BACKGROUND: Randomised trials show that treatment of obstructive sleep apnoea (OSA) with nasal continuous positive airway pressure (CPAP) greatly improves sleepiness and also lowers diurnal systemic blood pressures (BP). Such patients consume more coffee than controls (presumably to combat their sleepiness) and might reduce their consumption following effective treatment, thus lowering BP by this mechanism rather than via a direct effect of alleviating OSA. METHODS:Plasma caffeine levels before and after treatment with either therapeutic (n=52) or subtherapeutic (control, n=49) CPAP were measured in stored blood samples from a previous randomised controlled trial of CPAP for 4 weeks in patients with OSA. RESULTS: There was a small significant rise in caffeine levels when the two groups were analysed as a whole (p=0.02), but not individually. Despite the fall in sleepiness measured objectively in the therapeutic CPAP group, there was no difference in absolute (or change in) caffeine levels between the two groups (mean (SE) micro mol/l; therapeutic CPAP 9.2 (1.2), 10.2 (1.0), subtherapeutic 6.7 (0.9), 8.6 (0.9) before and after treatment, respectively). CONCLUSION: Reduced coffee consumption is unlikely to be the explanation for the falls in BP following treatment of OSA.
RCT Entities:
BACKGROUND: Randomised trials show that treatment of obstructive sleep apnoea (OSA) with nasal continuous positive airway pressure (CPAP) greatly improves sleepiness and also lowers diurnal systemic blood pressures (BP). Such patients consume more coffee than controls (presumably to combat their sleepiness) and might reduce their consumption following effective treatment, thus lowering BP by this mechanism rather than via a direct effect of alleviating OSA. METHODS: Plasma caffeine levels before and after treatment with either therapeutic (n=52) or subtherapeutic (control, n=49) CPAP were measured in stored blood samples from a previous randomised controlled trial of CPAP for 4 weeks in patients with OSA. RESULTS: There was a small significant rise in caffeine levels when the two groups were analysed as a whole (p=0.02), but not individually. Despite the fall in sleepiness measured objectively in the therapeutic CPAP group, there was no difference in absolute (or change in) caffeine levels between the two groups (mean (SE) micro mol/l; therapeutic CPAP 9.2 (1.2), 10.2 (1.0), subtherapeutic 6.7 (0.9), 8.6 (0.9) before and after treatment, respectively). CONCLUSION: Reduced coffee consumption is unlikely to be the explanation for the falls in BP following treatment of OSA.
Authors: Justin C T Pepperell; Sharon Ramdassingh-Dow; Nicky Crosthwaite; Rebecca Mullins; Crispin Jenkinson; John R Stradling; Robert J O Davies Journal: Lancet Date: 2002-01-19 Impact factor: 79.321
Authors: G H Kamimori; D M Penetar; D B Headley; D R Thorne; R Otterstetter; G Belenky Journal: Eur J Clin Pharmacol Date: 2000-11 Impact factor: 2.953
Authors: A J Chauhan; Hazel M Inskip; Catherine H Linaker; Sandra Smith; Jacqueline Schreiber; Sebastian L Johnston; Stephen T Holgate Journal: Lancet Date: 2003-06-07 Impact factor: 79.321
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