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PubMed2004

Caffeine inhibits homology-directed repair of I-SceI-induced DNA double-strand breaks.

We recently reported that two Chinese hamster mutants deficient in the RAD51 paralogs XRCC2 and XRCC3 show reduced radiosensitization after treatment with caffeine, thus implicating homology-directed repair (HDR) of DNA double-strand breaks (DSBs) in the mechanism of caffeine radiosensitization. Here, we investigate directly the effect of caffeine on HDR initiated by DSBs induced by a rare cutting endonuclease (I-SceI) into one of two direct DNA repeats. The results demonstrate a strong inhibition by caffeine of HDR in wild-type cells, and a substantial reduction of this effect in HDR-deficient XRCC3 mutant cells. Inhibition of HDR and cell radiosensitization to killing shows similar dependence on caffeine concentration suggesting a cause-effect relationship between these effects. UCN-01, a kinase inhibitor that effectively abrogates checkpoint activation in irradiated cells, has only a small effect on HDR, indicating that similar to radiosensitization, inhibition of checkpoint signaling is not sufficient for HDR inhibition. Recombination events occurring during treatment with caffeine are characterized by rearrangements reminiscent to those previously reported for the XRCC3 mutant, and immunofluorescence microscopy demonstrates significantly reduced formation of IR-specific RAD51 foci after caffeine treatment. In summary, our results identify inhibition of HDR as a significant contributor to caffeine radiosensitization.

Animals↗
PubMed1994

Haemodynamic and neurohumoral effects of caffeine in elderly patients with symptomatic postprandial hypotension: a double-blind, randomized, placebo-controlled study.

1. The aim of this study was to determine the effects of caffeine on haemodynamic and neurohumoral responses to meal ingestion in elderly patients with a history of symptomatic postprandial hypotension. 2. Postprandial hypotension is a common disorder of blood pressure regulation in the elderly, associated with falls and syncope. The pathophysiological mechanism is thought to be related to impaired vascular compensation for splanchnic blood pooling after a meal. Since caffeine inhibits vasodilatory adenosine receptors in the splanchnic circulation, we postulated that caffeine would reduce splanchnic blood pooling and prevent the development of postprandial hypotension. 3. We conducted a randomized, double-blind, placebo-controlled, cross-over study in nine elderly patients [age 76 +/- 9 (SD) years] with histories of symptomatic postprandial hypotension. Standardized 1674kJ liquid meals with 250 mg of caffeine or placebo were given on two occasions, at least 1 week apart. Blood pressure, heart rate, forearm vascular resistance (by venous occlusion plethysmography), and plasma caffeine and catecholamine levels were measured. Cardiac and splanchnic blood volume were determined by radionuclide scans. 4. By 30 min after both caffeine and placebo meal studies, supine mean arterial blood pressure fell significantly (P = 0.006) by 31 +/- 7 and 19 +/- 6 mmHg, respectively (mean +/- SEM, between group difference was not significant). Heart rate, cardiac output and splanchnic blood volume increased significantly, but to a similar extent, after caffeine and placebo. Forearm vascular resistance was unchanged after both meals. 5. Oral caffeine given with a meal does not reduce splanchnic blood pooling nor prevent postprandial hypotension in symptomatic elderly patients.

Aged↗
PubMed2002

Caffeine in apnoeic Asian neonates: a sparse data analysis.

AIMS: To monitor plasma caffeine concentrations and adverse effects and to study the pharmacokinetics of caffeine in neonatal apnoea in the local Asian population after intravenous administration of caffeine. METHODS: Eighteen neonates with apnoea were treated with caffeine citrate at a loading dose of 10 mg caffeine base kg-1 and a maintenance dose of 2.5 mg kg-1 day-1. Blood samples, three after loading and two after the maintenance dose on day 2, 3, 7, 14 and 21 were taken and analysed for caffeine and its main metabolites using solid phase extraction and h.p.l.c. Adverse effects were monitored. Sparse data pharmacokinetic analysis was performed using P-Pharm. RESULTS: Mean caffeine concentrations varied from 10 to 20 mg l-1 throughout treatment (range 3.6-28.4 mg l-1). These concentrations were efficacious; less so in those with lower concentrations. Adverse effects included gastrointestinal disturbances, diuresis and hyperglycaemia. Pharmacokinetic parameter estimates [mean (coefficient of variation%)] were CL=0.00628 (17.5%) l h-1 and V=0.961 (20.3%) l. CL (l h-1)=0.004248 * wt(kg)+0.00154; r=0.8, P<0.01, explained 64% of the variation. V (l)=0.6299 * wt(kg)+0.259; r=0.67, P<0.01, explained 45% of variation. Model-predicted compared with observed plasma concentrations in a separate group of 10 neonates were unbiased and of good precision. CONCLUSIONS: The dosing regimen studied was suitable for our local Asian neonates as it resulted in therapeutic caffeine concentrations for adequate treatment of apnoea. Adverse effects were tolerable. Therefore, to avoid a higher incidence of adverse effects, this regimen should be retained and not increased as proposed by other workers. CL and V were within values of those reported for neonatal apnoea. Sparse data analysis showed that weight alone was adequate as the influential variable for the accurate prediction of individual pharmacokinetic parameters, plasma concentrations and for dosage adjustment if required.

Apnea↗
PubMed2000

Does caffeine confound relationships among adrenergic tone, blood pressure and sleep apnoea?

The purpose of this study was to determine whether caffeine consumption confounds the relationship among adrenergic tone, as measured by urinary norepinephrine (NE), blood pressure (BP) and obstructive sleep apnoea (OSA). Data were analysed using correlation and regression analysis, analysis of covariance and t-tests. Subjects included normotensives and hypertensives with and without OSA: 38 men, 23 women, aged 30-60 y; 100-150% of ideal body weight; without other major illness. Patients were studied using polysomnography, caffeine consumption was assessed, 24-h urinary NE levels were examined and ambulatory BP was recorded. Patients with OSA (N=27) reported significantly greater caffeine consumption than those without OSA (N=34) (295 vs. 103 mg, P=0.010), but caffeine was not significantly correlated with their ambulatory BP. In contrast, NE excretion correlated with caffeine consumption (r=0.24, P=0.041), apnoea severity (r=0.65, P < 0.001) and BP (r=0.34, P < 0.005). Significant OSA-NE and BP-NE relationships remained even after controlling for caffeine consumption. Patients with OSA consumed nearly three times the amount of caffeine as patients without OSA. While caffeine partially explains the increased adrenergic tone in patients with OSA and the relationship between BP and NE, it does not appear to contribute significantly to the relationship between OSA and elevated BP.

Adult↗
PubMedDate not supplied

Periextubation caffeine in preterm neonates: a randomized dose response trial.

OBJECTIVE: To compare the effectiveness of three dosing regimens of caffeine for preterm infants in the periextubation period. METHODS: A randomized double-blind clinical trial of three dosing regimens of caffeine citrate (3, 15 and 30 mg/kg) for periextubation management of ventilated preterm infants was undertaken. Infants born <32 weeks gestation who were ventilated for>48 h were eligible for the study. Caffeine citrate was given as a once daily dose for a period of 6 days commencing 24 h prior to a planned extubation, or within 6 h of an unplanned extubation. The primary outcome measure was extubation failure, defined as neonates who were unable to be extubated within 48 h of caffeine loading or who required reventilation or doxapram dose within 7 days of caffeine loading. Continuous recordings of oxygen saturation and heart rate were undertaken in a subgroup of enrolled infants. RESULTS: A total of 127 babies were enrolled into the study (42, 40, 45, in the 3, 15, and 30 mg/kg groups, respectively). No statistically significant difference was demonstrated in the incidence of extubation failure between dosing groups (19, 10, and 11 infants in the 3, 15, and 30 mg/kg groups, respectively), however, infants in the two higher dose groups had statistically significantly less documented apnoea than the lowest dose group. Of the 37 neonates with continuous pulse oximetry recordings, those on higher doses of caffeine recorded a statistically significantly higher mean heart rate, oxygen saturations and less time with oxygen saturations <85%. CONCLUSIONS: This trial indicated there were short-term benefits of decreased apnoea in the immediate periextubation period for ventilated infants born <32 weeks gestation receiving higher doses of caffeine. Further studies with larger numbers of infants assessing longer-term outcomes are necessary to determine the optimal dosing regimen of caffeine in preterm infants.

Apnea↗
PubMed2002

Caffeine stimulates Ca(2+) entry through store-operated channels to activate tyrosine hydroxylase in bovine chromaffin cells.

The ability of caffeine-induced store Ca(2+) mobilization to activate tyrosine hydroxylase was studied in bovine adrenal chromaffin cells. Caffeine increased tyrosine hydroxylase activity over 10 min with an EC(50) of 3 mm and maximum effect at 20 mm. The maximum response to caffeine was substantial, being almost one third that of the strongest agonists acetylcholine and PACAP-27, about half that for K(+) and similar to that for histamine. In contrast, catecholamine secretion evoked by caffeine was small, being less than 10% of the response to strong agonists. Caffeine-induced tyrosine hydroxylase activation was not mimicked or prevented by phosphodiesterase inhibition with isobutylmethylxanthine, nor was it mimicked by an equimolar concentration of sucrose. However, the effect of caffeine was prevented by depleting intracellular Ca(2+) stores by thapsigargin pretreatment, and reduced substantially by removing extracellular Ca(2+), by blocking Ca(2+) channels with Co(2+) or Ni(2+), or by inhibiting store-operated channels with 2-aminoethyl diphenylborate. It was not affected by inhibiting Ca(2+) entry through voltage-operated Ca(2+)-channels or by tetrodotoxin. The effect of caffeine was mimicked by acute thapsigargin treatment or by depleting intracellular Ca(2+) stores in Ca(2+)-free buffer and then reintroducing extracellular Ca(2+). The results indicate that mobilizing store Ca(2+) with caffeine is a very effective mechanism for activating tyrosine hydroxylase and that the majority of this response depends on extracellular Ca(2+) entry through store-operated channels. They also suggest that extracellular Ca(2+) entry through such channels regulates cellular responses differently to Ca(2+) entry through voltage-operated Ca(2+) channels.

Adrenal Medulla↗
PubMed2001

The safety and efficacy of pharmaceutical and herbal caffeine and ephedrine use as a weight loss agent.

Since passage of the Dietary Supplement Health and Education Act of 1994, the sale of herbal dietary supplements containing caffeine and ephedrine for weight loss has become widespread in the United States. Reports of adverse events associated with the use of these non-prescription supplements have raised concerns in the United States regulatory community. Restricting the use of these products is now being considered. Such restriction should be based upon controlled clinical trials. This review of the literature in Medline relative to the use of caffeine and ephedrine in the treatment of obesity concludes that caffeine and ephedrine are effective in causing weight loss. Caffeine and ephedrine give equivalent weight loss to Diethylpropion and superior weight loss compared to dexfenfluramine. Caffeine and ephedrine have a long history of safe, non-prescription use. The adverse events accompanying acute dosing are mild and transient. Adverse events with caffeine and ephedrine reach and remain at placebo levels after 4-12 weeks of continuous treatment, but data from randomized trials up to 6 months only are available. Obesity is chronic, requires chronic treatment, its incidence is increasing and it has few effective treatments. The benefits of caffeine and ephedrine in treating obesity appear to outweigh the small associated risks. Restriction of dietary herbal supplements containing caffeine and ephedrine, often with other ingredients, should be based on controlled clinical trials of these products.

Aminophylline↗
PubMed2002

Does caffeine intake protect from Alzheimer's disease?

Caffeine is the most widely consumed behaviourally active substance in the western world. Neuroprotective effects of caffeine in low doses, chronically administered, have been shown in different experimental models. If caffeine intake could protect against neurodegeneration in Alzheimer's disease (AD), then higher levels of caffeine consumption in normal subjects as compared with AD patients should be detectable in the presumably long period before diagnosis when insidious pathogenic changes are taking place. A case-control study was used: cases were 54 patients with probable AD fulfilling the National Institute of Neurologic and Communicative Disorders and Stroke and the AD and Related Disorders Association criteria, in a Dementia Clinics setting. Controls were 54 accompanying persons, cognitively normal, matched for age (+/-3 years) and sex. Patients with AD had an average daily caffeine intake of 73.9 +/- 97.9 mg during the 20 years that preceded diagnosis of AD, whereas the controls had an average daily caffeine intake of 198.7 +/- 135.7 mg during the corresponding 20 years of their lifetimes (P < 0.001, Wilcoxon signed ranks test). Using a logistic regression model, caffeine exposure during this period was found to be significantly inversely associated with AD (odds ratio=0.40, 95% confidence interval=0.25-0.67), whereas hypertension, diabetes, stroke, head trauma, smoking habits, alcohol consumption, non-steroid anti-inflammatory drugs, vitamin E, gastric disorders, heart disease, education and family history of dementia were not statistically significantly associated with AD. Caffeine intake was associated with a significantly lower risk for AD, independently of other possible confounding variables. These results, if confirmed with future prospective studies, may have a major impact on the prevention of AD.

Aged↗
PubMed1996

Exocytosis coupled to mobilization of intracellular calcium by muscarine and caffeine in rat chromaffin cells.

We used cultured rat chromaffin cells to test the hypothesis that Ca2+ entry but not release from internal stores is utilized for exocytosis. Two protocols were used to identify internal versus external Ca2+ sources: (a) Ca2+ surrounding single cells was transiently displaced by applying agonist with or without Ca2+ from an ejection pipette. (b) Intracellular stores of Ca2+ were depleted by soaking cells in Ca2+ -free plus 1 mM EGTA solution before transient exposure to agonist plus Ca2+. Exocytosis from individual cells was measured by microelectrochemical detection, and the intracellular Ca2+ concentration ([Ca2+]i) was measured by indo-1 fluorescence. KCl (35 mM) and nicotine (10 microM) caused an immediate increase in [Ca2+]i and secretion in cells with or without internal Ca2+ stores, but only when applied with Ca2+ in the ejection pipette. Caffeine (10 mM) and muscarine (30 microM) evoked exocytosis whether or not Ca2+ was included in the pipette, but neither produced responses in cells depleted of internal Ca2+ stores. Pretreatment with ryanodine (0.1 microM) inhibited caffeine- but not muscarine-stimulated responses. Elevated [Ca2+]i and exocytosis exhibited long latency to onset after stimulation by caffeine (2.9 +/- 0.38 s) or muscarine (2.2 +/- 0.25 s). However, the duration of caffeine-evoked exocytosis (7.1 +/- 0.8 s) was significantly shorter than that evoked by muscarine (33.1 +/- 3.5 s). The duration of caffeine-evoked exocytosis was not affected by changing the application period between 0.5 and 30 s. An approximately 20-s refractory period was found between repeated caffeine-evoked exocytosis bursts even though [Ca2+]i continued to be elevated. However, muscarine or nicotine could evoke exocytosis during the caffeine refractory period. We conclude that muscarine and caffeine mobilize different internal Ca2+ stores and that both are coupled to exocytosis in rat chromaffin cells. The nicotinic component of acetylcholine action depends primarily on influx of external Ca2+. These results and conclusions are consistent with our original observations in the perfused adrenal gland.

Adrenal Glands↗
PubMed2001

Ca(2+)-dependent K(+) current and exocytosis in responses to caffeine and muscarine in voltage-clamped guinea-pig adrenal chromaffin cells.

We characterized changes in membrane currents and the cytosolic Ca(2+) concentration, [Ca(2+)](i), in response to caffeine, and compared them with those in response to muscarine using the perforated patch-clamp technique and fura-2 microfluorimetry in guinea-pig adrenal chromaffin cells. Catecholamine release from single voltage-clamped cells was monitored with amperometry using carbon microelectrodes. Caffeine produced a transient outward current (I(out)) at holding potentials over - 60 mV, increasing in amplitude with increasing the potentials. It also evoked a rapid increase of [Ca(2+)](i) at all potentials examined. The current-voltage relation revealed that the activation of K(+) channels was responsible for the I(out) evoked by caffeine. Both current and [Ca(2+)](i) responses were reversibly abolished by cyclopiazonic acid, an inhibitor of Ca(2+)-pump ATPase. At - 30 mV, the caffeine-induced I(out), but not [Ca(2+)](i), was partly inhibited by either charybdotoxin or apamin. In the majority of cells tested, caffeine induced a larger I(out) but a smaller [Ca(2+)](i) increase than muscarine. Caffeine and muscarine increased catecholamine release from voltage-clamped single cells concomitant with the transient increase of [Ca(2+)](i), and there was a positive correlation between them. These results indicate that caffeine activates Ca(2+)-dependent K(+) channels and catecholamine secretion due to the release of Ca(2+) from internal stores in voltage-clamped adrenal chromaffin cells of the guinea-pig. There seems to be a spatial difference between [Ca(2+)](i) increased by Ca(2+) release from caffeine-sensitive stores and that released from muscarine (inositol 1,4,5-trisphosphate)-sensitive ones.

Adrenal Glands↗
PubMed1997

Alcohol, smoking, and caffeine use among headache patients.

We reviewed the charts of 151 headache patients, seen initially in a specialty headache center between 1988 and 1994, to collect information regarding reported alcohol consumption, smoking, daily number of caffeinated beverages, and medications. Charts of 50 patients in a general medicine clinic were reviewed for the same information. No significant differences between headache patients and general medicine patients were found in consumption of alcohol, smoking, or caffeinated beverages. Thirty headache patients (20%) used caffeine-containing medications more frequently than recommended; 24 of these patients used the products daily; 18 of those had a greater caffeine intake from medications than from beverages. Over-the-counter caffeine-containing analgesics were overused by 12 of the patients compared to 21 patients who overused prescription caffeine-containing preparations. Headache patients consume minimal amounts of alcohol, tobacco, and caffeinated beverages. However, headache patients often use caffeine-containing analgesics more frequently than recommended, which may lead to rebound and withdrawal headache.

Adolescent↗
PubMed2001

Urinary caffeine after coffee consumption and heat dehydration.

This study evaluated the effect of heat-induced dehydration on urinary caffeine excretion after the consumption of a strong coffee solution. Following ingestion of coffee (caffeine 4.9+/-0.1 [SE] mg/kg, 3-4 cups), ten healthy males were intermittently exposed to heat in a sauna until they had lost 2.9 % of lean mass. On a separate occasion, they consumed the same amount of coffee but remained quiet and euhydrated (control). Urine flow was reduced 7-fold in dehydration. At these low excretion rates (< 30 ml/h), caffeine concentration was negatively correlated with flow. Peak urinary caffeine (Cmax) was 7.6 +/- 0.4 (SE) microg/ml in dehydration and 7.1 +/- 0.2 microg/ml in the control (p > 0.05). Compared with the control, dehydration delayed Cmax by 1 hour, maintained higher saliva caffeine concentration (6.1 vs 5.2 microg/ml, p < 0.05) and a lower saliva paraxanthine/caffeine ratio (p < 0.001). The 24h-recovery of caffeine in urine was reduced (1.2 vs 2.8% of dose, p < 0.001), however at least 2.6% of dose were lost in sweat. These results suggest that the rise in circulating caffeine due to delayed metabolic clearance was partly opposed by a sizeable elimination in sweat. Therefore, heat dehydration did not lead to higher concentration of caffeine in urine after coffee ingestion.

Adult↗
PubMed1987

Effects of sucrose or caffeine ingestion on running performance and biochemical responses to endurance running.

To elucidate the effects of sucrose or caffeine ingestion on metabolic responses to prolonged exercise and on performance of a finishing spurt after the prolonged exercise, seven male physical education students performed four sets of 30 min running (62%-67% VO2 max) followed by progressive exhaustive running on a treadmill. Before each set, they took 350 ml solution containing either sucrose 23.8 g (97.5 kcal), caffeine 200 mg, or a placebo. The duration of the exhaustive running after sucrose, caffeine, or placebo ingestion was not significantly different. Exhaustion would possibly be attained not by depletion of muscle glycogen but by a decrease in the capacity of muscle cells to produce high tension for anaerobic metabolism. Total energy and energy from carbohydrate combusted during four sets of running were estimated at 1255 kcal and 810 kcal in the sucrose trial, 1271 kcal and 624 kcal in the caffeine trial, and 1248 kcal and 649 kcal in the placebo trial. Judging from the figures above, glycogen sparing during prolonged running seemed to be attained by sucrose ingestion but not by caffeine ingestion. The latter finding would be caused by lower intensity and a larger amount of ingested caffeine. In conclusion, performance of progressive exhaustive running following endurance running for 2 h could not be improved either by sucrose or caffeine ingestion. Glycogen sparing in the muscle, however, was suggested by sucrose ingestion but not by caffeine ingestion.

Adult↗
PubMed1982

Effects of caffeine ingestion on exercise performance at low and high altitudes in cross-country skiers.

The effect of caffeine on exercise time over a specified distance (approx. 21 km) was investigated in well-trained cross-country skiers (14 subjects) both at low (300 m above sea level) and high (2900 m above sea level) altitudes. Each subject participated in two races at both altitudes--one after caffeine ingestion (6 mg/kg body weight) and one after placebo on a double-blind basis. In each race 50% of the participants were medicated with caffeine, thereby after normalization (where the mean time was set at 100%), when the influence of weather and snow conditions were minimized, the difference between the race time with caffeine and placebo could be calculated for each individual and expressed as a percentage of the mean. At low altitudes, after half the distance, the race time with caffeine was decreased 0.94% of the mean time (corresponding to approx. 33 s) as compared to placebo (P less than 0.05), whereas after the full distance the corresponding decrease was 1.7% of the mean time (corresponding to approx. 59 s) (0.05 less than P less than 0.10). At high altitudes, the race time was significantly faster with caffeine than with placebo (P less than 0.001), both after one and two laps, 2.19% and 3.18% of the mean time, respectively (corresponding to approx. 101 s and 152 s). The perceived exertion was similar at low and high altitudes independent of medication. In conclusion, there are indications that caffeine induces an increased performance capacity for cross-country skiers at low altitudes. Furthermore, an even more marked improvement after caffeine as compared to placebo was found at high altitudes.

Adult↗
PubMed2000

Do caffeine-containing analgesics promote dependence? A review and evaluation.

OBJECTIVE: Debates about the suspected association between kidney disease and use of analgesics have led to concern about whether caffeine could stimulate an undesirable overuse of phenacetin-free combined analgesics. A committee was asked to critically review the pertinent literature and to suggest guides for clinical practice and for consideration of international regulatory authorities. PARTICIPANTS: A group of international scientists, jointly selected by the regulatory authorities of Germany, Switzerland, and Austria and the pharmaceutical industry. EVIDENCE: All invited experts evaluated relevant literature and reports and added further information and comments. CONCLUSIONS: Caffeine has a synergistic effectiveness with analgesics. Although caffeine has a dependence potential, the potential is low. Experimental data regarding dependence potential for caffeine alone may not correspond to the conditions in patients with pain. Withdrawal is not likely to cause stimulation or sustainment of analgesic intake. For drug-induced headache, no single or combined analgesic was consistently identified as causative, and no evidence exists for a special role of caffeine. Strong dependence behavior was observed only in patients using phenacetin-containing preparations, coformulated with antipyretics/analgesics and caffeine. This finding may have led to the impression that caffeine stimulates overuse of analgesics. SUMMARY: Although more experimental and long-term data would be desirable to show possible mechanisms of dependence and to offer unequivocal proof of safety, the committee concluded that the available evidence does not support the claim that analgesics coformulated with caffeine, in the absence of phenacetin, stimulate or sustain overuse.

Analgesics↗
PubMed2001

Urinary biomarkers for assessing dietary exposure to caffeine.

The feasibility of using metabolites specific to caffeine as urinary biomarkers to be employed in the estimation of dietary caffeine intake is reported. The influence of inter-individual differences in the metabolism of caffeine and the effect of volunteer phenotype on the interpretation of potential biomarkers has been investigated using urinary caffeine metabolite data. This method of phenotype determination accurately reflected the rate constant for the cytochrome P4501A2 (CYP1A2)-catalysed 3-demethylation of caffeine in vivo. Three studies with up to 20 human volunteers demonstrated that a 24-h urine collection after a caffeine dose allows quantification of the metabolites excreted; that the ratios of selected metabolites used to classify the volunteers into fast, intermediate or slow caffeine metabolizers by CYP1A2 phenotype gave a similar result (2:7:3, slow:intermediate:fast) to that found in the general population (1:7:2); and that three metabolites, 1,7-dimethylxanthine, 1,7-dimethyluric acid and 1-methylxanthine, could be studied further as potential biomarkers for caffeine dietary intake.

Adult↗
PubMed1994

Interactions between dietary caffeine and calcium on calcium and bone metabolism in older women.

OBJECTIVE: Our purpose was to determine the effect of 2 weeks of caffeine abstinence on calcium (Ca) and bone metabolism in women habitually consuming caffeine and either low or moderate amounts of Ca. METHODS: Participants were 25 women, aged 39-76 years (mean 65 years, median 57 years) habitually consuming at least 200 mg caffeine daily. Three days of dietary records and 24-hour urine collections were made immediately prior to collection of fasting blood and 1-hour urine in a metabolic unit. Women were classified as low Ca consumers (414-584 mg daily) or moderate Ca consumers (662-1357 mg daily) based on 6 days of diet records. RESULTS: Women in the low Ca group had higher levels of serum ultrafiltrable Ca (UFCa) after caffeine abstinence (1.40 mmol/L CAF+ vs 1.52 mmol/L CAF-, p < 0.01), while there were no differences between experimental periods for UFCa in the moderate Ca group (1.35 mmol/L CAF+ vs 1.38 mmol/L CAF-, ns). Women in the low Ca group also had lower serum bone isoenzyme alkaline phosphatase levels after caffeine abstinence (9.3 U/L CAF+ vs 8.8 U/L CAF-, p < 0.05), while no significant changes were seen in bone alkaline phosphatase in the moderate Ca consumers (8.7 U/L CAF+ vs 8.9 U/L CAF-, ns). Fasting total serum Ca, urinary hydroxyproline/creatinine, and Ca/creatinine ratios were unchanged in both dietary groups. Three-day mean 24-hour urinary Ca excretion decreased after caffeine abstinence in the moderate Ca group only. There were no differences in dietary intakes of Ca from dairy products between CAF+ and CAF- in either the low or moderate Ca groups. CONCLUSION: Abstinence from moderate caffeine intake (mean 5.8 mg/kg lean body mass, 383 mg/day caffeine) raises ultrafiltrable Ca and decreases bone alkaline phosphatase in older women consuming < 600 mg Ca daily.

Adult↗
PubMed2003

Interaction of metal ions with caffeine and theophylline: stability and structural features.

The interactions of caffeine and theophylline with divalent cadmium, mercury, strontium and barium ions were studied in aqueous solution and physiological pH. Fourier transform infrared spectroscopy (FTIR) and absorption spectra were used to determine the cation binding mode and association constants. Spectroscopic results showed that Cd(2+), Hg(2+), Sr(2+) and Ba(2+) bind strongly to caffeine and theophylline. Direct and indirect (through metal hydration shell) interactions were observed for caffeine and theophylline with Cd(2+), Hg(2+), Sr(2+) and Ba(2+) through O6 and N9 (caffeine) and O6, N9 and N7 atoms (theophylline). The overall binding constants are:k(Cd-caffeine) = 1.24 x 10(5) M(-1), k(Hg-caffeine) = 1.74 x 10(5) M(-1), k(Sr- caffeine) = 3.3 x 10(4) M(-1), k(Ba-caffeine) = 1.8 x 10(4) M(-1), k(Cd-theophylline) = 5.75 x 10(5) M(-1), k(Hg-theophylline) = 2.14 x 10(5) M(-1), k(Sr-theophylline) = 4.6 x 10(4) M(-1), k(Ba-theophylline) = 3 x 10(4) M(-1). These k values are evidence for weak and strong cation interactions in these metal complexes.

Caffeine↗