Coffee consumption and markers of inflammation and endothelial dysfunction in healthy and diabetic women

In several short-term studies, coffee consumption has been associated with impairment of endothelial function.

The objective was to assess the relation between long-term caffeinated and decaffeinated filtered coffee consumption and markers of inflammation and endothelial dysfunction.

We conducted a cross-sectional study of 730 healthy women and 663 women with type 2 diabetes from the Nurses' Health Study I cohort, who were aged 43-70 y and free of cardiovascular disease and cancer at the time blood was drawn (1989-1990). Dietary intake was assessed with a validated food-frequency questionnaire in 1986 and 1990.

About 77% of the healthy women consumed > or =1 cup (237 mL) caffeinated coffee/mo and 75% consumed > or =1 cup decaffeinated coffee/mo; the corresponding intakes for women with type 2 diabetes were 74% and 63%, respectively. In healthy women, no appreciable differences in plasma concentrations of the markers were found across categories of caffeinated coffee intake. In women with type 2 diabetes, higher caffeinated coffee consumption was associated with lower plasma concentrations of E-selectin (adjusted percentage change per 1 cup/d increment = -3.2%; P = 0.05) and C-reactive protein (adjusted percentage change = -10.2%; P < 0.001). Higher decaffeinated coffee consumption was associated with lower plasma concentrations of E-selectin (adjusted percentage change = -2.5%; P = 0.08) and C-reactive protein (adjusted percentage change = -7.9%; P = 0.02) only in healthy women. The results were similar when we also adjusted the models for other dietary factors and blood lipids and when we excluded participants with hypertension or hypercholesterolemia.

These results indicate that neither caffeinated nor decaffeinated filtered coffee has a detrimental effect on endothelial function. In contrast, the results suggest that coffee consumption is inversely associated with markers of inflammation and endothelial dysfunction.