Article

The impact of caffeine use on tobacco cessation and withdrawal

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Abstract

Continuous caffeine consumption with smoking cessation has been associated with more than doubled caffeine plasma levels. Such concentrations may be sufficient to produce caffeine toxicity symptoms in smoking abstinence conditions. To test whether caffeine abstinence influences smoking cessation, 162 caffeine-using smokers were enlisted from American Lung Association smoking cessation programs. Volunteers were randomly assigned by clinic to caffeine-use and caffeine-abstinence conditions and measured for 3 weeks post-smoking cessation, at 6 months and one year. Results showed a significant linear increase in caffeine sputum levels across 3 weeks post cessation for those who quit smoking and continued using caffeine. Three weeks after cessation, concentrations reached 203% of baseline for the caffeine user. Typical nicotine withdrawal symptoms occurred during the first 16 days of cessation. The caffeine abstainers, but not continued users of caffeine, reported increased fatigue during the first 3 days of cessation. Among complete caffeine abstainers, compared with caffeine users, there was a significant increase in fatigue, a decrease in stimulation, and a marginal increase in caffeine craving immediately following tobacco cessation. There were no differences between the groups on other withdrawal symptoms or in cessation success at 16 days, 6 months, or 12 months.

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... W poprzednio cytowanej pracy Benowitza zaobserwowano w osoczu: 269% po 12 tygodniach i 266% po 26 tygodniach. Swanson sugeruje mo¿liwoae istnienia liniowego trendu [24]. W ci¹gu 16 dni od zaprzestania palenia, badani wci¹¿ pij¹cy kawê cierpieli na typowy nikotynowy zespó³ abstynencki. ...
... W 21 dniu eksperymentu wci¹¿ nie obserwowano ¿adnych ró¿nic. Picie kawy lub napojów zawieraj¹cych kofeinê nie wydaje siê, wiêc nie mieae wp³ywu na sukces w zaprzestaniu palenia przez pierwszy tydzieñ [24]. ...
... Eksperyment Swansona nie daje podstaw do nie picia kawy w krótkim czasie po zaprzestaniu palenia, ale nie s¹ to wyniki przes¹dzaj¹ce sprawê. Byae mo¿e lepiej jest, jak sugerowa³ Benowitz, ograniczyae kofeinê tak¿e ze wzglêdu na wp³yw wysokich jej stê¿eñ na zdrowie, nie tylko w odniesieniu do nikotynowego zespo³u abstynenckiego [24]. ...
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... Cessation of smoking significantly reduces caffeine clearance and changes the pattern of caffeine metabolism bringing the two steps of caffeine demethylation back to normal (Brown et al., 1988). Three weeks after smoking cessation and continued caffeine use, caffeine concentrations reach 203% of baseline for caffeine users (Swanson et al., 1997). ...
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... These findings confirm the need to consider both coffee and smoking together when considering the health implications of coffee or caffeine in population studies. In addition, given that it has been hypothesized that overlap in symptoms between caffeine toxicity and nicotine withdrawal could increase risk of relapse to smoking, 45 our findings may have implications for smoking cessation if individuals trying to quit smoking experience caffeine toxicity due to reduced caffeine metabolism. ...
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... In a similar pattern, individuals might experience symptoms of caffeine intoxication following reduction or abstinence from smoking. 16 ...
... Hypothesized behavioral mechanisms for this association include reduced caffeine consumption as a marker for healthy lifestyle change (Fernandez et al., 1997) and coffee consumption as a cue for tobacco use (Krall, Garvey, & Garcia, 2002). Proposed pharmacological explanations are accelerated caffeine metabolism during tobacco consumption leading to caffeine toxicity during cessation (Swanson, Lee, Hopp, & Berk, 1997), reduced nicotine uptake due to oral acidification by caffeinated beverages (Henningfield, Radzius, Cooper, & Clayton, 1990;Tomar & Henningfield, 1997), and enhancement of nicotine's neurologic effects by caffeine (Tanda & Goldberg, 2000). To date no studies have examined the effect of simultaneous caffeine reductions on the success of ST cessation. ...
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Today, two generations after the first Surgeon General's report, and with abundant evidence of the catastrophic consequences of smoking, no serious person can be unaware that smokers risk their lives and health. We also know that quitting smoking--at any age--promises significant health benefits. When offered the tools they need, older smokers quit smoking at rates comparable to those of younger smokers despite their skepticism, fatalism, and self-doubt. Older smokers should be encouraged to enter programs that stress the health benefits derived and identify the risks they are avoiding by quitting smoking. These programs establish quit dates, use sound behavioral modification techniques, provide strategies for stress management and relaxation, treat withdrawal symptoms, and provide regular and continuing follow-up. The patient is asked to make an existential change, and the physician should provide encouragement and promote self-confidence by emphasizing that, despite setbacks, with repeated efforts, success can be achieved. Clinicians can influence patients to quit smoking, and they should.
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This study examined the relationship between smoking, drinking and heavy caffeine use (> three caffeinated drinks per day) among pregnant women who reported smoking cigarettes and drinking alcohol prior to conception. Demographic predictors of smoking, drinking and caffeine use during pregnancy were also identified. Pregnant women (n = 237) attending a university-based, public clinic were identified during screening for a larger intervention study. Logistic regression analyses revealed a significant relationship between pregnancy smoking and drinking (OR= 8.1), as well as between smoking and harmful caffeine use (OR=3.1). Age predicted smoking and drinking in pregnancy, with older women being more likely to use both substances. Caucasian women were more likely to continue smoking, while African-American women were more likely to continue drinking. Increased attention should be paid to the co-occurrence of multiple health risk behaviours during pregnancy and to the specific needs of subgroups of high-risk women.
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Coffee, tea, chocolate and caffeinated drinks are the main sources of caffeine, which is consumed in almost all ages and socioeconomic levels. Caffeine acts as a non-selective adenosine receptor antagonist in the central nervous system. Its main effects are as psychostimulant, acting in addition on the respiratory, muscular and cardiovascular systems. Basically, caffeine is metabolized by the hepatic cytochrome P-450 1A2 enzymes (CYP1A2). Several drugs can interact with its metabolism. The observed interindividual differences of its effects can be explained by variations in its metabolism. The main therapeutic use of caffeine is bronchodilator in respiratory diseases. Other possible uses are under investigation. Acute or chronic consumption of caffeine can induce several adverse effects, including intoxication that can be lethal. Finally, caffeine can be considered a drug of abuse. It has positive reinforcing actions, produces tolerance, and a withdrawal syndrome after stopping its consumption. Caffeine can cause different mental disorders such as dependence, which is not included in the DSM-IV-R, withdrawal syndrome and intoxication. Depending on its use, caffeine can be considered a nutrient, a drug or a drug of abuse.
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1. A large body of research on the demography of caffeine use and its potential health consequences has been undermined by the absence of empirical data on the reliability of retrospective self-reports of caffeine consumption. 2. The principal aim of the present study was to use standard bioanalytic method to assess the reliability of subjects' self-reported caffeine use. Saliva samples were obtained from 142 first-and second-year medical students and assayed for caffeine and paraxanthine. 3. Self-reported caffeine use was found to be significantly correlated with salivary caffeine (r = 0.31, P less than 0.001) and paraxanthine (r = 0.42, P less than 0.001), thereby providing qualified support for use of questionnaires to estimate patterns of caffeine consumption. 4. A secondary aim of the study was to extend previous research concerning the symptomatology of caffeine use by examining the association between caffeine exposure and a variety of measures of somatic and psychological health. Caffeine consumption was reliably associated with the self-reported occurrence of somatic symptoms, but not psychological well-being.
Chapter
Why do people habitually consume tobacco and how does tobacco use influence the health of the habitual user? Complete answers to these questions are many years away. But a beginning is an understanding of the human pharmacology of nicotine, which is the primary pharmacologically active substance in tobacco. Central issues include: (1) What are the pathways and rate of metabolism? (2) How does elimination rate influence effects of nicotine or smoking behavior? (3) What is the time course of nicotine in the body during regular tobacco use? (4) What is the relationship between dose, concentration, and effects? (5) How does tolerance influence effects of nicotine? We will review a number of studies conducted in our laboratory examining these issues.
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The absorption, distribution, and elimination of caffeine, 2 mg/kg by mouth, were evaluated in six smokers and six nonsmokers before and on the fourth day of administration of cimetidine, 300 mg by mouth every 6 hr. Caffeine absorption, assessed by the maximal serum caffeine concentration (Cmax) and the time to reach Cmax (tmax), was very rapid relative to elimination. The total body clearance (TBC) of caffeine was higher (2.49 0.35 and 1.59 0.19 ml/kg/min, P < 0.05) and the elimination half-life (t½) shorter (190 15 and 276 30 min, P < 0.05) in smokers than nonsmokers, but Cmax, tmax, and the apparent volume of distribution (Vd,app) did not differ (P > 0.05). Cimetidine decreased the TBC of caffeine by 31% (to 1.73 0.28 ml/kg/min, P < 0.05) and by 42% (to 0.92 0.11 ml/kg/min,, P < 0.01) in smokers and nonsmokers. The increases in t½ were 45% (to 276 25 min, P < 0.05) and 96% (to 542 123 min, P < 0.05). Cmax, tmax, and Vd,app were unaffected by cimetidine. Caffeine induced similar slight increases in blood pressure and pulse rate in smokers and nonsmokers both before and during cimetidine dosing.
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Commercial chocolate products were analyzed for theobromine and caffeine content by High Performance Liquid Chromatography, Levels in 22 samples of chocolate liquor averaged 1.22% theobromine and 0.21% caffeine. Commercial cocoas contained, on the average, 1.89% theobromine and 0.21% caffeine. Sweet chocolate averaged 0.46% theobromine and 0.07% caffeine, while milk chocolate averaged 0.15% theobromine and 0.02% caffeine. Hot cocoa (chocolate) beverages averaged 65 mg of theobromine and 4 mg of caffeine per 5 ounce serving and chocolate milk prepared from a variety of cocoa-sugar mixes averaged 58 mg of theobromine and 5 mg of caffeine per 8 ounce serving. Theobromine and caffeine levels varied widely in individual samples within the product categories examined. Also, the ratio of theobromine to caffeine varied widely among different chocolate liquors ranging from a low of 2.5:1 to a high of 23.0:1.
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The elimination of caffeine from saliva was compared in groups of healthy smokers (n = 13) and nonsmokers (n = 13). Mean caffeine t1/2 in smokers (3.5 hr) was shorter than that in the nonsmokers (6.0 hr). The body clearance of caffeine in the smokers (155 +/- 16 ml . kg-1 . hr-1) was greater than that in the nonsmokers (94 +/- 18 ml . kg-1 . hr-1) (p less than 0.05). No significant difference was noted in the apparent volume of distribution in smokers (720 +/- 67 ml . kg-1) and nonsmokers (610 +/- 80 ml . kg-1). These differences probably reflect the induction of hepatic aryl hydrocarbon hydroxylase (AHH) activity in smokers. The increased clearance of caffeine by smokers may contribute to the higher consumption of coffee reported to occur in this group.
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We describe a rapid, sensitive method for the routine simultaneous determination of nicotine and cotinine in 1 mL of plasma. Extraction in 10-mL screw-capped Teflon tubes with methylene chloride after deproteinization with trichloroacetic acid eliminated emulsion formation. The extract, after evaporation and reconstitution in 30 microL of mobile phase, is injected into a reversed-phase C-18 ion-pair column of an isocratic high-performance liquid-chromatographic unit. Absorbance is monitored at 256 nm. The mobile phase is a citrate-phosphate (30 mmol each per liter) buffer mixture containing 50 mL of acetonitrile and 1 mmol of sodium heptanesulfonate per liter. 2-Phenylimidazole is the internal standard. The detection limit is 1 microgram/L for nicotine and 3 micrograms/L for cotinine. The standard curve is linear from 0 to 700 micrograms/L for both compounds. The average CV for nicotine in the concentration range 0-100 micrograms/L is 6.5%, and that for cotinine in the concentration range 50-700 micrograms/L is 4%.
Article
Caffeine metabolism is known to be accelerated in cigarette smokers, but the effects of smoking on the kinetics and pattern of metabolism in a daily consumption pattern have not been described. We investigated the effects of tobacco abstinence on the rate and pattern of caffeine metabolism in nine habitual smokers who consumed six cups of coffee per day, each cup containing 2 mg/kg caffeine. Abstinence from smoking for 4 days resulted in a 46% increase in the 24-hour AUC. Thus, significant, although probably not complete, normalization of the enzyme-inducing effects of cigarette smoking can be seen after 4 days abstinence. During abstinence, 24-hour urine ratios of dimethylxanthines to caffeine and mono-dimethylxanthines to dimethylxanthines were reduced, suggesting that cigarette smoking accelerates both demethylation steps. Other metabolic pathways were unaffected.
Article
Measurement of cotinine, a nicotine metabolite, has been studied as a method for monitoring smoking behavior and determining smoking status. We describe a specific, sensitive method for quantifying it in plasma and saliva by reversed-phase paired-ion liquid chromatography and detection by absorbance at 257 nm. The cotinine is extracted with methylene chloride, and 2-phenylimidazole is the internal standard. Cotinine peak heights are linearly related to the amount on the column from 0 to 500 ng. The mean (+/- SD) concentration of cotinine in plasma of 31 passively exposed nonsmokers was 2.1 +/- 1.6 micrograms/L (range, 0-7.9 micrograms/L). The regression of saliva cotinine concentration (y) on plasma cotinine concentration (x) at 0, 24, and 48 h in 10 smokers who refrained from smoking for 48 h was y (micrograms/L) = 1.155x (micrograms/L) + 0.245 (r = 0.986). The efficiency of cotinine as a biological marker was determined at 0, 24, and 48 h of smoking abstinence. Within-run CVs were 3.5% (n = 5) and day-to-day CVs 4.4% (n = 6) at 150 micrograms/L.
Article
An improved high-performance liquid chromatographic method for the simultaneous determination of caffeine and its N-demethylated metabolites in plasma is described. Excellent resolution of all components is provided by reversed-phase chromatography using a mobile phase consisting of 1% acetic acid-methanol (83:17) at a flow-rate of 2.7 ml/min, in conjunction with a Waters Assoc. Nova-Pak C18 column which was protected by a Waters Assoc. Guard-Pak precolumn module containing a Guard-Pak CN cartridge. Rapid extraction of caffeine and the dimethylxanthines from plasma was achieved using reversed-phase octadecylsilane bonded-silica columns (Bond-Elut C18). With only 100 microliters of sample, plasma levels in the region of 50 ng/ml for the dimethylxanthines and 100 ng/ml for caffeine can be determined using ultraviolet detection at 273 nm. The method has been used for measuring umbilical cord plasma samples to provide information regarding foetal exposure to caffeine and its metabolites and is also suitable for therapeutic drug monitoring of caffeine and theophylline levels in the treatment of neonatal apnoea.
Article
Data collection and questionnaire design are significant to both researchers and clinical practitioners in the field of adult smoking cessation. Unfortunately, minimal standards for data collection are typically neglected by public service and proprietary programs and are all too often neglected by researchers as well. The purpose of the current paper is not to recommend new standards in this area. Instead, discussion will focus upon some existing standards that profitably can be applied in research and public service settings.
Article
Two experiments designed to assess the relationship between coffee intake and smoking are reported. In Experiment I, coffee drinking smokers were randomly assigned to four groups in which they received 0, 1, 2, or 3 cups of coffee during two one-hour sessions while they worked on crossword puzzles. Results showed that subjects receiving coffee in any amount smoked more than subjects who were not provided coffee. Moderate and low rate smokers were then randomly assigned to one of five groups in Experiment II, in which they were provided no drink, water, Postum® (a coffee substitute), caffeinated, or decaffeinated coffee. These groups were selected to assess the characteristics of coffee that may have influenced increased smoking. Results for number of cigarettes smoked and puff rate generally showed that subjects receiving caffeinated or decaffeinated coffee smoked more than subjects in the no drink or water control groups. The results of this study provide experimental evidence of the role of coffee in setting the occasion for smoking, as well as ruling out the presence of a liquid or caffeine as the important characteristics of coffee in influencing smoking.
Article
The relative influence of nicotine and coffee on cigarette consumption was examined in a laboratory setting. During the first half hour of the experimental session, subjects were either preloaded with two cigarettes or nicotine deprived. During the subsequent hour, subjects were given two cups of either coffee or water, and number of cigarettes smoked during this period was assessed. Results showed a significant preload effect, with non-preloaded subjects smoking an average of .88 cigarettes per hour more than preloaded subjects. A nonsignificant increase in smoking was found for the coffee condition. The implications of these findings for relative effects of pharmacological and environmental events on smoking are discussed.
Article
There is a strong, significant relationship between coffee consumption and smoking. In six epidemiological studies reviewed and analyzed here, 86.4% of smokers consumed coffee versus 77.2% of nonsmokers. Exsmokers use more coffee than nonsmokers but somewhat less than smokers. Seventeen experimental studies suggest that the pharmacologic effect of caffeine in coffee may be partially but not totally responsible for the relationship. Conditioning, a reciprocal interaction (caffeine intake increases anxiety/arousal--nicotine decreases it), or joint effect of a third variable (e.g., stress, alcohol) may account for the relationship. In abstinent smokers, blood caffeine levels increase and remain elevated for as long as 6 months. These higher caffeine plasma levels may be sufficient to produce caffeine toxicity syndrome. A review of 86 studies of nicotine withdrawal, caffeine withdrawal, and caffeine toxicity suggests that the symptoms are similar enough to be confused, and that reported nicotine withdrawal symptoms may be a mixture of nicotine withdrawal and caffeine toxicity.
Mean self-report caffeine and nicotine (in milligrams per measurement day), sputum caffeine
  • Fig
Fig. 1. Mean self-report caffeine and nicotine (in milligrams per measurement day), sputum caffeine (in kg/ mL), and cotinine concentrations (in &mL) during baseline, and days post-cessation.
1620) = 1.99, p = .003, p(Huynh-Feldt Epsilon) = .005. Figure 2 shows that the baseline low and high caffeine users slept longer than moderate-caffeine users in both Changes in rate and pattern of caffeine metabolism after cigarette abstinence
  • J A Swanson
Finally, a statistically significant interaction was found for self-reported hours slept, F(24,1620) = 1.99, p =.003, p(Huynh-Feldt Epsilon) =.005. Figure 2 shows that the baseline low and high caffeine users slept longer than moderate-caffeine users in both J. A. SWANSON et al. Brown, C. R., Jacob, III, I?, Wilson, M. & Benowitz, N. L. (1988). Changes in rate and pattern of caffeine metabolism after cigarette abstinence. Clinicat Pharmacology & Therapeutics 43,488491.
Effects of cimetidine on caffeine dispo-sition in smokers and nonsmokers Clinical Pharmacology and Therapeutics, 31 Relative effects of nicotine and coffee on cigarette smoking
  • D C May
  • C H Jarboe
  • A B Vanbakel
  • W M Williams
May, D. C., Jarboe, C. H., VanBakel, A. B., & Williams, W. M. (1982). Effects of cimetidine on caffeine dispo-sition in smokers and nonsmokers Clinical Pharmacology and Therapeutics, 31.656661. Ossip, D. J., & Epstein, L. H. (1981). Relative effects of nicotine and coffee on cigarette smoking. Addictive Behaviors, 6,35-39.
Tar, nicotine, and carbon monoxide of the smoke of 475 varieties of domestic cigarettes
  • U.S. Department of Health and Human Services