Abstract
BackgroundThe role of coffee intake as a risk factor for coronary heart disease (CHD) has been debated for decades. We examined whether the relationship between coffee intake and incidence of CHD events is dependent on the metabolism of circulating catecholamines, as determined by functional polymorphism of the catechol-O-methyltransferase (COMT) gene.Methodology/Principal FindingsIn a cohort of 773 men who were 42 to 60 years old and free of symptomatic CHD at baseline in 1984–89, 78 participants experienced an acute coronary event during an average follow-up of 13 years. In logistic regression adjusting for age, smoking, family history of CHD, vitamin C deficiency, blood pressure, plasma cholesterol concentration, and diabetes, the odds ratio (90% confidence interval) comparing heavy coffee drinkers with the low activity COMT genotype with those with the high activity or heterozygotic genotypes was 3.2 (1.2–8.4). Urinary adrenaline excretion increased with increasing coffee intake, being over two-fold in heavy drinkers compared with nondrinkers (p = 0.008 for trend).Conclusions/SignificanceHeavy coffee consumption increases the incidence of acute coronary events in men with low but not high COMT activity. Further studies are required to determine to which extent circulating catecholamines mediate the relationship between coffee intake and CHD.
Highlights
Despite decades of research, controversy persists regarding the effects of coffee consumption on cardiovascular health [1,2]
We examined whether the functional polymorphism of the catechol-O-methyltransferase (COMT) gene, resulting in several-fold differences in the metabolism of circulating catecholamines, modifies the effect of heavy consumption of caffeine-containing coffee on the risk of acute coronary events in a cohort of middle-aged eastern Finnish men initially free from symptomatic coronary heart disease (CHD)
In the supplemental analysis of urinary catecholamine excretion among 258 participants, the amount of adrenaline excreted was over two-fold in the heavy coffee intake category compared with non-drinkers (p = 0.008 for trend); for noradrenaline, the respective difference was 30% (p = 0.039 for trend)
Summary
Controversy persists regarding the effects of coffee consumption on cardiovascular health [1,2]. We have recently reported a U-shaped dose–response relationship between intake of caffeine-containing coffee and incidence of acute coronary events [7]; similar findings have been reported from at least two other studies [8,9]. Caffeine is a potent stimulator of plasma renin activity and adrenomedullary secretion; acute ingestion results in substantial increases in plasma concentrations of adrenaline and noradrenaline [10]. Tolerance to these acute humoral effects may develop in the course of one to four days of habitual consumption [11], but is not complete [12] and may be lost after abstinence for as little as 12 hours [13,14].
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