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ORIGINAL RESEARCH COMMUNICATION |
1 From the Julius Center for Health Sciences and Primary Care, University Medical Center, Utrecht, Netherlands (CSPMU, PHMP, and DEG); the Centers for Prevention and Health Services Research (WMMV), for Nutrition and Health (HBBdM, MO, and EJMF), and for Information Technology and Methodology (HCB), National Institute of Public Health and the Environment, Bilthoven, Netherlands; and the Division of Human Nutrition, Wageningen University, Wageningen, Netherlands (JMG)
2 The Doetinchem Cohort Study was financially supported by the Ministry of Public Health, Welfare, and Sports of the Netherlands and the National Institute of Public Health and the Environment, Bilthoven. CSPMU was provided an unrestricted grant by the organization for Physiological Effects of Coffee (PEC) in Paris, France.
3 Reprints not available. Address correspondence to CSPM Uiterwaal, Julius Center for Health Sciences and Primary Care, University Medical Center, PO Box 85500, 3508 GA Utrecht, Netherlands. E-mail: c.s.p.m.uiterwaal{at}umcutrecht.nl.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Objective: The objective was to assess whether coffee intake is associated with the incidence of hypertension.
Design: This study was conducted on a cohort of 2985 men and 3383 women who had a baseline visit and follow-up visits after 6 and 11 y. Baseline coffee intake was ascertained with questionnaires and categorized into 0, >0–3, >3–6, and >6 cups/d. Hypertension was defined as a mean systolic blood pressure (SBP) 
140 mm Hg over both follow-up measurements, a mean diastolic blood pressure (DBP) 90 mm Hg over both follow-up measurements, or the use of antihypertensive medication at any follow-up measurement.
Results: Coffee abstainers at baseline had a lower risk of hypertension than did those with a coffee intake of >0–3 cups/d [odds ratio (OR): 0.54; 95% CI: 0.31, 0.92]. Women who drank >6 cups/d had a lower risk than did women who drank >0–3 cups/d (OR: 0.67; 95% CI: 0.46, 0.98). Subjects aged 39 y at baseline had 0.35 mm Hg (95% CI: –0.59, –0.11 mm Hg) lower SBP per cup intake/d and 0.11 mm Hg lower DBP (95% CI: –0.26, 0.03 mm Hg) than did those aged <39 y at baseline, although the difference in DBP was not statistically significant.
Conclusions: Coffee abstinence is associated with a lower hypertension risk than is low coffee consumption. An inverse U-shaped relation between coffee intake and risk of hypertension was observed in the women.
Key Words: Coffee • hypertension • cohort study
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Most evidence on the relation between coffee and blood pressure stems from cross-sectional studies. This evidence, however, is inconsistent. Some of these studies showed a positive relation (2), no relation (3), or even an inverse relation (4). Such cross-sectional studies have important limitations with respect to causal inference.
Conclusive information about coffee as a cause for hypertension cannot be expected to come from randomized trials, because those would require unrealistically long-term interventions. Rather, long-term observational cohort studies will have to provide such information. There have been few follow-up studies on the relation between coffee intake and blood pressure or risk of hypertension (5, 6, 7). In 1017 young men, a small positive association between coffee intake and blood pressure rise over many years of follow-up was indicated to play a small role in the development of hypertension (6). In women participating in the Nurse's Health Studies, an inverse U-shaped relation was recently found between hypertension and caffeine consumption, but no association was found with caffeinated coffee consumption (7).
Because the long-term longitudinal evidence for a relation between coffee intake and hypertension is relatively scarce, we used a Dutch cohort study to address that issue. This cohort allowed for studying the relation of baseline coffee intake to the incidence of persistent hypertension on the basis of repeatedly measured blood pressure levels in subjects at 5 y intervals during a follow-up of 11 y. Our specific research question was whether coffee intake in subjects who are not hypertensive is associated with the incidence of hypertension.
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SUBJECTS AND METHODS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Dietary variables and exposure categories
Coffee intake at baseline of PPHV was estimated by the question "How many cups of coffee do you drink per day?," a question on the type of coffee used (regular, decaffeinated, or other), and a question about the use of additives (none, milk, sugar, etc). In MORGEN-EPIC, the subjects were asked to indicate how frequently they usually drank coffee, the type of coffee [regular (instant), decaffeinated, or other], use of additives (sugar, milk, and type of milk) with color photographs to indicate the strength of coffee and the standard size of a cup equaling 125 g. In a food-frequency questionnaire, the respondents were instructed to record what, on average, they had eaten and drunk in the past year. The MORGEN-EPIC food-frequency questionnaire was also used in the third follow-up (11). Similar questions were asked about tea intake. Coffee intake at baseline was divided into 4 categories: 0 cups/d, >0–3 cups/d, >3–6 cups/d, and >6 cups/d. The category of >0–3 cups/d was chosen as the reference category rather than the non-coffee drinking category because it contained larger numbers of subjects and yielded more stable estimates.
At baseline of PPHV, the subjects filled out a mailed questionnaire about demography, family history of cardiovascular disease, other chronic disease (eg, diabetes mellitus), current medication use, prescribed diets, selected dietary habits, and reproductive history for women. Pregnant women were excluded from the study. Questionnaires were used to assess alcohol intake (glasses/d), smoking status (none, ever, or current smoking of cigarettes), educational level (low, medium, or high) based on highest educational level achieved, and occupational status (paid work, housekeeping, unemployed, or retired or other).
Anthropometric and biological variables
Body height was measured to the nearest 0.5 cm without shoes. Body weight was measured without shoes and heavy clothing to the nearest 0.1 kg.
At all visits, nonfasting blood samples were obtained by using a standardized protocol. Plasma total and HDL cholesterol were measured at the Clinical Chemistry Laboratory of the University Hospital "Dijkzigt" in Rotterdam, which is the Lipid Reference Laboratory for standardized cholesterol determinations in the Netherlands. Total cholesterol was measured enzymatically by using a Boehringer test kit (12). HDL-cholesterol concentrations were measured after precipitation of apolipoprotein B–containing lipoproteins with magnesium phosphotungstate (13).
Outcome measurements and definitions
In PPHV, blood pressure was measured by trained technicians using a random zero sphygmomanometer while the subject was in a sitting position. The cuff size (12 x 23 cm) was applied to the left upper arm. A larger cuff (15 x 33 cm) was used in 1.1% and a smaller cuff (9 x 18 cm) in 0.4% of all examined subjects. Systolic blood pressure was recorded at the appearance of sounds (first-phase Korotkoff) and diastolic blood pressure at the disappearance of sounds (fifth-phase Korotkoff). After the first measurement, the heart rate was measured for 30 s followed by a second blood pressure measurement. In MORGEN-EPIC and at the third visit, the blood pressure measurement procedure was identical to that performed in PPHV. No restrictions were made with regard to coffee drinking before the measurements were taken.
Hypertension was defined by using cutoffs according to the recommendations in the 7th report of the Joint National Committee (JNC) of the National Heart, Lung, and Blood Institute (14), which classifies stage 1 hypertension as a systolic blood pressure of 140–159 mm Hg or a diastolic blood pressure of 90–99 mm Hg and stage 2 hypertension as having systolic blood pressure of 160 mm Hg or diastolic blood pressure 100 mm Hg, use of antihypertensive medication, or both. To have sufficient numbers of hypertensives in each category of coffee intake, these categories of hypertension were pooled to at least JNC stage 1 hypertension. Persistent hypertension was defined as having a mean systolic blood pressure 140 mm Hg or a mean diastolic blood pressure 90 mm Hg calculated over both follow-up measurements at a 5-y interval, the use of antihypertensive medication at any of the follow-up measurements, or both. The association between baseline coffee intake and incident hypertension as defined above was assessed among those who did not have hypertension at baseline. No hypertension at baseline was defined as having a systolic blood pressure <140 mm Hg and a diastolic blood pressure <90 mm Hg and no use antihypertensive medication.
Statistical analysis
The association between baseline coffee intake and incident hypertension as defined above was assessed among those who did not have hypertension at baseline as defined above. Logistic regression was used with presence of persistent hypertension (yes or no) as the dependent variable and baseline coffee intake and confounders as independent variables. Furthermore, effects of changes in coffee intake as a predictor of change of blood pressure were examined. A repeated-measures analysis with time-varying covariates was used with changes between repeated blood pressure measurements as dependent variables and time-varying changes in coffee intake and confounders as independent variables. In all analyses, we adjusted for the following possible confounders: age, sex, body height and weight, smoking, alcohol intake, tea intake, educational level, occupational status, and total energy intake.
All analyses were expressed as measures of association with corresponding 95% CIs, regarding intervals not including the respective null values as statistically significant. Analyses were performed by using SPSS version 11.0 or SAS Proc Mixed for repeated-measures analysis (SPSS Inc, Chicago, IL).
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RESULTS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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. The prevalence of hypertension, as defined in Methods, at baseline was 23% in the men and 14.5% in the women.
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. The interaction between sex and coffee intake in relation to hypertension was borderline statistically significant (P = 0.08), and therefore we decided to do both sex-specific analyses and analysis of the total group. The unadjusted odds ratios indicated a lower risk among noncoffee drinkers than in those who drank >0–3 cups/d. After adjustment, this association was slightly attenuated but was still detectable in the total group. Furthermore, women who drank >6 cups/d had a lower risk of hypertension than did women who drank >0–3 cups/d. Among coffee drinking women, there was a statistically significant trend over coffee intake categories (P = 0.023). Because age played a central role in confounding adjustments, we further explored to what extent the association between baseline coffee intake and later blood pressure differed with age. In linear regression models with the mean systolic or diastolic blood pressure from the last 2 visits as the dependent variable and coffee intake (cups), age, and a coffee intake x age interaction term as independent variables, there was a statistically signficant interaction for systolic blood pressure (P < 0.0001) as well as for diastolic blood pressure (P < 0.0001). The association between baseline coffee intake and systolic and diastolic blood pressure by median age at baseline and after full adjustment in the subjects who were not treated for hypertension at baseline is shown in Figure 1. Below the median age, there was no significant relation between coffee and blood pressure. In the group above the median, there was an inverse relation for systolic blood pressure (linear regression coefficient: –0.35 mm Hgcup–1d–1; 95% CI: –0.59, –0.11 mm Hgcup–1d–1) and diastolic blood pressure (–0.11 mm Hgcup–1·d–1; 95% CI: –0.26, 0.03 mm Hgcup–1d–1), although the latter was not statistically significant.
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Finally, we found in our cohort a lower risk of persistent hypertension in the 231 total abstainers from coffee than in the 411 users of strictly decaffeinated coffee. Using stage 1 or stage 2 hypertension as outcome, the unadjusted odds ratio was 0.35 (95% CI: 0.20, 0.60). Adjustment for confounding attenuated this odds ratio to a nonsignificant 0.72 (95% CI: 0.34, 1.49).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Nonresponses may have been related to coffee intake or blood pressure, but not likely to specific associations between coffee and blood pressure. We cannot rule out that professional advice to lower coffee consumption to persons with higher baseline intakes has led to a spurious association between higher intake and lower blood pressure. However, we analyzed persons who were normotensive at baseline to whom such advice was unlikely given. Although there may be residual or unmeasured confounding, we accounted for most confounders that are known to be risk factors for high blood pressure. We had no baseline information about intake of caffeine-containing sodas, which was recently shown to be associated with incidence of hypertension (7). We can only speculate about the effects of adjustment for that intake, but consumption of such sodas in the Netherlands in middle-aged persons in that period was probably low. A strong feature of our study is that it pertains to a large sample from the general population with >10 y of follow-up. Moreover, our outcome classification—the incidence of hypertension persisting over a 5-y period—better reflects true hypertension incidence than does measurement at a single occasion. This outcome was based on actual blood pressure measurements or hypertension treatment, rather than on self-reporting of a physician diagnosis, such as in the Nurse's Health Study (7). Finally, although we have addressed a limited number of hypotheses concerning the association between coffee intake and hypertension, we cannot rule out chance as an explanation, neither for the main effects nor for the interactions with age.
Our findings in men agree with those of a previous report on a long-term follow-up conducted in 1017 males showing a nonsignificant relation between coffee intake and hypertension incidence, despite a small positive effect on blood pressure levels (6). Our findings in women may be compatible with recent findings in the women participating in the Nurse's Health Studies I and II, where an inverse U-shaped association was found between caffeinated coffee intake and hypertension risk (7). Among normotensives at baseline, we showed a lower hypertension risk for coffee abstainers than for users of >0–3 cups/d.
From short-term randomized trials, it is known that coffee and caffeine have a blood pressure–raising effect (1). The prevailing explanation for such effect is that caffeine antagonizes endogenous adenosine, resulting in vasoconstriction and elevated total peripheral vascular resistance (15). The question is how low coffee intake is associated with a higher risk of hypertension, whereas high coffee intake is not. One explanation could be that effects of coffee on blood pressure do depend on consumption habits, with higher blood pressure levels observed in nonhabitual than in habitual coffee consumers (16, 17). Thus, a higher hypertension risk in consumers of >0–3 cups/d than in nondrinkers and consumers of >6 cups/d may be based on a lower adaptation to the effects of coffee when used in moderate to low amounts. Alternatively, coffee may have more general protective effects, because our finding of heavier coffee intake leading to lower blood pressure does not seem to be specific. A lower risk for type 2 diabetes mellitus in heavy coffee users compared with non- or moderate users was first shown by one of us (18) and recently confirmed by others (19-23) and is somewhat stronger in women than in men (21). In agreement with our findings for hypertension, it was shown that women with low coffee use (<1 cup/d) had a higher risk of type 2 diabetes mellitus than did non-coffee users (20). However, it remains unclear whether and to what extent an association between coffee intake and blood pressure can explain the association with diabetes mellitus. Some studies could only adjust for known hypertension (18, 23), which may be misclassified and leave residual confounding by blood pressure as an explanation. One study adjusted for systolic blood pressure levels, whereas diastolic blood pressure levels were most strongly associated with diabetes mellitus risk (21). In other studies, there was no explicit adjustment for blood pressure or hypertension (19, 20, 22). Finally, there may be a blood pressure–lowering compound in coffee that explains lower hypertension risk with higher intake. It was recently shown in a cross-sectional study that higher habitual tea intake was associated with lower risk of hypertension (24). This effect of tea combined with our observations on coffee may indicate a central role of serum potassium concentrations. A higher intake of potassium is clearly associated with lower blood pressure (25), and tea and particularly coffee are rich sources of potassium in Western diets (26). This, however, would not explain the observed lower hypertension risk in coffee abstainers.
Overall, higher baseline coffee intake in our study was associated with lower later blood pressure only from middle age onwards, wheras there was no such relation in younger persons. We can only speculate about the mechanisms for such age-dependent effects. It may agree with the results from short-term randomized trials, in which blood pressure–raising effects of coffee were reported to be stronger in younger than in older subjects (1) and which may point at more habituation to coffee in older persons (15, 16). Alternatively, if there is a protective salt constituent in coffee, such as potassium, it may be through increasing salt-sensitivity and higher blood pressure levels observed with increasing age (27, 28) that the protective effects of higher coffee intake become apparent. Finally, there is recent evidence to suggest that genetically determined slow caffeine metabolism in relation to cardiovascular disease risk is present only in relatively younger persons (29).
From a public health point of view, a direct implication of our study may be to reduce the incidence of hypertension by measures aimed at refraining from moderate coffee intake, but that would be unpractical if at all effective. The most important merit of our study is the elucidation of the role of coffee intake through its relation with hypertension in increasing the risk of cardiovascular disease. Although there are reports claiming coffee to be hazardous (30, 31), the larger cohorts show no association between coffee intake and cardiovascular morbidity or mortality (32) or with the prognosis of myocardial infarction (33). We consider it likely that the extent to which coffee intake explains hypertension risk is too small to be detected in relation to cardiovascular disease. A practical implication from our findings would therefore be to abstain from professional advice concerning coffee intake in normotensive individuals, which indeed agrees with the latest clinical guidelines on hypertension (14). We cannot preclude that associations between coffee intake and cardiovascular outcomes are different among hypertensive individuals (34). In conclusion, coffee abstinence was associated with a lower hypertension risk than was low coffee consumption, and an inverse U-shaped relation between coffee intake and risk of hypertension was observed in women.
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ACKNOWLEDGMENTS |
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WMMV was the project leader. WMMV, HBBdM, and MO were involved in the design and conduct of the cohort. CSPMU, HCB, and DEG analyzed the data. All authors played a role in data-interpretation and writing of the manuscript. CSPMU was provided an unrestricted grant by the organization on Physiological Effects of Coffee (PEC) in Paris. No other authors had any conflicts of interest.
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REFERENCES |
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This article has been cited by other articles:
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  S. Voutilainen, T.-P. Tuomainen, J. Mursu, and J. T Salonen Coffee intake and the incidence of hypertension Am. J. Clinical Nutrition, October 1, 2007; 86(4): 1248 - 1248. [Full Text] [PDF]
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C. S. Uiterwaal, W. M. Verschuren, and D. E Grobbee Reply to S Voutilainen et al Am. J. Clinical Nutrition, October 1, 2007; 86(4): 1249 - 1249. [Full Text] [PDF]
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| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
) and diastolic (•) blood pressures over the 2 follow-up visits per each extra daily cup of coffee at baseline, separated by those aged below and above the median age (39 y) at baseline in the study cohort. Data pertain to 5694 subjects without antihypertensive treatment at any visit. All estimates are adjusted for sex, height and weight, smoking, alcohol intake, tea intake, total cholesterol, HDL cholesterol, education level, occupational status, and total energy intake. In linear regression models with the mean systolic or diastolic blood pressure from the 2 follow-up visits as the dependent variable and coffee intake (in cups), age, and an coffee intake x age interaction term as independent variables, there was a statistically significant interaction for systolic blood pressure and for diastolic blood pressure (P < 0.0001 for both). 95% CIs not crossing the null line are considered statistically significant.