Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Caffeine”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources
PubMed1999

The frequency of caffeine withdrawal in a population-based survey and in a controlled, blinded pilot experiment.

Reports of symptoms when regular caffeine consumption is stopped have appeared in the medical literature, but the frequency and significance of this phenomenon have remained controversial. The objective of this study was to collect information on the prevalence and severity of caffeine withdrawal in the general population and determine the incidence and type of symptoms reported on blind abrupt and gradual caffeine cessation among coffee drinkers reporting past episodes of caffeine-withdrawal symptoms. A community-based telephone survey was followed by a stratified, randomized, double-blind controlled study. Participants included 11,112 persons spontaneously calling to inquire about studies not related to caffeine and 57 regular caffeine users selected from among the callers because of self-reported caffeine-withdrawal symptoms. Gradual or abrupt withdrawal from caffeine was compared to continuation of the same caffeine level. In a survey of 11,112 persons, 61% reported daily caffeine consumption, and 11% of the caffeine consumers reported symptoms upon stopping caffeine. Among the regular caffeine users, only 0.9% of males and 5.5% of females reported symptoms significant enough to interfere with normal activities when they abruptly stopped caffeine. A group of those reporting withdrawal symptoms were randomly assigned to three subsamples. In the group subjected to abrupt withdrawal (N = 18), 6 (33.3%) reported symptoms (e.g., headaches and tiredness). Including decreases in functional ratings, a total of 7 of the 18 (38.8%) could be considered to have experienced caffeine withdrawal. The gradual withdrawal group (N = 20) reported minimal if any caffeine withdrawal symptoms. A third group (N = 18) was kept on a level dose of caffeine for comparison. When participants are unaware of the caffeine-withdrawal focus of the study, these results suggest that both the frequency and severity of caffeine-withdrawal symptoms are much lower than found in some previous reports and that clinically significant symptoms may be uncommon events among the general population.

Adult↗
PubMed2001

Caffeine levels in saliva: associations with psychosocial factors and behavioural effects.

The present study had two main aims. The first was to examine associations between psychosocial factors, health-related behaviours, regular level of caffeine consumption, time of day and levels of caffeine in saliva following acute caffeine challenges. The second aim was to determine whether individual differences in changes in performance following ingestion of caffeine were related to levels of caffeine in saliva. One hundred and forty-four young adults participated in the study. Questionnaires were administered prior to the study to measure psychosocial characteristics, health-related behaviours and habitual levels of caffeine consumption. Two double-blind acute caffeine challenges were then carried out 1 week apart. Volunteers were given either placebo or 1.5 or 3 mg/kg of caffeine on each occasion. The challenges were carried out at 8 : 00, 11 : 00, 14 : 00 or 18 : 00 h so that the impact of time of day could be assessed. In the week between the two challenges the volunteers consumed either caffeinated or decaffeinated products. This allowed investigation of the effects of caffeine withdrawal on caffeine metabolism. Prior to each caffeine challenge volunteers performed a range of tasks, and a baseline saliva sample was taken. The tasks were repeated 1 h after ingestion of the caffeine, with saliva samples being taken at the start and end of the 1 h test battery. The results showed that the level of caffeine in the saliva was a good indicator of the dose of caffeine consumed and of compliance with the withdrawal manipulation. Caffeine levels were not influenced by time of day, habitual caffeine consumption, psychosocial factors or health-related behaviours. Individual differences in caffeine levels in saliva were not related to the individual variation in the effects of caffeine on performance. Copyright 2001 John Wiley & Sons, Ltd.

Journal Article↗
PubMed1992

Oral caffeine consumption by rats: the role of flavor history, concentration, concurrent food, and an adenosine agonist.

Some determinants of caffeine consumption by rats were examined using the two-bottle choice test. To describe the role of flavor history, groups of eight rats each received one of three fluids as their only source of fluid beginning at 29 days of age and continuing throughout the experiments. One group ("water") received tapwater, a second group ("caffeine") received 0.5 mg/ml caffeine in tapwater, and a third group ("quinine") received 0.01 mg/ml quinine in tapwater. Two-bottle choice tests began when rats were 40 days old. In the initial tests, caffeine rats drank more caffeinated water than water rats. Quinine rats were midway between these two groups. On a second block of tests, quinine and water rats' caffeine consumption increased so that the three groups were indistinguishable. When 0.5 mg/ml caffeine was available for 24 h, about one third of the total fluid consumption was of caffeinated water for all three groups. The presence of food greatly increased both caffeine and water consumption across a range of caffeine concentrations spanning 0.125-4.0 mg/ml. Increasing caffeine concentration generally increased consumption of plain water and decreased that of caffeinated water (but not total caffeine consumed) for water rats. Caffeine rats generally drank more caffeine than water rats, largely due to a tendency toward increased consumption of the 0.5-mg/ml concentration. Consumption of caffeinated water peaked at 0.5 mg/ml and showed graded decreases at higher and lower concentrations. Caffeine consumption showed dose-related increases with presession administration of l-phenylisopropyl adenosine. The serines of experiments characterize some of the determinants of caffeine consumption in rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed2006

Fewer but heavier caffeine consumers in schizophrenia: a case-control study.

According to the literature, there is an association between schizophrenia and caffeine consumption, but it is not clear whether schizophrenia is associated with either higher prevalence of daily caffeine intake or the amount consumed. In this study we compared our previously published schizophrenia patients (n=250) with a control sample (n=290) after controlling for demographic variables and tobacco and alcohol consumption. Current caffeine intake was less frequent in schizophrenia patients (59%, 147/250) than in controls (70%, 204/290). In the multivariate analyses, caffeine intake was less frequent at an older age and in schizophrenia patients, and more frequent in smokers and alcohol users. Among caffeine consumers, heavy caffeine intake (> or =200 mg/day) was significantly associated with schizophrenia (64%, 94/147 in schizophrenia versus 36%, 73/204 in controls), as well as older age and smoking. Daily amount of caffeine intake and smoked cigarettes correlated significantly in the schizophrenia group but not in the control group; the correlation of caffeine intake with nicotine dependence was low and non-significant in both groups. The association between current smoking and heavy caffeine intake may be partly explained by a pharmacokinetic effect: tobacco smoke compounds induce caffeine metabolism by the cytochrome P450 1A2. Although schizophrenia by itself may be associated with heavy caffeine intake in caffeine users, part of this association was explained by the association between schizophrenia and smoking. The relationship between caffeine and alcohol intake appeared to be more complex; alcohol and caffeine use were significantly associated, but within caffeine users alcohol was associated with less frequent heavy caffeine consumption among smokers. In future studies, the measurement of plasma caffeine levels will help both to better define heavy caffeine intake and to control for smoking pharmacokinetic effects.

Adolescent↗
PubMedDate not supplied

Acute but not chronic caffeine impairs functional responses to ischaemia-reperfusion in rat isolated perfused heart.

1. The effect of acute (50 micromol/L) and chronic (0.06% in drinking water for 14 days) caffeine on the response to ischaemia-reperfusion was studied in Wistar rat isolated perfused hearts. 2. Neither acute nor chronic caffeine modified normoxic heart rate or left ventricular pressures. However, acute caffeine decreased coronary flow by up to 20%, while chronic caffeine consumption increased coronary flow by approximately 15% and abolished the vasoconstrictor effect of acute caffeine (P<0.05). 3. After 15 min global ischaemia, chronic caffeine treatment did not alter the recovery of left ventricular diastolic pressure (LVDP), end-diastolic pressure (EDP) or heart rate during reperfusion, but did enhance coronary flow rate (P<0.05). Acute caffeine inhibited the recovery of LVDP and elevated postischaemic EDP in both caffeine-naive and chronic caffeine-treated groups. Acute caffeine also significantly inhibited coronary reflow in naive but not chronic caffeine-treated groups and produced a transient tachycardia during reperfusion in hearts from chronic caffeine-treated rats. 4. The incidence of arrhythmias was unaltered by chronic caffeine treatment, but was increased by acute caffeine in both naive and chronic caffeine hearts. 5. In conclusion, chronic caffeine intake alone has no detrimental effects on recovery from ischaemia; however, acute caffeine worsens postischaemic contractile function in hearts from naive and chronic caffeine-treated rats.

Animals↗
PubMed2006

Psychostimulant and other effects of caffeine in 9- to 11-year-old children.

BACKGROUND: Recent research on adults suggests that "beneficial" psychostimulant effects of caffeine are found only in the context of caffeine deprivation; that is, caffeine improves psychomotor and cognitive performance in habitual caffeine consumers following caffeine withdrawal. Furthermore, no net benefit is gained because performance is merely restored to "baseline" levels. The effects of caffeine in children is an under-researched area, with only a handful of studies being carried out in the US where children's consumption of caffeine appears to be lower on average than in the UK. METHOD: Twenty-six children aged between 9 and 11 years completed a double-blind, placebo-controlled study. Habitual caffeine consumers (mean daily caffeine intake = 109 mg) and non/low-consumers (12 mg) were tested on two separate days following overnight caffeine abstinence. On each day measures of cognitive performance (a number search task), and self-rated mood and physical symptoms, including alertness and headache, were taken before and after administration of 50 mg of caffeine, or placebo. RESULTS: At baseline (before treatment), the habitual consumers showed poorer performance on the cognitive test than did the non/low-consumers, although no significant differences in mood or physical symptoms were found between the two groups. There were significant habit by treatment (caffeine vs. placebo) interactions for accuracy of performance and headache, and a significant main effect of treatment for alertness. Post hoc comparisons showed that caffeine administration improved the consumers' accuracy on the cognitive test (to near the level displayed by the non/low-consumers at baseline), but that it had no significant effect on the non/low-consumers' performance. In the consumers, caffeine prevented an increase in headache that occurred after placebo, and it increased alertness relative to placebo. Again, however, caffeine did not significantly affect levels of headache or alertness in the non/low-consumers. CONCLUSIONS: These results suggest that, like adults, children probably derive little or no benefit from habitual caffeine intake, although negative symptoms associated with overnight caffeine withdrawal are avoided or rapidly reversed by subsequent caffeine consumption.

Affect↗
PubMed1988

Inhibitory effects of caffeine on contractions and calcium movement in vascular and intestinal smooth muscle.

1. The mechanism of the inhibitory effect of caffeine was investigated using vascular smooth muscle of rabbit aorta and intestinal smooth muscle of taenia isolated from guinea-pig caecum. 2. Caffeine, 0.5-10 mM, relaxed the sustained contraction induced by 65.4 mM KCl or 10(-6) M noradrenaline in aorta, and by 45.4 mM KCl or 10(-6) M carbachol in taenia. The inhibitory effect of caffeine on the high K+-induced contraction was antagonized by external Ca2+ but not by the Ca2 channel activators, Bay K 8644 (10(-7) M) or CGP 28,392 (10(-7) M). Forskolin (2 x 10(-7) M) potentiated the inhibitory effect of caffeine on the noradrenaline-induced contraction but not on the high K+- or carbachol-induced contraction. Caffeine induced a time- and concentration-dependent increase in the cyclic AMP content of aorta and forskolin caused a further augmentation. 3. 45Ca2+ uptake was increased by high K+ or noradrenaline in aorta and by high K+ or carbachol in taenia. The increments were inhibited by caffeine at concentrations needed to inhibit muscle contractions. 4. 45Ca2+ in the cellular releasable site in aorta was decreased either by noradrenaline or by caffeine. Simultaneous application of noradrenaline and caffeine did not induce an additive decrease. 5. In aorta treated with a Ca2+-free solution, caffeine induced only a small contraction. Noradrenaline induced a greater contraction which was inhibited by caffeine. After washout of caffeine and noradrenaline, the second application of noradrenaline induced a transient contraction suggesting that caffeine does not deplete the noradrenaline-sensitive store. 6. It was concluded that caffeine has multiple sites of action in smooth muscle. Caffeine releases Ca2+ from a store which is apparently not sensitive to noradrenaline. Caffeine may inhibit noradrenalineinduced Ca2' release. Caffeine itself induces only a small contraction possibly because it decreases the Ca2+ sensitivity of contractile filaments and/or increases Ca2+ extrusion. Further, caffeine seems to inhibit stimulated Ca2+ influx. Cyclic AMP may be only partly responsible for the inhibitory effect of caffeine.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1997

Effects of caffeine on the influx of extracellular calcium in GH4C1 pituitary cells.

Caffeine increases intracellular Ca2+ concentrations ([Ca2+]i) in a variety of cell types by triggering the mobilization of Ca2+ from intracellular Ca2+ stores. Caffeine also can change [Ca2+]i by affecting Ca2+ influx through voltage-operated Ca2+ channels (VOCCs). In the present study, we investigated the effects of caffeine on Ca2+ entry in GH4C1 pituitary cells. Pretreatment of the cells with caffeine attenuated the high K+-evoked influx of 45Ca2+ in a dose-dependent manner. This inhibition was not secondary to the caffeine-evoked elevation of [Ca2+]i because caffeine was able to inhibit VOCCs also in the presence of the intracellular Ca2+ chelator BAPTA. However, the inhibitory effect of caffeine on 45Ca2+ entry appeared to be dependent on the degree of depolarization of the plasma membrane. Only in cells depolarized with relatively high concentrations of K+ (20, 35, and 50 mM) was the caffeine-induced inhibition observed. A similar inhibitory effect of caffeine on the high K+-evoked calcium and barium entry was observed in experiments using Fura 2. Neither IBMX, forskolin nor dibutyryl cAMP reduced the enhanced [Ca2+]i induced by 50 mM K+, suggesting that the effect of caffeine was not due to increased intracellular cAMP. Furthermore, high doses of caffeine inhibited the plateau level of the TRH-induced increase in [Ca2+]i, which is caused partly by influx of Ca2+ through VOCCs. The inhibitory effect of caffeine was, in part, due to an hyperpolarization of the plasma membrane observed at high doses of caffeine. On the other hand, low doses of caffeine enhanced depolarization-evoked Ba2+ entry as well as the TRH-evoked plateau level of [Ca2+]i. We conclude that caffeine has a dual effect on Ca2+ entry through activated VOCCs in GH4C1 cells: at low concentrations caffeine enhances Ca2+ entry, whereas high concentrations of caffeine block Ca2+ entry.

Animals↗
PubMed2002

Oral caffeine maintenance potentiates the reinforcing and stimulant subjective effects of intravenous nicotine in cigarette smokers.

RATIONALE: Epidemiological, clinical and pre-clinical observations suggest that caffeine can potentiate the reinforcing and discriminative effects of nicotine. OBJECTIVE: The present study examined whether chronic exposure to moderate doses of caffeine affects the reinforcing and subjective effects of intravenously administered nicotine. METHODS: The effects of oral caffeine maintenance on the subjective and physiological effects of intravenously administered nicotine and caffeine were examined using double-blind methods in nine volunteers with current use of tobacco, caffeine, and cocaine. Each subject was exposed to two chronic drug phases (200 mg/70 kg oral caffeine t.i.d. and placebo t.i.d.), each of at least 12 days duration. Within each drug phase, the subject received intravenous injections of placebo, nicotine (1.0 and 2.0 mg/70 kg), and caffeine (200 and 400 mg/70 kg) in mixed order. Physiological and subjective data were collected before and repeatedly after drug or placebo injection. RESULTS: Both intravenous nicotine and caffeine produced significant increases in ratings of drug effect, stimulated, rush, and bad effect, with only nicotine significantly increasing ratings of liking and good effect. Caffeine maintenance significantly increased ratings of drug effect and stimulated after the high dose of nicotine, and significantly decreased ratings of bad effect after the low dose of nicotine. Caffeine maintenance also significantly increased the identification of the low dose of nicotine as a stimulant. A drug versus money measure of reinforcement showed that subjects were willing to pay money to receive nicotine injections, but willing to forfeit money to avoid caffeine injections. Furthermore, subjects were willing to pay significantly more money to receive the high dose of nicotine in the caffeine maintenance phase than in the abstinence phase. Both intravenous nicotine and caffeine increased diastolic blood pressure and decreased skin temperature, and nicotine also increased heart rate. These physiological effects of intravenous nicotine and caffeine as well as the subjective effects of intravenous caffeine were not influenced by caffeine maintenance. CONCLUSIONS: The results extend recent clinical and preclinical findings by showing that oral caffeine maintenance can potentiate the reinforcing and stimulant subjective effects of nicotine.

Administration, Oral↗
PubMed1998

Conditioned flavour preference negatively reinforced by caffeine in human volunteers.

This study examined whether 100 mg caffeine could reinforce preference for the flavour of a novel drink in moderate caffeine users, both after overnight caffeine abstinence and 2 h after receiving 100 mg caffeine, using a two-stage between-groups procedure with 36 volunteers. In the first stage, liking for a test drink (fruit tea) was assessed at breakfast following overnight caffeine abstinence, with half the subjects receiving caffeine. Liking for the tea increased significantly over four trials for subjects receiving caffeine, and decreased significantly in those without caffeine. These effects were greatest in subjects who rated the drink as highly novel. In stage two, subjects evaluated a second drink (fruit-juice) 2 h after receiving the tea, and again half the subjects received caffeine Those subjects who received caffeine in stage two but not stage one showed a significant increase in liking for the fruit-juice over the 4 test days, whereas subjects who did not receive caffeine at either stage showed a progressive decrease in liking for this drink. In contrast, no significant change in liking for the fruit-juice was seen at stage two for subjects who had received caffeine in stage one, regardless of the presence or absence of caffeine at stage two. Caffeine at breakfast increased ratings of energetic and lively, and energetic ratings also increased following caffeine in the fruit-juice in subjects who had not had caffeine at breakfast. Overall, these data are consistent with a negative reinforcement model of caffeine reinforcement, and demonstrate further the utility of the conditioned flavour preference method for evaluating reinforcing effects of drugs in humans.

Adult↗
PubMed2001

No evidence for latent learning of liking for flavours conditioned by caffeine.

RATIONALE: The ability of caffeine to condition liking for flavours depends on the caffeine deprivation status of subjects; however, it is not known if a latent liking for a flavour can be acquired in an undeprived state, which subsequently emerges when consumers are caffeine deprived. OBJECTIVES: To determine if exposure of undeprived caffeine consumers to a novel drink containing caffeine leads to increased liking for this drink when they are subsequently tested when caffeine-deprived. METHODS: In a double-blind placebo controlled study, four groups of 13 moderate caffeine consumers evaluated a novel flavoured drink on 5 days. The test group consumed this drink with 100 mg caffeine when undeprived on days 1-4, and in a deprived state on day 5. Three control groups had the same conditions on all 5 days, with an undeprived group receiving the caffeinated drink, and two deprived groups receiving the drink with caffeine or placebo. RESULTS: The pleasantness of the drink did not change over the 4 training days in the test group, and did not alter when this group was tested when caffeine-deprived. At no stage did these ratings differ between the test and undeprived control groups. Pleasantness increased significantly over the 5 days in the deprived group who received caffeine, and decreased in the deprived group who received placebo. CONCLUSIONS: These results suggest that repeated pairing of a novel flavour with the effects of caffeine in subjects who are not caffeine deprived does not lead to an emergent liking for that flavour when subsequently tested caffeine-deprived. However, the pleasantness of the same caffeinated drink increased if it was consumed when caffeine deprived.

Adult↗
PubMed2003

A pilot study of plasma caffeine concentrations in a US sample of smoker and nonsmoker volunteers.

Even though 85% of adults drink caffeinated beverages daily, very limited studies on plasma caffeine concentration in the US population have been published. Smoking induces cytochrome P450 1A2 (CYP1A2), which is the main enzyme involved in caffeine metabolism. The current naturalistic pilot study explores plasma caffeine concentrations in a US sample, and presents a mathematical model of the relationship between caffeine intake and plasma concentrations for smokers and nonsmokers. Caffeine intake and average plasma caffeine concentrations from morning (7:30-9:30 a.m.) and afternoon (2:00-4:00 p.m.) samples were studied in 69 volunteers (21 smokers and 48 nonsmokers). The mean caffeine intake obtained from caffeinated beverages was 3.02 mg/kg/day, which is similar to the intake in the US population. Almost all subjects in the present sample (99%; 95% confidence interval [CI]: 96-100) had detectable plasma caffeine concentrations. Smokers had significantly higher caffeine intake than nonsmokers. The ratio of concentration/dose of caffeine from caffeinated beverages was approximately four-fold higher in nonsmokers (1.33 kgxday/l) than in smokers (0.29 kgxday/l). According to the model, the median plasma caffeine concentration was two- to three-fold higher in nonsmokers for each level of caffeine intake. Our model improves our understanding of the interactions between caffeine and smoking. Additional studies are needed to replicate the model. This model may help epidemiologists to correct for the effects of smoking on caffeine intake and pharmacologists to screen for the activity of CYP1A2.

Adult↗
PubMed1995

Caffeine-evoked, calcium-sensitive membrane currents in rabbit aortic endothelial cells.

1. Single cell photometry and whole-cell patch clamp recording were used to study caffeine-induced intracellular Ca2+ signals and membrane currents, respectively, in endothelial cells freshly dissociated from rabbit aorta. 2. Caffeine (5 mM) evoked a transient increase in [Ca2+]i in fura-2-loaded endothelial cells. Pretreatment of cells with 10 microM ryanodine did not alter resting [Ca2+]i but irreversibly inhibited the caffeine-induced rise in [Ca2+]i. The caffeine-induced increase in [Ca2+]i was not attenuated by the removal of extracellular Ca2+ and did not stimulate the rate of Mn2+ quench of fura-2 fluorescence. 3. Bath application of caffeine evoked a dose- and voltage-dependent outward current. The rate of onset and amplitude of the caffeine-evoked outward current increased with higher caffeine concentrations and membrane depolarization. The relationship between caffeine-evoked current amplitude and membrane potential was non linear, suggesting that the channels underlying the current are voltage-sensitive. 4. In the absence of extracellular Ca2+, the amplitude of the caffeine-evoked outward current was reduced by approximately 50% but the duration of the current was prolonged compared to that observed in the presence of external Ca2+. Ca(2+)-free external solutions produced an unexpected increase in both the frequency and amplitude of spontaneous transient outward currents (STOCs). 5. Inclusion of heparin (10 micrograms ml-1) in the patch pipette abolished the acetylcholine (ACh)-induced outward current but failed to inhibit either STOCs or the caffeine-evoked outward current in native endothelial cells. In the absence of extracellular Ca2+, heparin did not affect either STOCs or the caffeine-induced outward current. 6. Externally applied tetraethylammonium ions (TEA, 3-10mM) reversibly inhibited unitary Ca2+-activated K+ currents and STOCs in endothelial cells but failed to inhibit completely the outward current evoked by 20 mM caffeine.7. Bath application of 0.1 mM zinc ion (Zn2+), a chloride channel blocker, did not affect unitary currents or STOCs but reduced the amplitude of the caffeine-evoked current by >75% compared to control. Replacement of extracellular NaCl with Na gluconate also reduced the amplitude of the caffeine-induced outward current. Bath application of 0.1 mM Zn2+ and 10 mM TEA completely blocked the caffeine-evoked outward current in endothelial cells.8. Caffeine-induced Ca2+ release from intracellular stores evokes a transient rise in [Ca2+1, which is correlated with a large, transient outward current. The ionic dependence and inhibition of the caffeine sensitive current by TEA and Zn2+ suggests that Ca2+-activated K+ and Cl- conductances contribute to the caffeine response in rabbit aortic endothelial cells.

Animals↗
PubMed1992

Caffeine inhibits the agonist-evoked cytosolic Ca2+ signal in mouse pancreatic acinar cells by blocking inositol trisphosphate production.

The inhibitory effects of caffeine on receptor-activated cytosolic Ca2+ signal generation in isolated mouse pancreatic acinar cells were investigated. Using the ability of caffeine to quench Indo-1 fluorescence we measured simultaneously the free intracellular Ca2+ concentration ([Ca2+]i) and the intracellular caffeine concentration ([caffeine]i). We also measured inositol 1,4,5-trisphosphate (InsP3) production with a radioreceptor assay. When caffeine was added to the extracellular solution during a sustained receptor-activated increase in [Ca2+]i, [caffeine]i rose to its steady level within a few seconds. This was accompanied by a decrease of [Ca2+]i, which started only after [caffeine]i had reached an apparent threshold concentration (about 2 mM in the case of 0.5 microM acetylcholine (ACh) stimulation). Above this [caffeine]i level there was a linear relationship between [caffeine]i and [Ca2+]i. Throughout the caffeine exposure [Ca2+]i remained at a steady low level. Following removal of caffeine from the bath, [caffeine]i decreased to zero within seconds. There was no significant increase in [Ca2+]i until [caffeine]i had been reduced to the threshold level (about 2 mM at 0.5 microM ACh). Caffeine inhibited Ca2+ signals evoked by ACh, cholecystokinin, and ATP and also inhibited signals generated in the absence of external Ca2+. Caffeine application had the same effect as removal of agonist allowing recovery from apparent desensitization. Caffeine inhibited the agonist-evoked production of InsP3 in a dose-dependent manner. Our results demonstrate the acute and reversible dose-dependent inhibition of agonist-evoked cytosolic Ca2+ signal generation due to rapid intracellular caffeine accumulation and washout. The inhibition can be explained by the reduction of agonist-evoked InsP3 production.

Acetylcholine↗
PubMed2000

Acquisition and extinction of flavour preferences conditioned by caffeine in humans.

Previous research has shown that moderate caffeine users develop a liking for the flavour of a novel caffeinated drink only if they experience this drink in a caffeine-deprived state. This study tested how sensitive these conditioned-flavour preferences are to subsequent changes in deprivation state and the continued presence or absence of caffeine. Thirty-six moderate caffeine consumers were given 4 training days during which they evaluated a novel flavoured caffeinated drink consumed mid-morning after 12 h caffeine deprivation. Subjects were then divided into four groups depending on whether or not they remained caffeine-deprived and whether the test drink continued to contain caffeine. They then re-evaluated the novel drink over a further 4 test days. As expected, liking for the test drink increased across the 4 training days, and this increased liking was maintained across the 4 test days in the group who continued to receive the caffeinated version of the drink in a caffeine-deprived state. Liking decreased in the test phase in the caffeine-deprived group who no longer received caffeine (extinction). It is surprising that both groups who were tested in a non-deprived state showed a marked decrease in liking on all 4 test days relative to the last training day. This implies that conditioned-flavour preferences may not be expressed in the absence of the relevant motivational state (caffeine deprivation). Together, these data suggest that flavour preferences conditioned by caffeine are very sensitive to changes in the contingent relationship between deprivation state and caffeine content of the drink.

Adult↗
PubMed1994

Caffeine-induced calcium release in sea urchin eggs and the effect of continuous versus pulsed application on the mitotic apparatus.

Unfertilized and fertilized eggs of the sea urchins Strongylocentrotus purpuratus and Lytechinus pictus, injected with the fluorescent probe calcium green dextran (Molecular Probes, Inc.) and monitored with single cell fluorimetry, rarely responded to 10 mM caffeine, but with 20 mM caffeine they produced a transient rise in intracellular calcium. Unfertilized eggs of both species produced a sharp peak approximately 2/3 the height of the normal fertilization peak, with the L. pictus response usually slightly lower and more variable. Image-intensified video microscopy of S. purpuratus eggs showed that this release originated in the center of the egg as well as in the cortex. When caffeine was applied to fertilized eggs within 10-15 min after the fertilization peak, during the period of elevated calcium, the size of the resulting calcium release increased with the elapsed time between the peak and the time of caffeine application. For example, there was no release when caffeine was applied at the height of the peak. When caffeine was washed out after the calcium level returned to baseline, there was a secondary peak (in the absence of caffeine) whose size decreased in proportion to the elapsed time. The source of this secondary calcium release is not known. Caffeine applied after the fertilization peak had returned to baseline produced a transient peak that was not followed by a secondary peak. The caffeine response gradually increased during the cell cycle. Although 10 mM caffeine did not produce a measurable calcium release, light microscopy of fixed and sectioned material showed that fertilized eggs incubated throughout the cell cycle in 7-10 mM caffeine-sea water had greatly reduced numbers of microtubules. Eggs treated at prometaphase with 10 mM caffeine rapidly lost a formed mitotic apparatus by shortening of the spindle and movement of the two centrosomes to the metaphase plate. Within 15 min all the mitotic apparatus-associated vesicles, which are known to sequester calcium, aggregated into two dense spheres of packed membranes located at the sites of the former asters. Microtubules and asters rapidly recovered when caffeine was removed. These observations suggest: (1) that the caffeine-sensitive store contributes to the fertilization calcium release and is an important sink for calcium after the fertilization peak, (2) that the caffeine-sensitive store in unfertilized eggs is located in the central part of the egg as well as in the cortex, and (3) that the caffeine-sensitive store is associated with the membrane system of the mitotic apparatus and may serve as a regulator of microtubule polymerization.

Animals↗
PubMed2005

Food sources and intakes of caffeine in the diets of persons in the United States.

This study provides information on the caffeine intakes of a representative sample of the US population using the US Department of Agriculture 1994 to 1996 and 1998 Continuing Survey of Food Intakes by Individuals. The percentage of caffeine consumers of the total sample (N=18,081) and by age and sex groups and for pregnant women were determined. Among caffeine consumers (n=15,716), the following were determined: mean intakes of caffeine (milligrams per day and milligrams per kilogram per day) for all caffeine consumers, as well as for each age and sex group and pregnant women; mean intakes (milligrams per day) of caffeine by food and beverage sources; and the percent contribution of each food and beverage category to total caffeine intake for all caffeine consumers, as well as each age and sex group and pregnant women. Eight-seven percent of the sample consumed food and beverages containing caffeine. On average, caffeine consumers' intakes were 193 mg caffeine per day and 1.2 mg caffeine per kilogram of body weight per day. As age increased, caffeine consumption increased among people aged 2 to 54 years. Men and women aged 35 to 64 years were among the highest consumers of caffeine. Major sources of caffeine were coffee (71%), soft drinks (16%), and tea (12%). Coffee was the major source of caffeine in the diets of adults, whereas soft drinks were the primary source for children and teens.

Adolescent↗
PubMed2006

Caffeine content of decaffeinated coffee.

Caffeine is the most widely consumed drug in the world with coffee representing a major source of intake. Despite widespread availability, various medical conditions necessitate caffeine-restricted diets. Patients on certain prescription medications are advised to discontinue caffeine intake. Such admonition has implications for certain psychiatric patients because of pharmacokinetic interactions between caffeine and certain anti-anxiety drugs. In an effort to abstain from caffeine, patients may substitute decaffeinated for caffeinated coffee. However, decaffeinated beverages are known to contain caffeine in varying amounts. The present study determined the caffeine content in a variety of decaffeinated coffee drinks. In phase 1 of the study, 10 decaffeinated samples were collected from different coffee establishments. In phase 2 of the study, Starbucks espresso decaffeinated (N=6) and Starbucks brewed decaffeinated coffee (N=6) samples were collected from the same outlet to evaluate variability of caffeine content of the same drink. The 10 decaffeinated coffee samples from different outlets contained caffeine in the range of 0-13.9 mg/16-oz serving. The caffeine content for the Starbucks espresso and the Starbucks brewed samples collected from the same outlet were 3.0-15.8 mg/shot and 12.0-13.4 mg/16-oz serving, respectively. Patients vulnerable to caffeine effects should be advised that caffeine may be present in coffees purported to be decaffeinated. Further research is warranted on the potential deleterious effects of consumption of "decaffeinated" coffee that contains caffeine on caffeine-restricted patients. Additionally, further exploration is merited for the possible physical dependence potential of low doses of caffeine such as those concentrations found in decaffeinated coffee.

Caffeine↗