Yet, kinetics and concentrations of paraxanthine have rarely been considered when studying the physiological and cognitive outcomes of caffeine intake in humans.ĭespite the common pattern of regular intake, studies on the kinetics of caffeine and paraxanthine in humans after daily caffeine intake are surprisingly scarce. Paraxanthine has as high potency at antagonizing adenosine receptors as caffeine ( 8) and exerts several similar effects as caffeine, such as wake-promotion ( 9), psychostimulation ( 10), elevating blood pressure, and release of epinephrine ( 11). Following the peak concentration after a single administration of 5–8 mg/kg caffeine, plasma concentrations of caffeine decline rapidly and are surpassed by the paraxanthine levels at around 8–10 h after the intake ( 7). Approximately 84% of caffeine is transformed into paraxanthine through the process of 3-methyl demethylation by the hepatic cytochrome P450 1A2 enzyme (CYP1A2) ( 2, 5). The average half-life of caffeine after an acute consumption is 2.5–5 h ( 2), while it can be modulated by the ingested dosages, smoking, genetic variance, health status, oral contraceptives and pregnancy, and various other factors ( 3– 6). administration, 99% of the caffeine is rapidly absorbed within ~45 min ( 1), which brings the peak plasma concentration of caffeine at 1–2 h after the intake. They also suggest investigating the consequences of a paraxanthine accumulation during daily caffeine intake.Ĭaffeine is the most frequently consumed psychostimulant worldwide. Our findings unveil that conventional daily caffeine intake does not provide sufficient time to clear up psychoactive compounds and restore cerebral responses, even after 36 h of abstinence. After 36 h of caffeine deprivation, the previously reported caffeine-induced GM reduction was partially mitigated, while CBF was elevated compared to placebo. The results indicated that levels of paraxanthine and caffeine remained high and were carried overnight during daily intake, and that the levels of paraxanthine remained elevated after 24 h of caffeine deprivation compared to placebo. We assessed gray matter (GM) intensity and cerebral blood flow (CBF) after acute caffeine deprivation as compared to changes in the caffeine condition from our previous report. On day 10, we determined the course of salivary caffeine and paraxanthine using liquid chromatography-mass spectrometry coupled with tandem mass spectrometry. In this report, we leveraged the data of a laboratory study with N = 20 participants and three within-subject conditions: caffeine (150 mg caffeine × 3/day × 10 days), placebo (150 mg mannitol × 3/day × 10 days), and acute caffeine deprivation (caffeine × 9 days, afterward placebo × 1 day). The neural impact of such adaptions is virtually unexplored. First evidence indicates that, during daily intake, the elimination of caffeine may slow down, and the primary metabolite, paraxanthine, may accumulate.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |