Variability of caffeine metabolism in humans.

  • 1 January 1985
    • journal article
    • Vol. 35, 319-24
Abstract
The metabolic disappearance of caffeine from blood is subject to substantial inter- and intra-individual variation. Smoking of cigarettes and other inducers of aryl hydrocarbon hydroxylase tend to enhance the caffeine metabolism; pregnancy, the use of oral contraceptives, and various kinds of liver disease prolong the caffeine half-life. A genetic component affecting caffeine half-life has not yet been systematically searched for, but might be expected to affect the response to cigarette smoke and similar inducing agents, rather than to provide direct control of caffeine metabolism. The secondary metabolisms of the primary caffeine metabolites are strongly affected by the well-known genetic polymorphism of the N-acetyltransferase of human liver (a polymorphism originally discovered by studies of isoniazid metabolism). Since the proportion of slow acetylators differs in different ethnic populations, many ethnic differences in the ultimate fate of caffeine are to be expected. An observed difference of paraxanthine excretion between Caucasian and Oriental subjects might reflect a difference in the capacity for renal tubular reabsorption of that substance, but further metabolic differences cannot be excluded. The renal elimination of the dimethylxanthines is urinary flow dependent while that of the water soluble metabolites 1-methylxanthine and AFMU (5-acetylamino-6-formylamino-3-methyluracil) is not. Thus, the urinary metabolite pattern can be expected to vary from time to time. However, habitual coffee intake does not affect the metabolite pattern of caffeine.

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