Effect of smoking on caffeine clearance

Parsons, William D.; Neims, Allen H.

doi:10.1002/cpt197824140

Cited by 283 publications

(126 citation statements)

References 7 publications

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“…It is possible that this may have biased the clearance values in this group although overall there was no statistical relationship between pre-study caffeine intakes and any of the pharmacokinetic variables. Caffeine clearance has been shown to increase in smokers (Parsons & Neims, 1978). In the present study, none of the patients with decompensated cirrhosis smoked and in the patients with compensated cirrhosis, no significant differences were observed in kinetic variables between the smokers and non-smokers.…”

Section: Discussioncontrasting

confidence: 60%

The pharmacokinetics of caffeine and its dimethylxanthine metabolites in patients with chronic liver disease.

Scott

Stambuk

Chakraborty

et al. 1989

Brit J Clinical Pharma

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1. Serum and salivary concentrations of caffeine (1,3,7‐ trimethylxanthine) and its dimethylxanthine metabolites were measured in 10 healthy control subjects and in 19 patients with cirrhosis, for up to 96 h following a 400 mg oral caffeine load. 2. Serum and salivary caffeine concentrations correlated significantly (r = 0.954; P less than 0.001) and no significant differences were observed in the pharmacokinetic data derived from the respective concentration‐time curves. 3. In the control subjects, basal salivary caffeine concentrations did not exceed 0.4 mg l‐1. The median (range) basal salivary caffeine concentrations in patients with compensated cirrhosis (n = 10), 0.2 (0‐0.7) mg l‐1 and decompensated cirrhosis (n = 9), 0.7 (0‐5.8) mg l‐1, were not significantly different from control values, although three patients with decompensated cirrhosis had basal salivary caffeine values above 2.0 mg l‐1. 4. In the patients with compensated cirrhosis, the median peak salivary caffeine concentration, 10.9 (8.2‐ 16.5) mg l‐1 was significantly greater than in controls, 7.1 (4.7‐11.8) mg l‐1 (P less than 0.01) and the median apparent volume of distribution was significantly reduced, 0.38 (0.19‐0.49) vs 0.41 (0.23‐ 0.63) l kg‐1 (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussioncontrasting

confidence: 60%

The pharmacokinetics of caffeine and its dimethylxanthine metabolites in patients with chronic liver disease.

Scott

Stambuk

Chakraborty

et al. 1989

Brit J Clinical Pharma

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“…The metabolism is slowed during pregnancy (Knutti et al, 1981) and in women taking oral contraceptives (Callahan et al, 1983). On the other hand, the clearance rate of caffeine is greater in smokers than in non-smokers (Parsons & Neims, 1978).…”

Section: Introductionmentioning

confidence: 88%

“…Moreover, in a cross-sectional observational study using 24 h ambulatory blood pressure monitoring, moderate smokers and coffee drinkers with mild hypertension had signi®cantly higher daytime blood pressure than nonsmokers and those who did not drink coffee (Narkiewicz et al, 1995), which suggests that the effect might recur throughout the day, despite the increased caffeine catabolism in smokers (Parsons & Neims, 1978).…”

Section: Acute Intake Of Coffee or Caffeine And Blood Pressurementioning

confidence: 99%

Coffee, caffeine and blood pressure: a critical review

et al. 1999

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Objective: We review the published data relating to intake of coffee and caffeine on blood pressure in man. We also refer to studies on the possible mechanisms of actions of these effects of caffeine. Design: The MEDLINE and Current Contents databases were searched from 1966 to April 1999 using the text words`coffee or caffeine' and`blood pressure or hypertension'. Controlled clinical and epidemiologic studies on the blood pressure effects of coffee or caffeine are reviewed. We also refer to studies on the possible mechanisms of action of these effects of caffeine. Results: Acute intake of coffee and caffeine increases blood pressure. Caffeine is probably the main active component in coffee. The pressor response is strongest in hypertensive subjects. Some studies with repeated administration of caffeine showed a persistent pressor effect, whereas in others chronic caffeine ingestion did not increase blood pressure. Epidemiologic studies have produced contradictory ®ndings regarding the association between blood pressure and coffee consumption. During regular use tolerance to the cardiovascular responses develops in some people, and therefore no systematic elevation of blood pressure in long-term and in population studies can be shown. Conclusions:We conclude that regular coffee may be harmful to some hypertension-prone subjects. The hemodynamic effects of chronic coffee and caffeine consumption have not been suf®ciently studied. The possible mechanisms of the cardiovascular effects of caffeine include the blocking of adenosine receptors and the inhibition of phosphodiesterases.

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“…Although previous studies have shown that caffeine can enhance the reinforcing effects of nicotine (Shoaib et al, 1999;Jones and Griffiths, 2003), no study has evaluated whether nicotine enhances the reinforcing effects of caffeine. However, it is known that cigarette smoking decreases the half-life of caffeine by as much as 50% (Parsons and Neims, 1978;May et al, 1982). Thus, higher rates of caffeine consumption among cigarette smokers may be due to the faster rate of caffeine elimination.…”

Section: Effects Of Nicotine Maintenance On Intravenous Caffeinementioning

confidence: 99%

Transdermal Nicotine Maintenance Attenuates the Subjective and Reinforcing Effects of Intravenous Nicotine, but not Cocaine or Caffeine, in Cigarette-Smoking Stimulant Abusers

Sobel

Sigmon

Griffiths

2004

Neuropsychopharmacol

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The effects of transdermal nicotine maintenance on the subjective, reinforcing, and cardiovascular effects of intravenously administered cocaine, caffeine, and nicotine were examined using double-blind procedures in nine volunteers with histories of using tobacco, caffeine, and cocaine. Each participant was exposed to two chronic drug maintenance phases (21 mg/day nicotine transdermal patch and placebo transdermal patch). Within each drug phase, the participant received intravenous injections of placebo, cocaine (15 and 30 mg/70 kg), caffeine (200 and 400 mg/70 kg), and nicotine (1.0 and 2.0 mg/70 kg) in mixed order across days. Subjective and cardiovascular data were collected before and repeatedly after drug or placebo injection. Reinforcing effects were also assessed after each injection with a Drug vs Money Multiple-Choice Form. Intravenous cocaine produced robust dose-related increases in subjective and reinforcing effects; these effects were not altered by nicotine maintenance. Intravenous caffeine produced elevations on several subjective ratings; nicotine maintenance did not affect these ratings. Under the placebo maintenance condition, intravenous nicotine produced robust dose-related subjective effects, with maximal increases similar to the high dose of cocaine; nicotine maintenance significantly decreased the subjective and reinforcing effects of intravenous nicotine. The results of the present study demonstrate that chronic nicotine maintenance produces tolerance to the effects of intravenous nicotine, but does not affect the subjective or reinforcing effects of cocaine or caffeine.

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Effect of smoking on caffeine clearance

Cited by 283 publications

References 7 publications

The pharmacokinetics of caffeine and its dimethylxanthine metabolites in patients with chronic liver disease.

The pharmacokinetics of caffeine and its dimethylxanthine metabolites in patients with chronic liver disease.

Coffee, caffeine and blood pressure: a critical review

Transdermal Nicotine Maintenance Attenuates the Subjective and Reinforcing Effects of Intravenous Nicotine, but not Cocaine or Caffeine, in Cigarette-Smoking Stimulant Abusers

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