medications, study design, type of control, method of blood pressure, baseline blood pressure, change in blood pressure, coffee intake, run-in period, method of preparation, and amount of coffee was abstracted from every article. If different treatments were used in the same report, they were analyzed as separate trials and delineated by a and b suffixes, as indicated in Table 1. When studies had both ambulatory and resting blood pressure, ambulatory blood pressure measurement was used in the analysis.32 33 34 37 38 39 Ambulatory measurements were used for 2 reasons. First, information needed to calculate the net effect of coffee intake on blood pressure was not available for resting blood pressure measurements in 2 studies.38 39 More importantly, ambulatory measurements provide a more precise measurement of blood pressure than do resting measurements because multiple determinations of blood pressure are obtained. This improved precision permits greater statistical power to detect blood pressure changes in clinical trials.51 Two studies32 39 did not provide baseline ambulatory blood pressure, and therefore resting blood pressure was recorded as pretreatment blood pressure. In the study by Superko et al,39 several ambulatory blood pressure readings were provided for different time periods. Measurements from 3 PM to 6 PM were arbitrarily chosen for calculating effect size.


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  		Table 1. Participant and Study Design Characteristics in 11 Coffee Consumption Trials

Statistical Analysis
In trials with multiple treatment groups,14 25 27 31 the effect of coffee intake was assessed by comparing the treatment groups with the no-coffee control group. For parallel trials, net changes in blood pressure were calculated as the mean difference (coffee minus control) of the changes (follow-up minus baseline) in these mean values. For crossover trials, net changes were calculated as the mean difference in values between the end of the coffee supplementation and control periods. In a few instances, these values had to be estimated from figures.24 25 26 To calculate the pooled effects of treatment, each study was assigned a weight consisting of the reciprocal of its total variance. Because the variances for net changes in blood pressure were not reported directly in most articles, they were calculated from CIs, t statistics, probability value, or the individual variances for intervention and control groups (parallel trials) or intervention and control periods (crossover trials). For parallel trials in which the variance of paired differences during the trial was reported separately for each group, we calculated a pooled variance for net change using standardized methods.52

Estimates of the mean effect of coffee consumption on blood pressure and the corresponding 95% CIs were calculated using random-effects models.53 The assumption of heterogeneity implied by the use of the random-effects model is plausible because duration of the trials varied and they were conducted in samples that differed by age, hypertension status, and other covariates. To explore further the possible influence of covariates on net change in blood pressure, a series of subgroup analyses was performed on the basis of biological knowledge and our review of the literature. Finally, univariate and multivariate linear regression models were weighted by the inverse of variance for change in blood pressure. For each trial, covariates were calculated as average values at baseline or during the study or as the average change from baseline. Variables that demonstrated statistical significance in the univariate analyses as well as age were included in the multivariate models. When information on mean age was missing (4 trials), we used an average of the minimum and maximum values for that trial. Information on race was not reported with the exception of 1 trial. For crossover trials, we used the mean blood pressure during the control period as a baseline value. For the 1 trial in which baseline blood pressure information was not available for the entire group,22 we used an average of the values for the remaining 10 trials. To examine potential publication bias, we plotted sample size against effect size.


*    Results
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Participant and study design characteristics of the 11 clinical trials included in our meta-analysis are presented in Table 1. Table 2 displays daily habitual intake of coffee before start of the study, duration of the run-in period, method of preparation, and amount of coffee and caffeine content (milligrams) consumed in the trials.


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  		Table 2. Characteristics of Participants and Variables Related to Treatment in 11 Coffee Consumption Trials

Compared with control, coffee administration was associated with an average net change in blood pressure that ranged from -2.1 to 6.1 mm Hg for systolic and -0.9 to 3.1 mm Hg for diastolic blood pressure (Figure 1). Systolic and diastolic blood pressure increased in the coffee administration arm compared with the corresponding control group in 9 (82%) of the 11 trials; in 6 trials (55%), the lower bound of the 95% CI was >0. For diastolic blood pressure, an intervention-related increase in blood pressure was also noted in 9 (82%) of the 11 trials, and the lower bound of the 95% CI was >0 in 6 (55%) of the 11 studies. For both systolic and diastolic blood pressure, there was considerable variation across the 11 trials in the estimate of intervention-related average net change in blood pressure and in the width of the associated 95% CI. On the basis of a test of homogeneity, the variation in estimated in effect size was significant for both systolic and diastolic blood pressure (P<0.001).



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  		Figure 1. Net change in systolic and diastolic blood pressure associated with coffee drinking in 11 clinical trials. The overall effect is weighted by the inverse of the total variance of each trial. References are as in Tables 1 and 2.

Pooled estimates of the effect of coffee supplementation on systolic and diastolic blood pressure are provided in Table 3. The overall pooled estimates of treatment effect associated with coffee drinking were 2.4 mm Hg (95% CI, 1.0 to 3.7) for systolic (P=0.005) and 1.2 mm Hg for diastolic (95% CI, 0.4 to 2.1) (P=0.015) blood pressure. There was evidence favoring a greater effect on systolic blood pressure in studies with a run-in period of <7 days and those that administered more coffee. Diastolic blood pressure also increased more in trials with younger participants. There was no statistically significant difference in effect size between other subgroups. The pooled effect of drinking 1 cup of coffee, estimated in linear regression analysis, was 0.8 mm Hg for systolic pressure (P<0.001) (Figure 1) and 0.5 mm Hg for diastolic pressure (P<0.01).


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  		Table 3. Mean Net Systolic and Diastolic Blood Pressure Changes in Subgroups of Trials Defined by Participant and Study Design Characteristics

Because the study population in the trial of treated hypertensive persons may have differed from that in the other trials, the analysis was performed with the exclusion of this trial.38 The overall estimate of the change in blood pressure in the remaining 10 trials was virtually identical to the overall results for both systolic pressure (2.4 mm Hg; 95% CI, 1.0 to 3.8 mm Hg) and diastolic pressure (1.2 mm Hg; 95% CI, 0.4 to 2.1 mm Hg). To make certain that use of ambulatory measurements did not bias the results, the meta-analysis was also repeated using resting blood measurements for those studies for which they were available. Results were unchanged.

In multiple linear regression analysis, 3 variables were independently associated with systolic blood pressure. The variables (effect sizes) were age (-2.22 mm Hg/y; P<0.005), coffee consumption (0.52 mm Hg/cup; P<0.04), and sample size (0.06 mm Hg/person; P<0.002). The same 3 variables were included in the multivariate model for diastolic blood pressure. The effect sizes were -0.11 mm Hg/y (P=0.01) for age, 0.25 mm Hg/cup (P=0.12) for coffee intake, and 0.03 mm Hg/person for sample size (P<0.01). Approximately 82% of the variance in systolic and 72% of the variance in diastolic blood pressure–related treatment effect size could be explained by the 3 variables included in the multivariate model.

The plot of sample size versus effect size showed a typical "funnel" shape with little variation in effect size for large sample studies and increasing spread of effect size with smaller sample sizes. The distribution of effect sizes seen in individual studies was symmetrically distributed around the pooled mean effect size.


*    Discussion
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 up arrowAbstract
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 *Discussion
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To our knowledge, this is the first quantitative review of clinical trials of the effect of long-term coffee consumption on blood pressure. It demonstrates that, on average, coffee drinking was associated with a 2.4 mm Hg higher systolic blood pressure and 1.2 mm Hg higher diastolic blood pressure. For every cup of coffee consumed, systolic pressure increased by 0.8 mm Hg and diastolic pressure by 0.5 mm Hg. The pressor effect of coffee drinking was more pronounced in studies with younger participants, those that administered more coffee, and those with larger sample size. The relationship between coffee intake and blood pressure, however, was independent of the mean age of the study participants and study characteristics such as run-in time. The effect associated with coffee drinking in this analysis is substantially less than that seen in a quantitative summary of trials lasting <24 hours.54 The smaller effect of coffee administration in this analysis of studies lasting >2 weeks almost certainly reflects adaptation to the cardiovascular effects of coffee drinking.55

Previous reviews have suggested that coffee consumption is associated with an increase in both systolic and diastolic blood pressure.16 17 18 53 Results from observational studies, however, have been inconsistent and difficult to interpret. A few cross-sectional studies have shown a positive association between habitual coffee consumption and blood pressure.1 2 3 4 5 In the Busselton study, coffee consumption was directly related to blood pressure change over 6 years of follow-up.11 In contrast to these reports, several observational studies have failed to identify a pressor effect of habitual coffee consumption.6 7 8 9 10

In the present analysis, trials using a control group that consumed no coffee yielded the same results as the small number employing a control group that consumed decaffeinated coffee. This suggests that the effects of coffee on blood pressure are related to the presence of caffeine rather than another ingredient.24 Smits et al26 also reported that the cardiovascular effects of drinking coffee appears to be primarily related to caffeine content. The effect of caffeine on blood pressure appears to be mediated through an increase in systemic vascular resistance brought about by its ability to block adenosine receptors.56

The average effect size noted in the 11 trials included in our meta-analysis was relatively small. Small effects on blood pressure, however, can translate into important reductions in the incidence of hypertension and community burden of cardiovascular disease.57 Observational studies have consistently identified the presence of an important continuous, graded, independent relationship between systolic and diastolic blood pressure levels and risk of stroke, coronary heart disease, and end-stage renal disease.58 59

It is very likely that the association of coffee administration with an increase in blood pressure is causal. The 95% CIs around the estimate of effect size make it unlikely that the associations noted reflect a chance finding. The dose-response relationship observed between coffee intake and systolic blood pressure also supports a causal association, as does replication of the relationship in studies conducted in different populations and with different study designs. Finally, the association is biologically plausible. This meta-analysis, however, is limited by the trials available for inclusion. There were few trials, and most of them were of relatively small size, were conducted in persons with normotensive levels of blood pressure, and were of relatively short duration. Dietary interventions that influence blood pressure usually have a more profound effect in hypertensive persons.60 On the other hand, longer-term studies may have shown even less of an effect because of continued adaptation to the pressor effects of coffee ingestion. Adaptation occurs quickly,55 however, and there was no relation between study duration and effect of coffee intake in this group of trials. Lastly, this meta-analysis included only published studies. Exclusion of unpublished research may have biased the results because negative studies are less likely to be published. On examination of the funnel plots, however, there was no evidence of publication bias.

In summary, our findings provide support for a relationship between coffee intake and higher blood pressure. A high priority for the future should be the conduct of trials of longer duration and in groups who are at higher than average risk of hypertension or who already have high blood pressure. In addition, there is a need for further exploration of the role of factors such as cigarette smoking and stress in modifying the effect of coffee consumption on blood pressure.15 42



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  		Figure 2. Plot of net change in systolic blood pressure by amount of coffee supplementation in 11 trials. Diameter of circles is proportional to the inverse of the total variance of each trial.


*    Acknowledgments
 
This study was supported in part by grant AG01760 and Outpatient General Clinical Research Center grant 5M01RR00722 from the National Institutes of Health. Computational assistance was received from National Institutes of Health grant RR00035. Dr Jee was supported by a Post Doctoral Fellowship Award from the World Health Organization. Dr He was supported by training grant 5T32HL07024-21 from the National Institutes of Health, National Heart, Lung, and Blood Institute.


*    Footnotes
 
Reprint requests to Michael J. Klag, MD, MPH, Welch Center for Prevention, Epidemiology, and Clinical Research, The Johns Hopkins Medical Institutions, 2024 E Monument St, Suite 2-600, Baltimore, MD 21205-2223.

Received August 21, 1998; first decision September 10, 1998; accepted October 15, 1998.


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 *References
 

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