Abstract

“…our data suggest that coffee consumption may modestly reduce the risk of stroke among healthy women.”
The association between coffee consumption and health is of enormous interest because of the high consumption of this beverage among the population. Although coffee consumption has been traditionally assumed to increase the risk of having a cardiovascular event, recent evidence from large cohort studies suggests that coffee consumption does not increase the risk of cardiovascular disease [1–3].
Our group has recently examined the effect of coffee on several cardiovascular end points in the Nurses' Health Study (NHS) [101], a very large cohort of American nurses that have been followed for more than 30 years in an effort to understand how diet and other lifestyles modify the risk of having diseases in this population. The NHS cohort was established in 1976. Diet information has been assessed with a food frequency questionnaires every 4 years. In each questionnaire, participants were asked how often (on average) during the previous year they had consumed coffee and decaffeinated coffee. Other information from the participants has been updated every 2 years. Women who reported a cardiovascular event in a questionnaire were asked for permission to access their medical records. Deaths were identified using information provided by the next of kin or postal authorities or by systematic searches of the National Death Index. In this article we have summarized the main findings from our research about coffee and cardiovascular health in this group of women.
We first examined the association between long-term habitual coffee consumption and risk of coronary heart disease (CHD) [4]. Previous studies had found mixed results: some of them reported an increased risk [5,6], whereas others reported a lower risk among individuals with higher coffee consumption [1,2], and finally, other studies suggested that both high and low coffee intakes were associated with an increase in the risk of CHD, compared with moderate coffee consumption [7,8]. Our analyses demonstrated that for consumption of up to six or more cups of coffee per day, no increase in CHD risk was observed with increasing consumption. Similar results were found for consumption of two cups per day of nonfiltered coffee. Decaffeinated coffee, tea and caffeine intakes were also unrelated to CHD risk. Finally, consumption of caffeinated and decaffeinated coffee was not significantly associated with blood lipid levels. These results were consistent with analyses performed in parallel with a cohort of men [4]. The main implication of this work is that decreasing coffee consumption is not necessary to prevent the development of CHD.
Data on the relationship between coffee consumption and stroke are sparse, especially among women. The previous studies that addressed this association were performed in groups of men with very different risks of stroke, such as healthy men, men with Type 2 diabetes, hypertensive individuals and even smokers [9–12]. In our cohort of women, we found that for consumption of two or more cups of coffee per day, a 20% reduction in the risk of stroke was observed [13]. After additional adjustment by potential mediators of the relationship between coffee consumption and stroke, such as high blood pressure, hypercholesterolemia and Type 2 diabetes mellitus, the inverse association was slightly attenuated. The association was stronger among nonsmokers than among current smokers. Decaffeinated coffee was also associated with a lower risk of stroke but other drinks containing caffeine were not associated with stroke. Our results provide evidence that coffee consumption does not increase the risk of stroke in women. On the contrary, our data suggest that coffee consumption may modestly reduce the risk of stroke among healthy women.
Finally, we examined the effect of coffee consumption and mortality, motivated by recent findings that associate coffee with a lower risk of Type 2 diabetes [14] and a lower risk of some cancers [15,16], and by findings that suggest a beneficial effect of coffee for preventing cardiovascular disease [2,17]. When accounting for other risk factors, such as body size, smoking, diet and specific diseases, we found that people who drink more coffee were less likely to die prematurely during the follow-up period [18]. This was mainly owing to the lower risk for heart disease deaths among coffee drinkers. No association was found between coffee drinking and cancer deaths. These effects did not seem to be due to caffeine because people who drank decaffeinated coffee also had lower death rates than people who did not drink coffee.
“…coffee has some beneficial effects on inflammation and endothelial function, both of which are amongst the first stages of cardiovascular disease development.”
How can these findings be explained? New biological pathways have been described in the last few years, beyond the well-known acute effects of caffeine. First, it has been discovered that coffee has some beneficial effects on inflammation and endothelial function, both of which are amongst the first stages of cardiovascular disease development. Thus, phenolic compounds in this beverage (chlorogenic acid, ferulic acid and p-coumaric acid) have a strong antioxidant capacity [19], which reduces the risk of endothelial dysfunction and expression of inflammatory molecules. In addition, magnesium, trigonelline and quinides in coffee have been associated with improved insulin sensitivity [20], which reduces the risk of Type 2 diabetes, one of the main risk factors for cardiovascular disease. As a result of these pathways, we think that in the long term, these beneficial effects may counterbalance the detrimental short-term effects of caffeine on health.
However, there are some difficulties when analyzing the association between coffee and cardiovascular diseases. Since sicker people may be less likely to drink coffee, the association could simply reflect the fact that heavy coffee drinkers are healthier than nondrinkers. We tried to address this issue in our analysis in several ways. First, we used the cumulative coffee consumption (updated every 4 years) instead of the most recent data preceding the cardiovascular event. This avoided misclassification of patients from possible changes in consumption after diagnosis. Second, we made use of updated information of chronic diseases diagnosed during the follow-up to perform several sensibility analyses, adjusting our results for hypertension, hypercholesterolemia and Type 2 diabetes. Third, we performed additional analyses excluding participants in the lower category of coffee consumption to test whether specific characteristics of this group confounded the association. We also conducted analyses excluding participants who reduced their consumption in the 10 years preceding the study, excluding the first 4 years of follow-up (when participants could have undiagnosed diseases), using only the most recent coffee consumption (to assess short-term effects), or adjusting the results for perceived health (a marker of subclinical disease). In all cases, our findings were robust for the associations found.
Another important complication is the fact that smoking tends to be very closely linked to coffee consumption, making it necessary to remove this effect. In all the above studies, we performed analyses separately for smokers and nonsmokers and found that the potential effect of coffee on cardiovascular disease was only apparent among nonsmokers. We believe that smoking has such a detrimental effect on health that any beneficial lifestyle effect is counterbalanced by the deletereous effect of this exposure.
“…more research is necessary before we can recommend consuming coffee for health reasons.”
A final question when studying the effect of coffee is whether coffee may be detrimental to people who are not totally healthy but already have cardiovascular risk factors, such as high blood pressure, diabetes or high cholesterol levels. To address this question, we performed our analyses separately in people with these diseases and found no protective effect of coffee. However, there is not enough evidence on this matter to conclude anything. We feel that more research is needed on the effect of coffee consumption among individuals with a previous cardiovascular disease (heart attack or stroke) or with factors that increase the risk of cardiovascular disease (e.g., high blood pressure, diabetes or hypercholesterolemia) to provide accurate recommendations to these patients. In addition, we need to investigate the effect of nonfiltered coffee (e.g., espresso), because of the known cholesterol-raising effect of diterpenes present in boiled coffee [21]. In the NHS, the consumption of nonfiltered coffee was modest, so our work does not exclude a relation between high nonfiltered coffee consumption and increased cardiovascular risk.
In summary, our results suggest that long-term regular coffee consumption does not increase the risk of cardiovascular disease in women and may have several beneficial effects on health. However, more research is necessary before we can recommend consuming coffee for health reasons. We need to replicate these results in different populations, in people with chronic diseases, and we also need to assess the effect of other types of coffee on health. However, what we can say is that healthy coffee drinkers (including consumers who have up to six cups of coffee per day) can be quite sure that coffee does not increase their risk of cardiovascular disease. Women with diseases or conditions that may be worsened by coffee (e.g., insomnia, anxiety, hypertension or heart problems) should ask their doctor about their specific risks related to coffee consumption.
Footnotes
This study was funded in part by FIS research grant 09/00104. Dr Esther Lopez-Garcia's research was supported by a ‘Ramón y Cajal’ contract'. The author has no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
