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PubMed2006

Association of caffeine to MDMA does not increase antinociception but potentiates adverse effects of this recreational drug.

Ecstasy (MDMA) street tablets often contain several other compounds in addition to MDMA, particularly caffeine. Then, it becomes necessary to study the consequences of caffeine plus MDMA combination. MDMA (1 mg/kg) elicited an analgesic response both at the spinal and supraspinal levels. However, when associated, MDMA and caffeine did not show any synergistic interaction. When caffeine was administered prior to MDMA, a potentiation of locomotor activity was observed, which consisted in an increase in maximal values and in a prolonged time of activity. In the neurotoxicity studies, a hyperthermic effect of MDMA was observed. Although caffeine alone failed to alter body temperature, it potentiated MDMA-induced hyperthermia. This association also significantly increased MDMA lethality (from 22% to 34%). Following administration of MDMA to rats, there was a persistent decrease in the number of serotonin transporter sites in the cortex, striatum and hippocampus, which was potentiated by caffeine co-treatment. This MDMA toxicity in rats was accompanied by a transient dopaminergic impairment in the striatum, measured as decreased [(3)H]WIN35428 binding sites, by 31% 3 days after treatment, which was not modified by caffeine. A transient down-regulation of 5-HT(2) receptors occurred in the cortex of MDMA-treated rats, whose recovery was slowed by co-treatment with caffeine. In conclusion, the association of MDMA with caffeine does not generate any beneficial effects at the antinociceptive level. The acute effects stemming from this association, in tandem with the final potentiation of serotonergic terminals injury, provide evidence of the potentially greater long-term adverse effects of this particular recreational drug combination.

Analgesics↗
PubMed2006

The enigmatic effects of caffeine in cell cycle and cancer.

Caffeine may very well be the most frequently ingested neuroactive drug in the world. Mechanistically, caffeine has been reported to affect cell cycle function, induce programmed cell death or apoptosis and perturb key cell cycle regulatory proteins. Although the effects of caffeine have been heavily investigated, much of the research data regarding caffeine's effects on cell cycle and proliferation seem ambiguous. One important factor may be that caffeine has been used experimentally in numerous cell types under a variety of conditions at concentrations ranging from micromolar to high millimolar. Physiologically, achieving experimental blood levels of caffeine would be extremely difficult without adverse side effects. Therefore, the relevance of experimental data obtained by using high concentrations of caffeine is not clear and may account for some of the discrepancies in the literature. This review attempts to reconcile data regarding the cellular effects of caffeine by examining reported effects on cell cycle, proliferation and apoptosis with careful attention to differences in experimental conditions and caffeine concentration utilized.

Animals↗
PubMed2005

Release and sequestration of Ca2+ by a caffeine- and ryanodine-sensitive store in a sub-population of human SH-SY5Y neuroblastoma cells.

We have used single cell fluorescence imaging techniques to examine the role that ryanodine receptors play in the stimulus-induced Ca(2+) responses of SH-SY5Y cells. The muscarinic agonist methacholine (1mM) resulted in a Ca(2+) signal in 95% of all cells. Caffeine (30 mM) however stimulated a Ca(2+) signal in only 1-7% of N-type (neuroblastic) cells within any given field. The caffeine response was independent of extracellular Ca(2+), regenerative in nature, and abolished in a use-dependent fashion by ryanodine. In caffeine-responsive cells, the magnitude of the methacholine-induced Ca(2+) signal was inhibited by 75.07 +/- 5.51% by pretreatment with caffeine and ryanodine, suggesting that the caffeine-sensitive store may act as a Ca(2+) source after muscarinic stimulation. When these data were combined with equivalent data from non-caffeine-responsive cells, the degree of apparent inhibition was significantly reduced. In contrast, after store depletion by caffeine, the Ca(2+) signal induced by 55 mM K(+) was potentiated 2.5-fold in the presence of ryanodine, suggesting that the store may act a Ca(2+) sink after depolarisation. We conclude that a caffeine- and ryanodine-sensitive store can act as a Ca(2+) source and sink in SH-SY5Y cells, and that effects of the store can become obscured if data from caffeine-insensitive cells are not excluded.

Caffeine↗
PubMed2006

A taste receptor required for the caffeine response in vivo.

Caffeine is a methylxanthine present in the coffee tree, tea plant, and other naturally occurring sources and is among the most commonly consumed drugs worldwide. Whereas the pharmacological action of caffeine has been studied extensively, relatively little is known concerning the molecular mechanism through which this substance is detected as a bitter compound. Unlike most tastants, which are detected through cell-surface G protein-coupled receptors, it has been proposed that caffeine and related methylxanthines activate taste-receptor cells through inhibition of a cyclic nucleotide phosphodiesterase (PDE) . Here, we show that the gustatory receptor Gr66a is expressed in the dendrites of Drosophila gustatory receptor neurons and is essential for the caffeine response. In a behavioral assay, the aversion to caffeine was specifically disrupted in flies missing Gr66a. Caffeine-induced action potentials were also eliminated, as was the response to theophylline, the methylxanthine in tea. The Gr66a mutant exhibited normal tastant-induced action potentials upon presentation of theobromine, a methylxanthine in cocoa. Given that theobromine and caffeine inhibit PDEs with equal potencies , these data further support the role of Gr66a rather than a PDE in mediating the caffeine response. Gr66a is the first gustatory receptor shown to be essential for caffeine-induced behavior and activity of gustatory receptor cells in vivo.

Animals↗
PubMed2006

Enhancement of antinociception by co-administration of ibuprofen and caffeine in arthritic rats.

It has been observed that caffeine improves antinociceptive efficacy of some non-steroidal antiinflammatory drugs (NSAIDs) in several experimental models, however, these effects have been questioned in humans. Controversy in clinical studies may be due to the use of different protocols as well as to high interindividual variability in patient response. In addition, the antinociceptive interaction of ibuprofen+caffeine has not been studied. To assess a possible synergistic antinociceptive interaction, the antinociceptive effects of ibuprofen, and caffeine administered either separately or in combinations were determined in a model of arthritic pain: "Pain-induced functional impairment in the rat (PIFIR model). The antinociceptive efficacies were evaluated using several dose-response curves and time courses. The antinociceptive effects from the combination that produced the greater effect were compared with the maximal antinociceptive effect of either morphine or acetylsalicylic acid alone. The animals were administered with 0.05 ml intra-articular (i.a.) of uric acid to induce nociception. Groups of six rats received either acetylsalicylic acid, morphine, ibuprofen or caffeine, or a combination ibuprofen+caffeine (18 combinations). We report here that caffeine (17.8 and 31.6 mg/kg) is able to potentiate the antinociceptive effect of ibuprofen. This investigation showed that six combinations presented effects of potentiation and twelve combinations only showed antinociceptive effects not different from that of ibuprofen alone. The maximum antinociceptive effect was 270.7+/-12.7 area units (au), produced by ibuprofen 100 mg/kg+caffeine 17.8 mg/kg; this effect was greater than the maximum produced by morphine 17.8 mg/kg (244.7+/-22.9 au) in these experimental conditions. The maximum potentiation was 197 % produced with the combination of ibuprofen 17.8 mg/kg+caffeine 17.8 mg/kg. These results suggest that the antinociceptive effect of ibuprofen was significantly potentiated by doses of caffeine that by themselves are ineffective in this model.

Analgesics↗
PubMed2005

Inhibition of human TREK-1 channels by caffeine and theophylline.

Caffeine (1,3,7-trimethylxanthine) and theophylline (1,3-dimethylxanthine) are used for therapeutic purposes and can cause life-threatening convulsive seizures due to systemic toxicity. The mechanisms for the epileptogenicity of caffeine and theophylline are not clear. TWIK-related K(+) channels (TREK-1) are highly expressed in the human central nervous system and have a major role in the control of neuronal excitability by regulating the resting membrane potential. In view of their physiological significance, inhibition of TREK-1 channels may be implicated in caffeine- and theophylline-induced seizures. We thus investigated, using whole-cell patch-clamp technique, modulation of hTREK-1 channels expressed in Chinese hamster ovary (CHO) cells by caffeine and theophylline. Caffeine and theophylline produced reversible inhibition of TREK-1 channels in a concentration-dependent manner. The half-maximal inhibitory concentrations (IC(50)) for caffeine and theophylline were 377+/-54microM and 486+/-76microM, respectively. Caffeine and theophylline depolarized the membrane potential of CHO(TREK-1) cells in a reversible and concentration-dependent manner. Inhibition by caffeine (5mM) and theophylline (2mM) was attenuated in TREK-1 channels with mutation of the PKA consensus sequence at serine 348, suggesting the involvement of cAMP/PKA pathway in the inhibitory process. Inhibition of TREK-1 channels and consequent membrane depolarization may contribute to the convulsive seizures induced by toxic levels of caffeine and theophylline.

Animals↗
PubMed2004

Caffeine-dependent stimulus-triggered oscillations in the CA3 region of hippocampal slices from rats chronically exposed to lead.

Yoshimura et al. [Yoshimura, H., Sugai, T., Onoda, N., Segami, N., Kato, N., 2002. Age-dependent occurrence of synchronized population oscillation suggestive of a developing functional coupling between NMDA and ryanodine receptors in the neocortex. Dev. Brain Res., 136, 63-68.] have shown that caffeine can elicit synchronized oscillations (10-12 Hz) dependent on calcium-induced calcium release in rat neocortex neurons. In the present work, synchronized oscillations in the CA3 region of rat hippocampus were studied by recording field excitatory postsynaptic potentials (fEPSPs) in vitro. In the presence of 0.1 mM caffeine, in CA3 of 44 of 45 (97.8%) slices from chronic lead-exposed rats, single electrical stimuli triggered a burst of high-frequency oscillations (approximately 230 Hz), whereas in CA3 of caffeine-treated slices from control rats, such oscillations could be elicited in only 2 of 24 (8.3%) slices. The complete (but fully reversible) block of caffeine-dependent oscillations by 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX; 20 microM) indicates that alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors are necessary for the high-frequency synchronized oscillations. 2-Amino-5-phosphonopentanoate (AP-5; 50 micoM) partially reduced the amplitude of caffeine-dependent oscillations without significantly altering their frequency. Caffeine-dependent oscillations could be abolished by application of AP-5 and 3 mM Mg2+ during the initial period of bursting, indicating that N-methyl-D-aspartate (NMDA) receptors play an important role in the generation of oscillations. The Ca2+ chelator ethylene glycol bis-(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA; 5 mM) added in standard artificial cerebrospinal fluid (ACSF) containing 0.1 mM caffeine fully blocked the oscillations. Caffeine-dependent oscillations are insensitive to an antagonist of gamma-aminobutyric acid (GABAA) receptors (10 microM bicuculline), L-type Ca2+ channels (10 muM nicardipine), L-type and N-type voltage-dependent calcium channels (100 microM Cd2)), and T-type Ca2+ channels (100 microM Ni2+). Previous studies have demonstrated that expression and function of NMDA and AMPA receptors are altered in the hippocampus of chronic lead-exposed rats. We propose that caffeine-dependent stimulus-induced oscillations in CA3 area of hippocampus from chronic lead-exposed rats are mainly mediated by the entry of extracellular Ca2+ through NMDA and non-NMDA receptors, without participation of GABAA receptors. Additionally, the underlying mechanisms are also discussed.

Animals↗
PubMed2006

Induction of two cytochrome P450 genes, Cyp6a2 and Cyp6a8, of Drosophila melanogaster by caffeine in adult flies and in cell culture.

To examine whether caffeine, the most widely used xenobiotic compound, would induce insect cytochrome P450 or CYP gene expression, upstream DNA fragments of Cyp6a2 (0.12, 0.26, 0.52 and 0.98-kb) and Cyp6a8 (0.06, 0.1, 0.2, 0.5 and 0.8-kb) genes of Drosophila melanogaster were individually fused to the firefly luciferase (luc) reporter gene. Promoter activities of these constructs were examined in Drosophila SL-2 cells using luciferase assays. Activity of 0.2- and 0.8-kb upstream DNA of Cyp6a8 was also measured in transgenic female flies. When these flies were treated with 2 mM pure caffeine or Vivarin caffeine, both DNA fragments showed a 4-5-fold induction of promoter activity. Endogenous Cyp6a8 and Cyp6a2 genes in these flies also showed caffeine-induced expression. In addition, both 0.2- and 0.8-kb DNAs showed differential basal and caffeine-induced activity in head, ovaries, gut, cuticle plus fat body and malpighian tubules. However, in all tissues 0.8-kb DNA always showed higher basal and caffeine-induced activities compared to the 0.2-kb DNA, suggesting that the additional DNA present in the 0.8-kb fragment has sequences that enhance both activities. In SL-2 cells, all reporter constructs of each Cyp6 gene showed significantly higher basal activity than the empty vector. Sequences that boost basal activity are located in -265/-129 and -983/-522 DNA of Cyp6a2, and -199/-109 and -491/-199 DNA of Cyp6a8 genes. While the 0.12- and 0.1-kb upstream DNAs of Cyp6a2 and Cyp6a8 genes respectively did not show caffeine-inducibility in SL-2 cells, the longest upstream DNA of each gene gave the highest level of induction. Caffeine-responsive sequences are not clustered at one place; they appear to be dispersed in -983/-126 and -761/-109 regions of Cyp6a2 and Cyp6a8 genes which also contain many binding sites for activator protein 1 (AP1) and cyclic AMP response element binding protein (CRE-BP). Significance of these binding sites in caffeine-inducibility has been discussed.

Animals↗
PubMed2004

Caffeine suppresses TNF-alpha production via activation of the cyclic AMP/protein kinase A pathway.

This study investigated the effect of in vitro exposure to caffeine, and its major metabolite paraxanthine, at concentrations relevant to typical caffeine consumption in humans, on lipopolysaccharide (LPS)-stimulated cytokine production in human whole blood. In addition, a role for the cyclic AMP/protein kinase A (PKA) pathway in the immunomodulatory effect of caffeine was investigated. Diluted whole blood (taken following >/=15 h abstinence from caffeine-containing food and beverages) was preincubated with caffeine or paraxanthine (10-100 microM) and stimulated with LPS (1 proportional, variant g/ml) for 24 h. The proinflammatory cytokines tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta and IL-12, and the antiinflammatory cytokine IL-10 were measured in cell-free supernatants. Whilst caffeine and paraxanthine had little or no effect on IL-10, IL-1beta, or IL-12 production, TNF-alpha production was suppressed in all individuals studied. The effect was statistically significant at 100 microM and consistent across seven experiments performed. Although not statistically significant, a similar effect was observed with paraxanthine. Caffeine (100 microM) also increased intracellular cyclic AMP concentrations in LPS-stimulated monocytes isolated from whole blood. Moreover, the effect of caffeine on TNF-alpha production was abolished by pretreatment with the protein kinase A inhibitor Rp-8-Br-cAMPS (10(-4) and 10(-5)M). To conclude, this study demonstrates that concentrations of caffeine that are relevant to human consumption consistently suppress production of the proinflammatory cytokine TNF-alpha in human blood and that this effect is mediated by the cyclic AMP/protein kinase A pathway.

Adult↗
PubMed2004

Smoking and caffeine have a synergistic detrimental effect on aortic stiffness and wave reflections.

OBJECTIVES: We investigated the acute and chronic combined effect of cigarette smoking and caffeine intake on aortic stiffness and wave reflections. BACKGROUND: We have shown that smoking and caffeine separately increase arterial stiffness. Aortic stiffness and wave reflections are important determinants of the efficient performance of the cardiovascular system and prognosticators of cardiovascular risk. METHODS: The acute effects of smoking (one cigarette), caffeine (200 mg, equivalent to 2 cups of coffee), and smoking plus caffeine were studied in 24 healthy subjects according to a randomized, placebo- and sham procedure-controlled crossover design. The chronic effect of smoking and caffeine was studied in a population study that enrolled 160 healthy subjects. RESULTS: Acute study: there was a significant interaction between caffeine and smoking with regard to pulse-wave velocity (p < 0.01) and augmentation index (p < 0.05). When smoking followed caffeine intake, pulse-wave velocity and augmentation index increased further by 0.52 m/s and 13.4%, respectively, reaching a total of 0.85 m/s and 17.4%, 0.17 m/s and 9.2% in excess of the mere sum of caffeine effect (0.33 m/s and 4%) alone and smoking effect alone (0.35 m/s and 4.2%). Population study: there was a significant interaction of chronic coffee consumption and smoking regarding pulse-wave velocity (p < 0.05) and augmentation index (p = 0.001). CONCLUSIONS: The present study shows, for the first time, that when smoking and caffeine intake are combined, they interact and exert a synergistic, unfavorable effect on aortic stiffness and wave reflections on both an acute and chronic basis.

Adult↗
PubMed2006

Caffeine prevents protection in two human models of ischemic preconditioning.

OBJECTIVES: We studied whether caffeine impairs protection by ischemic preconditioning (IP) in humans. BACKGROUND: Ischemic preconditioning is critically dependent on adenosine receptor stimulation. We hypothesize that the adenosine receptor antagonist caffeine blocks the protective effect of IP. METHODS: In vivo ischemia-reperfusion injury was assessed in the thenar muscle by 99mTc-annexin A5 scintigraphy. Forty-two healthy volunteers performed forearm ischemic exercise. In 24 subjects, this was preceded by a stimulus for IP. In a randomized double-blinded design, the subjects received caffeine (4 mg/kg) or saline intravenously before the experiment. At reperfusion, 99mTc-annexin A5 was administered intravenously. Targeting of annexin was quantified by region-of-interest analysis, and expressed as percentage difference between experimental and contralateral hand. In vitro, we assessed recovery of contractile function of human atrial trabeculae, harvested during heart surgery, as functional end point of ischemia-reperfusion injury. Field-stimulated contraction was quantified at baseline and after simulated ischemia-reperfusion, in a paired approach with and without 5 min of IP, in the presence (n=13) or absence (n = 17) of caffeine (10 mg/l). RESULTS: Ischemic preconditioning reduced annexin targeting in the absence of caffeine (from 13 +/- 3% to 7 +/- 1% at 1 h, and from 19 +/- 2% to 9 +/- 3% at 4 h after reperfusion, p = 0.006), but not after caffeine administration (targeting 11 +/- 2% and 16 +/- 3% at 1 and 4 h). In vitro, IP improved post-ischemic functional recovery in the control group, but not in the caffeine group (8 +/- 3% vs. -8 +/- 5%, p=0.003). CONCLUSIONS: Caffeine abolishes IP in 2 human models at a dose equivalent to the drinking of 2 to 4 cups of coffee. (The Effect of Caffeine on Ischemic Preconditioning; http://clinicaltrials.gov/ct/show/NCT00184912?order=1; NCT00184912).

Adult↗
PubMed2004

The adenosine A1 receptor contributes to the stimulatory, but not the inhibitory effect of caffeine on locomotion: a study in mice lacking adenosine A1 and/or A2A receptors.

Caffeine has biphasic effects on locomotion, and blockade of the adenosine A(2A) receptor (A2AR) is necessary for the stimulatory effect of low doses of caffeine, but not for the locomotor depressant effect observed at high doses. We wanted to elucidate the role of the adenosine A(1) receptor (A1R) in mediating the locomotor effects of increasing doses of caffeine using wild-type mice (A1R(WT)), mice heterozygous for (A1R(HET)), and mice lacking the adenosine A(1) receptor (A1R(KO)). Caffeine had the typical biphasic dose-effect relationship in all three genotypes, but the stimulatory action of caffeine was facilitated in the A1R(KO) mice. In order to investigate the interaction between blockade of A1Rs and A2ARs, mice lacking both receptors (A1R(KO)/A2AR(KO)) were tested. Regardless of A1R genotype, animals lacking A2AR were not stimulated by caffeine, whereas animals heterozygous for A2AR were. As expected, the A1R is not crucial for the stimulatory effect of caffeine, but seems to modulate the effect of caffeine exerted via A2AR blockade. Furthermore, these results suggest that the inhibitory effect of high doses of caffeine is due neither to blockade of the A1R, nor of the A2AR, and an effect independent of these adenosine receptors is likely.

Adenosine A1 Receptor Agonists↗
PubMed2004

Dose-dependent effect of caffeine on reducing leg muscle pain during cycling exercise is unrelated to systolic blood pressure.

This double-blind, within-subjects experiment examined the effects of ingesting two doses of caffeine on perceptions of leg muscle pain and blood pressure during moderate intensity cycling exercise. Low caffeine consuming college-aged males (N=12) ingested one of two doses of caffeine (5 or 10 mg.kg(-1) body weight) or placebo and 1 h later completed 30 min of moderate intensity cycling exercise (60% VO2peak). The order of drug administration was counter-balanced. Resting blood pressure and heart rate were recorded immediately before and 1 h after drug administration. Perceptions of leg muscle pain as well as work rate, blood pressure, heart rate, and oxygen uptake (VO2) were recorded during exercise. Caffeine increased resting systolic pressure in a dose-dependent fashion but these blood pressure effects were not maintained during exercise. Caffeine had a significant linear effect on leg muscle pain ratings [F(2,22)=14.06; P < 0.0001; eta2=0.56 ]. The mean (+/-SD) pain intensity scores during exercise after ingesting 10 mg.kg(-1) body weight caffeine, 5 mg.kg(-1) body weight caffeine, and placebo were 2.1+/-1.4, 2.6+/-1.5, and 3.5+/-1.7, respectively. The results support the conclusion that caffeine ingestion has a dose-response effect on reducing leg muscle pain during exercise and that these effects do not depend on caffeine-induced increases in systolic blood pressure during exercise.

Adult↗
PubMed2006

Modulation of the hypothalamo-pituitary-adrenocortical axis by caffeine.

Although caffeine is the most consumed psychoactive substance in the world, the extents of many of its effects are unknown. High doses of caffeine have been shown to activate the HPA axis while the effects of low to moderate doses have usually not been described in detail. Moreover, although several lines of evidence suggest that low doses of caffeine may restrain some negative affective states, the possible modulatory role of caffeine on HPA axis activation induced by a stressful stimulus has not been described. Thus, the present studies investigated the possible modulatory effects of low to moderate doses of caffeine on moderate to high HPA axis activation induced by different intensities of loud noise. First, in order to test this modulation, time courses for adrenocorticotropic hormone (ACTH) and corticosterone responses to loud noise stress and to caffeine were defined, in rats. Plasma ACTH and corticosterone levels peaked 30 min from the onset of noise presentation, and rapidly declined after noise termination. A low caffeine dose of 2 mg/kg significantly increased plasma corticosterone and ACTH levels 30 min following injections, but levels returned to baseline 60 min following injections. Caffeine doses of 30 mg/kg and higher elevated plasma hormone levels for at least 2h. Doses of 2 or 10mg/kg, however, did not modulate endocrine responses to loud noise presentation. It is concluded that although caffeine activates the HPA axis, low to moderate doses do not modulate HPA axis responses to stressful stimuli.

Acoustic Stimulation↗
PubMed2006

Increased caffeine and nicotine consumption in community-dwelling patients with schizophrenia.

INTRODUCTION: It is known that people with schizophrenia make poor dietary choices and smoke at alarmingly high rates. There is also anecdotal evidence that they may ingest large amounts of caffeine. However, while smoking habits in this population have been examined, no recent study has quantified caffeine consumption taking into account various dietary caffeine sources unrelated to coffee including convenience foods such as candy bars, chocolate or soft drinks, and compared results to US population data. METHODS: We employed 24-h diet recalls to assess dietary habits in a sample of outpatients suffering from schizophrenia or schizoaffective disorder. Caloric intake and caffeine consumption were quantified and the relationship to various sociodemographic variables including body mass index (BMI) and dietary quality was examined. RESULTS: 146 patients were recruited. Mean BMI in the sample was 32.7+/-7.9. Patients ingested 3,057+/-1,132 cal on average. Patients smoked at higher rates (59.6% vs. 23.4%, p< or =0.001), higher numbers of cigarettes/day (24+/-14.4 vs. 13.5+/-11.3, t=8.549, p<0.001) and ingested more caffeine (471.6+/-584.6 mg vs. 254.2+/-384.9 mg, t=6.664, p<0.001) than US population comparisons. Caffeine consumption was correlated to the number of cigarettes smoked daily (r=0.299, p< or =0.001), but not to BMI (r=0.134, p=0.107) or dietary parameters such as caloric intake (r=0.105, p=0.207). CONCLUSION: Community-dwelling schizophrenia patients consume significantly more caffeine and nicotine than US population comparisons. Clinicians should be aware that while a significant proportion of patients are overweight and have poor dietary quality - which merits lifestyle counseling on its own - there is a lack of correlation between those factors and smoking and caffeine intake. Thus, lifestyle modification counseling in all patients should address smoking and caffeine intake concurrently.

Adult↗
PubMed2005

Sleep duration and caffeine consumption in a French middle-aged working population.

OBJECTIVE/BACKGROUND: To explore the association between sleep duration and daily caffeine intake in a working population. Caffeine acutely disrupts sleep in the laboratory, but the inter-relations between sleep and caffeine intake in daily life are ill-known. METHODS: Questionnaire and diary based survey of 1498 persons from the GAZEL cohort of employees of the National Electricity and Gas Company (EDF-GDF) working in various locations in the Paris and South-West France areas. We analyzed total sleep time, our primary measure, and time in bed, both by sleep logs. We assessed daily intake of caffeine, consumption of alcohol and tobacco, use of hypnotics, and daytime somnolence, all by questionnaire. RESULTS: Multiple linear regression analysis did not find a significant relationship between total sleep time and daily caffeine intake less than 8 cups of coffee per day, after controlling for age, gender, alcohol intake, smoking status, and use of hypnotics. By contrast, time in bed was reduced as caffeine intake increased (beta=-0.125; P<0.001). Higher caffeine intake was not related to a higher daytime somnolence. CONCLUSION: Despite the well-known acute effects of caffeine on sleep, habitual use of up to 7 cups of coffee (or 600 mg of caffeine equivalent) per day was not associated with decreased duration of sleep.

Beverages↗
PubMed2006

Caffeine challenge in insomniac patients after total sleep deprivation.

BACKGROUND AND PURPOSE: This study compared the effects of caffeine in patients with primary insomnia and normal volunteers. The main goal was to determine the differences in sensitivity to caffeine between the groups. We investigated the effects on daytime sleep of placebo or caffeine after a night of total sleep deprivation (SD). We hypothesized that insomniacs would be more affected by caffeine, which would suggest a change in adenosine receptor (number or sensitivity) in primary insomniacs. PATIENTS AND METHODS: Six primary insomnia patients (Diagnostic and Statistical Manual of Mental Disorders (DSM-IV)) and six normal volunteers with no sleep complaints participated in a double-blind study with caffeine or placebo administered under a cross-over design with each subject serving as his or her own control. The participants did not have a history of drinking coffee or caffeinated beverages. Data from all-night polysomnography and multiple sleep latency test (MSLT) were collected in the sleep research laboratory of National Institute of Medical Sciences and Nutrition Salvador Zubirán. RESULTS: During the baseline night, patients with insomnia had significantly less delta sleep and less total sleep time than the normal volunteers. Mean sleep latency under basal MSLT did not differ between the groups. However, insomnia patients had significantly less total sleep during each nap compared to normal volunteers. After one night of total SD and under caffeine administration, the insomniacs had significantly longer sleep latency and less total sleep time in MSLT compared to normal volunteers. After SD, healthy volunteers reduced sleep latencies in MSLT with or without caffeine. CONCLUSIONS: Patients with insomnia had a higher sensitivity to the diurnal awakening effect of caffeine even after one night of SD. This suggests that changes in the adenosine receptors could, in part, be responsible for the hyperarousal state that has been reported in primary insomnia.

Adult↗
PubMed2006

Stimulatory effect of oral administration of tea, coffee or caffeine on UVB-induced apoptosis in the epidermis of SKH-1 mice.

Oral administration of green tea or a caffeine solution, but not decaffeinated green tea, inhibits UVB-induced complete carcinogenesis in SKH-1 mice. Oral administration of green tea, coffee or a caffeine solution for 2 weeks enhanced UVB-induced increases in apoptosis in the epidermis, but these treatments had no effect in non-UVB treated normal epidermis. Our results suggest that administration of green tea, coffee and caffeine may inhibit UVB-induced carcinogenesis--at least in part--by enhancing UVB-induced apoptosis. Plasma levels of caffeine observed after its oral administration at cancer-preventive dose levels were within the range observed in moderate coffee drinkers. Topical applications of caffeine to mice previously treated with UVB for 20 weeks (high risk mice without tumors) inhibited the formation of tumors and stimulated apoptosis in the tumors but not in areas of the epidermis away from tumors. The selective effects of caffeine administration to stimulate UVB-induced apoptosis or apoptosis in tumors but not in normal epidermis or in areas of the epidermis away from tumors is of considerable interest, but the reasons for the selective effects of caffeine on apoptosis in DNA damaged tissues are unknown. Further studies are needed to determine mechanisms of these effects of caffeine and to determine the effects of caffeine administration on sunlight-induced actinic keratoses and squamous cell carcinomas in humans.

Administration, Oral↗