Results of the present study suggest that the relationship between obesity and plasma CRP levels is influenced by coffee consumption in overweight/obese, postmenopausal women who do not use HRT. As the positive relationship between obesity and plasma levels of CRP has been well-described in several studies, we found that, in women who reported drinking at least one daily cup of coffee, BMI was not associated with CRP. However, our results also suggest that this observation is limited to postmenopausal women who do not use HRT. As approximately half of postmenopausal U.S. women report using HRT (Brett and Chong 2001
), we believe that these findings could have an important impact in terms of chronic diseases prevention. Indeed, it is well recognized that women using HRT are characterized by increased plasma CRP levels (Cooper et al 2007
, Ridker et al 1999
). In our study, we found that this relationship was also independent from coffee consumption. Although the joint effects of obesity and HRT (or oral contraceptives) on plasma CRP levels have been previously documented (Buchbinder et al 2008
), our study suggests that coffee consumption might modify these relationships. To the best of our knowledge, the present study is the first ever conducted on this topic.
A few studies have investigated the association between coffee consumption and low-grade inflammation biomarkers such as CRP. In the ATTICA study, Zampelas and colleagues (Zampelas et al 2004
) investigated the relationship between coffee consumption and inflammatory markers in 1528 apparently healthy women (mean age=45±13 years) and reported that coffee consumption was positively associated with CRP levels. In that study, compared to women who did not drink coffee, those who consummated more than 400 mL/day had approximately 38% higher CRP levels. However, it is worth mentioning that although CRP levels were higher, mean plasma levels of CRP women drinking more than 400 mL/day remained in what is considered as a “normal” CRP range. The fact that our study population was limited to overweight/obese postmenopausal women compared to a study sample representative of women living in a Greek province (Attica) might explain, to a certain extent, this discrepancy. Similarly to what we observed in the present study, results of the Nurses’ Health Study suggest that plasma CRP levels were lower in women who reported drinking more than two cups of coffee per day compared with women who reported drinking less than one cup of coffee per day (Lopez-Garcia et al 2006
). However, this observation was limited to women with type 2 diabetes as healthy women had similar CRP levels across coffee consumption categories. It is of interest to mention that diabetic women of that cohort had BMIs and blood pressure values which were similar to those assessed in our study sample. Finally, in a sample of 459 community-living Japanese women aged 23–83, Kotani et al. (Kotani et al 2008
) reported that CRP was lower in women who reported consuming at least one cup of coffee per day compared to women who consumed less than one cup of coffee per day. Although they mentioned that this difference was higher in women aged >60 years of age, they did not investigate whether this relationship was still observed in women using or not using HRT.
Over the past few years, studies have reported that coffee consumption was associated with a lower risk of type 2 diabetes an inflammatory diseases in women (Andersen et al 2006
, van Dam and Hu 2005
). However, very few studies have examined how this relationships could be explained from a pathophysiological standpoint. Chung et al. (Chung et al 2004
) have shown that treatment of HepG2 cells with caffeic acid, a naturally occurring phenolic compound found in coffee might inhibit the function of the transcription nuclear factor κB, an important mediator of the inflammatory response. Although coffee might have anti-inflammatory or anti-oxidation properties, there is little pathophysiological evidence to support the results observed in the present study. Moreover, whether the relationship between HRT and CRP is the consequence of increased systemic inflammation or rather the consequence of the effects of estrogens on hepatic CRP production remains unclear (Ridker et al 1999
, Silvestri et al 2003
) and the possible biological pathways though which coffee might alter the relationship between obesity and CRP in postmenopausal women who do not use HRT need to be established.
Because of the cross-sectional design of our study, we cannot infer causality from our results. The prospective relationship between obesity, coffee consumption and plasma CRP levels and associated CVD and type 2 diabetes risk should be further investigated in population and/or intervention studies. Moreover, as our study sample was limited to overweight/obese postmenopausal women, we believe that this relationship should be documented in nonobese women from various ethnicities as well as in men. Similarly, since our study population was limited in size, lack of statistical power may have limited our ability to detect associations, especially for the analyses which required separating the study population into six groups. One other limitation of our study is the fact that coffee consumption was self-reported and that the food frequency questionnaire that was used did not enable us to measure the intake of the principal bioactive component of coffee: caffeine. Women of the study took the questionnaire once at the beginning of the study and therefore, we could not perform repeated assessment of coffee intake. Finally, the difference between consumption of boiled vs. filtered coffee was not assessed. However, these limitations would introduce an increased random measurement error that would likely attenuate the associations reported in the present study.
In conclusion, we found that BMI was positively associated with variations in plasma CRP levels and that coffee consumption was inversely associated with CRP, more specifically in overweight/obese postmenopausal women who did not take HRT. Our study also suggests that coffee consumption alters the relationship between obesity and plasma CRP levels in these women. In women who reported using HRT, BMI was positively associated with plasma CRP levels, with coffee consumption having no impact on this relationship. As the relationship between coffee consumption and CVD risk is not fully established, results of the present study do not support the view that coffee consumption could be deleterious to cardiovascular health. Rather, based on the results of our study, coffee consumption is associated with reduced levels of an inflammatory marker predictive of CVD risk in overweight/obese postmenopausal women who do not use HRT. However, whether coffee consumption should be encouraged to reduce CVD and/or type 2 diabetes risk associated with low-grade inflammation still needs to be further investigated. Additional studies and randomized trials will shed light on the specific mechanisms by which coffee consumption could possibly be linked to low-grade inflammation.