Epidemiological studies of long-term consumption of filtered coffee do not support the hypothesis that filtered caffeinated coffee is detrimental to BP. On the contrary, there is observational evidence that high intake (>4 cups per day) may even reduce the risk of hypertension, especially in women. The nature of the relationship between coffee and BP is not yet clear, and further investigation is needed to find out whether abstainers are at a lower or higher risk of hypertension than occasional coffee drinkers (1–2 cups per day). Findings from experimental studies suggest a BP-raising effect of coffee of a few mmHg in the short-term (<3 months), but apparently this effect does not translate into an increased risk of hypertension in the long-term. Both observational and experimental data suggest larger BP elevations during coffee intake at younger compared to older age (ie, >40 years). However, it should be noted that studies on coffee and BP in the elderly are sparse, as are studies in several other population subgroups, and long-term intervention studies.
A number of methodological issues need further consideration. Firstly, it has been well established that caffeinated coffee causes an acute rise in BP shortly after exposure (Nurminen et al 1999
), as is the case for other lifestyle factors such as smoking, alcohol intake, physical activity, and even talking. Such acute physiological responses are mostly transient, with BP returning to initial levels within hours. It is not yet clear whether repeated BP elevations during the day could eventually lead to persistent hypertension. For coffee, on basis of available evidence from prospective studies, this does not seem to be the case. In this respect, it should be noted that office BP measurements both in epidemiological and experimental studies are not always performed in fasting conditions. From available data, it is hard to judge to what extent coffee intake prior to BP assessment (ie, acute BP effects) influenced the outcomes of the studies. To illustrate, in a trial in young Swiss women, coffee consumption on the testing day was associated with elevated BP whereas no association was found with habitual intake (Höfer and Bättig 1993
). Also, ambulatory BP monitoring that captures repeated acute BP elevations during coffee intake throughout the day may point towards a BP raising effect of coffee, while such BP elevations are probably transient. It is recommended that in future studies a sufficient time period is incorporated between the last cup of coffee and BP assessment, to avoid measurement of acute effects. Also, investigators should clearly state in their papers the time when the last cup of coffee was consumed.
Secondly, it is unclear whether occasional coffee drinkers are at higher risk of hypertension than heavy coffee drinkers. Also here, acute BP effects may blur the view on the role of coffee in the development of hypertension. There is ample evidence that habitual coffee users develop tolerance to caffeine and show no elevation in BP shortly after intake. BP responses will probably not occur in people who take many cups of coffee throughout the day (‘continuous infusion’ with caffeine). In studies that have no proper time period between BP readings and the last intake of coffee or other caffeinated beverages (eg, cup of coffee or tea offered at the research center), BP may be temporarily increased in occasional, but not in heavy coffee drinkers.
Thirdly, observational epidemiological studies suggest that there may be a U-shaped relation between habitual coffee intake and BP. Such relation is less clear from RCTs, in which effects of coffee on BP are mostly in the positive direction or absent. This discrepancy may be related to the duration of trials compared to cohort studies, and it is possible that short-term BP effects are not persistent in time. However, other (methodological) aspects may also contribute to the discrepancy. Trials generally focus on one or two specific doses of coffee, mostly in the high range (around 5 cups per day), and there is a lack of experimental data on the effect of low intakes on BP. Furthermore, in many trials the control treatment comprises cessation of coffee use, which from a physiological point of view is truly different from non-use in observational studies. ‘Habitual abstainers’ do not drink coffee because of disliking, health problems (eg, stomach complaints), financial aspects, or other reasons. In addition, observational studies are often population-based, whereas trials are conducted in selected groups subjects. Finally, coffee consumption in trials is carefully monitored whereas observational studies make use of self-reported data. The latter could lead to misclassification of subjects. To illustrate, subjects who are aware of having high BP may find it socially desirable to report occasional use of coffee rather than higher levels of intake because of a general belief that coffee could be harmful to health. Random misclassification of coffee intake, as discussed previously, can lead to weakened associations between coffee and BP levels or hypertension.
In conclusion, it is at present unclear whether habitual coffee drinking is related to risk of hypertension, although most evidence suggest that this is not the case. At this moment, there is no reason to refrain from coffee for the prevention of hypertension. The precise nature of the relation between coffee and BP is not yet clear. More prospective studies of coffee intake and incident hypertension are needed, as are long-term randomized placebo-controlled trials. Future studies may focus on different doses of coffee, and on specific population subgroups such as the elderly, hypertensives, and non-Caucasians. With regard to underlying biological mechanisms, research should not only focus on the BP-raising properties of caffeine but also on the potentially beneficial effect of other substances in coffee, such as polyphenols, soluble fibre, and potassium.