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Coffee consumption has been shown to have adverse effects on various biological markers of coronary heart disease (CHD) risk, including serum cholesterol (1), blood pressure (2), insulin resistance (3), and plasma homocysteine (4). In contrast, higher coffee consumption has not been associated with a higher risk of CHD in prospective cohort studies (5)(6)(7). What could be the explanation for this “coffee paradox”? First, the acute effects of coffee consumption can be different from the effects of long-term habitual consumption. Second, the physiological effects of coffee can depend on the type of coffee consumed and are not necessarily the same as for caffeine in isolation. Third, coffee consumption may have beneficial effects on other biological pathways implicated in the development of CHD that could compensate for any adverse effects. Fourth, risk markers may not causally affect the development of CHD, or their effects may be too modest for any increase caused by coffee consumption to translate into a substantial increase in disease risk. Research supporting these explanations are discussed, with particular focus on the association between coffee consumption and homocysteine concentrations reported by Ulvik et al. in this issue of Clinical Chemistry (8).In caffeine-naive individuals, caffeine intake leads to a marked reduction in insulin sensitivity (3) and marked increases in postload glucose concentrations (9), epinephrine concentrations (10), and blood pressure (10). Within a week of initiating caffeine intake, however, an individual experiences an attenuation of coffee’s effects on epinephrine release and blood pressure (10). For blood pressure, only a partial tolerance develops, and a modest increase remains after several weeks (2). Given that caffeine’s stimulation of epinephrine release appears to contribute to insulin resistance (3), it is plausible that the effect of caffeine on glucose metabolism would also attenuate after continued caffeine intake. There is …

Coffee Consumption and Coronary Heart Disease: Paradoxical Effects on Biological Risk Factors versus Disease Incidence