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PubMed1988

Biochemical validation of self-reported caffeine consumption during caffeine fading.

Increasing concern about caffeine as a drug with potential for abuse has resulted in the development of procedures for effecting reductions in caffeine consumption among heavy users. However, the reliability of reported findings may be questioned, since previous studies have relied on subject self-report as the principal measure of caffeine use. The present study employed bioanalytic methods for assessing the reliability of self-reported caffeine intake during a caffeine-fading regime. Twelve subjects, each with a history of heavy caffeine use, provided baseline, treatment, and follow-up blood samples which were assayed for caffeine and its major metabolites. General support was provided for the reliability of self-report as a measure of caffeine consumption. The general efficacy of caffeine fading was also supported, although there were indications that maintenance effects may have been over-estimated in previous studies.

Adult↗
PubMed2000

Expression of flavour preferences conditioned by caffeine is dependent on caffeine deprivation state.

RATIONALE: The acquisition of a caffeine conditioned flavour preference depends on the caffeine deprivation status of subjects during conditioning. It is not known if the expression of an established flavour preference is also state-dependent. OBJECTIVES: To determine if the expression of a flavour preference conditioned by caffeine is dependent on the level of deprivation at the time of testing. METHODS: In a double-blind placebo controlled study, 44 subjects were given 4 days exposure to a novel flavoured drink following overnight abstinence from caffeine. Half the subjects received caffeine (100 mg) in the drink, while the remainder had placebo (maltodextrin, 100 mg). Subjects rated the pleasantness of the drink each time. On a fifth (test) day, the subjects were given additional caffeine (100 mg) or placebo 2 h before consuming and rating the pleasantness of the drink. RESULTS: Pleasantness ratings for the novel drink increased over the 4 conditioning days in subjects receiving caffeine, but decreased in those given placebo. On day 5, subjects who were trained and tested in the same caffeine deprivation state expressed pleasantness ratings similar to those for the final training day. In contrast, subjects who were trained and tested in different states expressed pleasantness ratings that were significantly different from those of the final training day. CONCLUSIONS: These results suggest that the expression of caffeine conditioned flavour preferences are acutely sensitive to current motivational state, and a number of possible explanations are discussed.

Adult↗
PubMed2004

Studies on the mechanism of caffeine action in alveolar macrophages: caffeine elevates cyclic adenosine monophosphate level and prostaglandin synthesis.

We have previously reported that the effects of caffeine on alveolar macrophages are dose-dependent; thus, at low concentrations caffeine prevents apoptosis and at moderate concentrations, the cells proceed into apoptosis. In the current study, the mechanism of caffeine action via prostaglandin synthesis and cyclic adenosine monophosphate (cAMP) was investigated using moderate concentrations of caffeine. The results show that the combination of caffeine with indomethacin, an inhibitor of prostaglandin synthesis, mediated caffeine's effect by increasing cellular viability and lowering superoxide anion production and DNA fragmentation. However, addition of exogenous prostaglandin E2 (PGE2) to the culture in the presence of caffeine had the opposite effect, in which the viability was decreased and anion superoxide production was increased. Incubation of macrophages with exogenous dibutyryl cAMP showed nearly similar effects to caffeine. At low concentrations (<50 micromol/L), higher viability and lower superoxide production pattern were evident and at higher concentrations (>50 micromol/L) the cells proceeded into apoptosis. Therefore, it is suggested that caffeine exerts its effects on macrophages by altering cAMP level and prostaglandin synthesis.

Animals↗
PubMed2004

How habitual caffeine consumption and dose influence flavour preference conditioning with caffeine.

This study investigated the effects of both habitual caffeine use and dose administered in determining the ability of caffeine to reinforce conditioned changes in flavour preference. Thirty overnight-withdrawn moderate caffeine consumers and 30 non or low-dose caffeine (non/low) consumers evaluated five novel-flavoured fruit teas. Subsequently, their median-rated tea was used in four ensuing conditioning sessions. Either placebo, 1 or 2 mg/kg of caffeine (n=10 consumers, 10 non/low consumers in each condition), was added to the target tea, and all five teas were reevaluated at a final tasting. Pleasantness ratings over the four conditioning sessions indicated that non/low consumers' liking increased for the noncaffeinated fruit tea with no change for the tea containing either 1 or 2 mg/kg of caffeine. Among consumers, pleasantness ratings tended to decrease for the noncaffeinated fruit tea but increased significantly at the 1-mg dose and showed a tendency to increase at the 2-mg dose. Similar effects were shown in the evaluations made before and after conditioning, with no change in the nonexposed drinks. These results show that 1.0 mg/kg of caffeine reinforces changes in flavour pleasantness in acutely withdrawn habitual consumers but not in nonconsumers or nondependent low-caffeine consumers, further endorsing the negative-reinforcement theory of conditioning with caffeine.

Adult↗
PubMed2002

Repetitive application of caffeine sensitizes caffeine-induced Ca2+ release in bullfrog sympathetic ganglion neurons.

Cytosolic free calcium concentration ([Ca(2+)](i)) was recorded from cultured bullfrog sympathetic ganglion cells loaded with the Ca(2+)-indicator Fura-2 or Fura-6F. Repetitive application of caffeine at a low concentration, which either failed to produce any [Ca(2+)](i) elevation or induced a small gradual increase in [Ca(2+)](i) at first challenge, produced a drastic increase in the amplitude of Ca(2+) release (caffeine response). The caffeine response eventually reached peak amplitude and then remained constant even if caffeine application were continued. This augmentation was maintained for up to 2 h, and was achieved not only by repetitive application but also by a long exposure of caffeine. However, this augmentation was neither achieved by repetitive administration of high K(+)-solution, nor caused by inhibition of phosphodiesterase by caffeine. The repetitive or sustained application of caffeine is suggested to increase the caffeine sensitivity of the calcium release channel to calcium, thus causing the potentiation of the caffeine response.

Animals↗
PubMed2006

Challenging sleep in aging: the effects of 200 mg of caffeine during the evening in young and middle-aged moderate caffeine consumers.

The aim of this study was to evaluate the effects of a 200-mg administration of caffeine on polysomnographic sleep variables and quantitative sleep electroencephalography (EEG) in 12 young (20-30 years) and 12 middle-aged (40-60 years) moderate caffeine consumers (one to three cups of coffee per day). All subjects were submitted to both a caffeine (200 mg) and placebo (lactose) condition in a double-blind cross-over design. The conditions were separated by 1 week. Compared with the placebo condition, the evening ingestion of caffeine lengthened sleep latency, reduced sleep efficiency, and decreased sleep duration and amount of stage 2 sleep in both age groups. Caffeine also reduced spectral power in delta frequencies in frontal, central and parietal brain areas, but not in prefrontal (PF) and occipital regions. Moreover, caffeine increased spectral power in beta frequencies in frontal and central brain areas in both age groups. A suppression of spectral power in the PF area in low delta frequencies (0.5-1.00 Hz) and a rise in spectral power in the parietal region in high alpha (10.00-12.00 Hz) and beta frequencies (17.00-21.00, 23.00-25.00, 27.00-29.00 Hz) occurred solely in middle-aged subjects. No such changes were noticeable in young subjects. Generally, caffeine produced similar effects in young and middle-aged subjects. Only a few frequency bins showed more effects of caffeine in middle-aged subjects compared with young subjects. Furthermore, sleep EEG results do not entirely support the hypothesis that caffeine fully mimics the effects of a reduction of homeostatic sleep propensity when following a normal sleep-wake cycle.

Adult↗
PubMed2000

Caffeine potentiates low frequency skeletal muscle force in habitual and nonhabitual caffeine consumers.

The mechanism of action underlying the ergogenic effect of caffeine is still unclear. Caffeine increases the force of muscular contraction during low-frequency stimulation by potentiating calcium release from the sarcoplasmic reticulum. Studies have also suggested an enhancement of lipid oxidation and glycogen sparing as potential mechanisms. Given that several studies have found an ergogenic effect of caffeine with no apparent metabolic effects, it is likely that a direct effect upon muscle is important. Twelve healthy male subjects were classified as habitual (n = 6) or nonhabitual (n = 6) caffeine consumers based on a 4-day diet record analysis, with a mean caffeine consumption of 771 and 14 mg/day for each group, respectively. Subjects were randomly allocated to receive caffeine (6 mg/kg) and placebo (citrate) in a double-blind, cross-over fashion approximately 100 min before a 2-min tetanic stimulation of the common peroneal nerve in a custom-made dynamometer (2 trials each of 20 and 40 Hz). Tetanic torque was measured every 30 s during and at 1, 5, and 15 min after the stimulation protocol. Maximal voluntary contraction strength and peak twitch torque were measured before and after the stimulation protocol. Caffeine potentiated the force of contraction during the final minute of the 20-Hz stimulation (P<0.05) with no effect of habituation. There was no effect of caffeine on 40-Hz stimulation strength nor was there an effect on maximal voluntary contraction or peak twitch torque. These data support the hypothesis that some of the ergogenic effect of caffeine in endurance exercise performance occurs directly at the skeletal muscle level.

Adult↗
PubMed1987

Caffeine enhances the slow-pressor response to angiotensin II in rats. Evidence for a caffeine-angiotensin II interaction with the sympathetic nervous system.

The purpose of this study was to determine if caffeine augments the slow-pressor response to chronic low-dose infusions of angiotensin II (AII) or the rapid-pressor response to acute infusions of AII. AII was infused (125 ng/min i.p.) for 12 d via mini-osmotic pumps in four groups of rats: group I, intact rats not treated with caffeine (n = 9); group II, intact rats treated with caffeine (0.1% in drinking water, n = 9); group III, rats previously sympathectomized with 6-hydroxydopamine, but not treated with caffeine (n = 10); and group IV, rats previously sympathectomized with 6-hydroxydopamine and treated with caffeine (n = 10). Chronic low-dose AII infusions slowly elevated systolic blood pressure in all groups. Caffeine greatly augmented this slow-pressor response to AII in intact animals; however, caffeine failed to enhance AII-induced hypertension in sympathectomized rats. Caffeine pretreatment did not enhance the rapid-pressor response to acute intravenous infusions of AII. We conclude that caffeine augmented the slow-pressor effect of chronic low-dose infusions of AII via a mechanism that involved the sympathetic nervous system.

Angiotensin II↗
PubMed1988

Increases in plasma concentrations of steroids in the rat after the administration of caffeine: comparison with plasma disposition of caffeine.

It was demonstrated that the altered endocrine environment caused by caffeine consumption could be equated with a stress-like pattern of response. A single acute treatment with caffeine (30 or 60 mg/kg) to male rats approximately 85 days old caused plasma concentrations of corticosterone, progesterone, testosterone and Na+ to rise significantly above control values. These changes were evident 3 min after caffeine administration and were maintained for 1-4 h before returning to normal. In animals exposed to daily chronic caffeine treatment for 10 days or more the levels of progesterone fell and Na+ rose significantly compared with control values at 24 h after administration. Following a single treatment of 30 mg/kg, caffeine was detected in blood plasma after 3 min, and reached peak levels by 1 h. After 24 h, less than 2% of the peak levels of caffeine remained. Metabolites of caffeine were detectable within 6 min and reached their peak levels 4 and 12 h later for theophylline and theobromine respectively. It is suggested that high steroid levels may in the long-term cause an altered hepatic clearance pattern affecting both steroid metabolism and caffeine elimination. A preliminary study of the morphology of livers from males chronically exposed to caffeine revealed that the hepatic cells lost cytoplasmic matrix, and that the sinusoids did not show up as clear spaces, compared with those in the controls.

Animals↗
PubMed1998

Caffeine consumption habits do not influence the exercise blood pressure response following caffeine ingestion.

BACKGROUND: The purpose of this study was to determine if the BP response during walking following caffeine ingestion differed between those who regularly consume caffeine and those who do not. METHODS: A double-blind cross-over experimental design was used. Data were collected in a research laboratory with a clinical exercise testing room. Eight regular caffeine users and eight men who did not habitually consume caffeine were studied. Each subject consumed of a beverage once with and once without 4.5 mg caffeine/kg fat-free mass added to the drink. Following consumption each subject walked at three intensities of exercise (30, 50, and 70% of VO2peak). Measures of BP were obtained by the auscultatory technique. RESULTS: Caffeine consumption resulted in significant increases in both systolic BP and diastolic BP at rest and during exercise. The elevation during exercise was 7-8 mmHg at all three exercise intensities for systolic BP; however, for diastolic BP there was only a significant elevation (4 mmHg) at the highest exercise intensity. No differences were noted between those men who regularly consume and those who regularly abstain from caffeine. There was a wide range in the resting BP response to caffeine (combined SBP and DBP ranged from 10-39 mmHg) suggesting that there are marked differences in sensitivity to caffeine, irrespective of individuals' consumption habits. CONCLUSIONS: Consideration should be given to caffeine intake prior to exercise in patients for whom an additional increase in BP during exercise would not be desirable.

Adult↗
PubMed1994

Caffeine reinforcement demonstrated in a majority of moderate caffeine users.

A mutually exclusive choice procedure was used to evaluate the reinforcing effects of caffeine in eleven normal subjects with histories of regular caffeine consumption (mean 256mg/day). Subjects participated for 24 weeks; each week consisted of three consecutive daily sessions (two sampling days followed by a choice day) during which subjects were required to abstain from dietary sources of caffeine. On each sampling day subjects ingested four capsules, one every 2h. Capsules contained placebo on one sampling day and caffeine (50 or 100mg/capsule) on the other sampling day. Placebo and caffeine were associated with different color-coded capsules. At the beginning of the choice day subjects chose one of the two color-coded capsules they wished to take on that day; they were required to ingest one capsule and, thereafter, they could ingest up to six additional capsules of the same color throughout the day. Across subjects and dose, caffeine was chosen over placebo on 80% of choice occasions; nine of 11 subjects (82%) chose caffeine on more than 70% of choice occasions and caffeine choice was replicable despite changes in capsule colors across blocks. This is the first study in a relatively uncontrolled outpatient context to demonstrate significant caffeine reinforcement in the majority of normal subjects.

Journal Article↗
PubMed2000

Postoperative caffeine for preventing apnea in preterm infants.

BACKGROUND: Growing ex-preterm infants who undergo general anesthesia for surgery at about term-equivalent age may have episodes of apnea, cyanosis and bradycardia during the early postoperative period. Caffeine treatment given at the time of operation might prevent these episodes. OBJECTIVES: In ex-preterm infants who undergo general anesthesia for surgery, does the prophylactic use of caffeine prevent episodes of apnea, cyanosis and bradycardia during the postoperative period without clinically important side effects? SEARCH STRATEGY: The standard strategy of the Neonatal Review Group was used. This included searches of the Oxford Database of Perinatal trials, Medline, previous reviews including cross references, abstracts, conferences and symposia proceedings, expert informants and journal handsearching mainly in the English language. SELECTION CRITERIA: All trials utilising random or quasi-random patient allocation, in which treatment was compared with placebo or no treatment, were included. DATA COLLECTION AND ANALYSIS: The standard methods of the Cochrane Collaboration and its Neonatal Review Group were used to select trials, evaluate quality and to extract data. The methodological quality of each trial was reviewed by the second author blinded to trial authors and institution(s). Each author extracted data separately, compared and resolved differences. Meta-analysis used relative risk and risk difference. MAIN RESULTS: In each trial apnea/bradycardia occurred in fewer treated than control infants. In two trials (Welborn 1989, LeBard 1989) continuous recordings of oxygen saturation detected hypoxaemic episodes (<90 %) in fewer treatment than control infants. No infant in any trial required intubation and mechanical ventilation. No adverse effects were reported. REVIEWER'S CONCLUSIONS: Implications for practice. Caffeine can be used to prevent postoperative apnea/bradycardia and episodes of oxygen desaturation in growing preterm infants if this is deemed clinically necessary. In view of the small numbers of infants studied in these trials and uncertainty concerning the clinical significance of the episodes, caution is warranted in applying these results to routine clinical practice. Implications for research. There is a need to determine which infants might benefit most by this treatment. Studies confined to those most at risk of apnea (prior history, younger postmenstrual age) and those that might require mechanical ventilation (chronic lung disease) would be of value.

Anesthesia, General↗
PubMed1975

Mitigation of caffeine-induced teratogenicity in mice by prior chronic caffeine ingestion.

Pregnant A/J female mice, which had drunk tap water or a 0.05% caffeine solution for 8-19 weeks after weaning, were each injected sc with 150 or 250 mg/kg caffeine once on day 13 of gestation. After 150 mg/kg caffeine the frequencies at term of fetal death, external malformation, and subcutaneous hematomas were significantly lower in the caffeine- than water-drinking group. After 250 mg/kg caffeine the frequency of fetal death but not of malformations and hematomas was lower in the group with caffeine pretreatment. These findings were explained by assuming that long-term ingestion of caffeine induced and increased rate of degradation of caffeine administered during pregnancy.

Abnormalities, Drug-Induced↗
PubMed1997

Caffeine-resistance in S. pombe: mutations in three novel caf genes increase caffeine tolerance and affect radiation sensitivity, fertility, and cell cycle.

Caffeine is a well known base analogue and is cytotoxic to both animal and yeast cells. There are two possible mechanisms by which yeast cells tolerate caffeine concentrations higher than normal, by mutation or by physiological adaptation. We have isolated novel caffeine-resistant mutants of S. pombe which define three distinct genes caf2, caf3 and caf4. These mutants achieved a level of caffeine resistance which is presumed to represent the upper limit attainable by mutation. The caf2-caf4 mutations, as well as the previously identified caf1 mutation, confer UV-sensitivity, caffeine-resistant UV repair, impaired fertility and sporulation, as well as a lengthened cell cycle. They are partially dominant for caffeine resistance and recessive for UV sensitivity. Some auxotrophic caf3-89 double mutants show drastically decreased caffeine resistance. The caf4 mutant is more resistant to gamma-radiation than wild-type cells and shows pH-sensitive growth. As each caf mutation can, individually, confer maximum caffeine resistance to the cells, all four genes are expected to operate in the same pathway. This pathway might also be responsible for the physiological adaptation since adaptation is lost in caf1-caf4 mutants.

Caffeine↗
PubMed1994

A simplified method for the measurement of caffeine in plasma and brain: evidence for a cortical-subcortical caffeine concentration differential in brain.

We describe a much simplified high-performance liquid chromatography (HPLC) method for the measurement of caffeine in plasma and brain. A particularly attractive feature of this method is that a simple methanol/water (60:40) mobile phase can be used both for plasma and brain samples. In addition, the method is compatible with solid-phase extraction for plasma samples and conventional brain tissue preparation for biogenic amine analysis with HPLC. Using this method to measure the concentrations of caffeine in plasma and brain of rats which received 10 or 50 mg/kg caffeine injections, we found substantial concentration differences between cortical and subcortical brain tissue. Specifically, at the 10 mg/kg dose, a nearly 2-fold difference between cortex and striatum caffeine concentrations was observed. A shortcoming of many neurobehavioral studies of caffeine effects is the absence of caffeine concentration measurements. The simplicity of the present method for the measurement of caffeine in plasma and brain tissue makes it a practical and feasible procedure to incorporate into neurobehavioral studies designed to elucidate the CNS actions of caffeine.

Animals↗
PubMed2006

Caffeine in the milk prevents respiratory disorders caused by in utero caffeine exposure in rats.

Consequences of postnatal caffeine exposure by the milk on ponto-medullary respiratory disturbances observed following an in utero caffeine exposure were analysed. Ponto-medullary-spinal cord preparations from newborn rats exposed to caffeine during gestation but not after the birth display an increase in respiratory frequency and an exaggeration of the hypoxic respiratory depression compared to not treated preparations. These data suggest that tachypneic and apneic episodes encountered in human newborns whose mother consumed caffeine during pregnancy are due in large part to central effect of caffeine at the ponto-medullary level. Both baseline respiratory frequency increase and emphasis of hypoxic respiratory depression are not encountered if rat dams consumed caffeine during nursing. Our hypothesis is that newborn rats exposed to caffeine during gestation but not after the birth would be in withdrawal situation whereas, when caffeine is present in drinking fluid of lactating dams, it goes down the milk and is able to prevent ponto-medullary respiratory disturbances.

Animals↗