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PubMed1980

Acute caffeine overdose in the neonate.

To our knowledge, the clinical course of acute caffeine poisoning in neonates has not been previously reported. Three full-term infants manifested CNS irritability after the parenteral administration of large doses of caffeine and benzoate sodium injection in the delivery room for respiratory depression. The infants received caffeine in doses that ranged from 36 to 136 mg/kg. On arrival in a regional newborn center, they exhibited one or more of the following symptoms: tachypnea, fine tremor of the extremities, opisthotonus, tonic-clonic movements, and nonpurposeful jaw and lip movements. The overdose of caffeine produced a clinical picture that suggested neonatal seizures and prompted therapy with anticonvulsants. A fourth infant (premature) attained a high plasma caffeine concentration, but this infant's symptoms were altered by intraventricular hemorrhage. The combination of caffeine overdose and perinatal asphyxia may precipitate or increase seizure activity in the neonate. Recognition of the potential toxic effects of caffeine overdose should guide patient care and stimulate further study to establish appropriate use of caffeine in the newborn infant.

Caffeine↗
PubMed1985

Increased anxiogenic effects of caffeine in panic disorders.

The effects of oral administration of caffeine (10 mg/kg) on behavioral ratings, somatic symptoms, blood pressure and plasma levels of 3-methoxy-4-hydroxyphenethyleneglycol (MHPG) and cortisol were determined in 17 healthy subjects and 21 patients meeting DSM-III criteria for agoraphobia with panic attacks or panic disorder. Caffeine produced significantly greater increases in subject-rated anxiety, nervousness, fear, nausea, palpitations, restlessness, and tremors in the patients compared with healthy subjects. In the patients, but not the healthy subjects, these symptoms were significantly correlated with plasma caffeine levels. Seventy-one percent of the patients reported that the behavioral effects of caffeine were similar to those experienced during panic attacks. Caffeine did not alter plasma MHPG levels in either the healthy subjects or patients. Caffeine increased plasma cortisol levels equally in the patient and healthy groups. Because caffeine is an adenosine receptor antagonist, these results suggest that some panic disorder patients may have abnormalities in neuronal systems involving adenosine. Patients with anxiety disorders may benefit by avoiding caffeine-containing foods and beverages.

Adult↗
PubMed1991

Caffeine self-administration, withdrawal, and adverse effects among coffee drinkers.

Twenty-two coffee drinkers (three to seven cups per day) underwent repeated double-blind trials to test for caffeine self-administration, withdrawal, and adverse effects. Each trial consisted first of a randomized crossover period of 1 day of decaffeinated coffee and 1 day of caffeinated coffee (100 mg) to assess withdrawal and adverse effects of caffeine. Next, subjects were given 2 days of concurrent access to the two coffees. The relative use of the two coffees was used to assess caffeine self-administration. Reliable caffeine self-administration occurred in three of 10 subjects in study 1 and seven of 12 subjects in study 2. Withdrawal symptoms were headaches, drowsiness, and fatigue. The major adverse effect from self-administration was tremulousness. The occurrence of headaches on substitution of decaffeinated coffee prospectively predicted subsequent self-administration of caffeine. These results indicate that some coffee drinkers exhibit signs of a caffeine dependence, ie, they self-administer coffee for the effects of caffeine, have withdrawal symptoms on cessation, and experience adverse effects.

Adult↗
PubMedDate not supplied

Effects of preconceptual caffeine exposure on pregnancy and progeny viability.

OBJECTIVE: A previous study demonstrated for the first time that a drug such as caffeine, administered prior to ovulation and genomic activation, causes a quantitative difference in growth-promoting energy utilization in a proportion of 5-day-old blastocysts. The objective of the present study was to investigate whether developmental changes induced by caffeine administered throughout the estrus cycle prior to fertilization are sustained throughout pregnancy and after birth. METHODS: Caffeine was administered to rats throughout the estrus cycle prior to fertilization, with control and experimental groups subdivided into preimplantation and postimplantation categories. Preimplantation fertilization rate was assessed on day 4 of pregnancy by a pregnancy-induced elevation in maternal plasma progesterone concentration, or by flushing each uterine horn on day 5 of pregnancy to determine the presence or absence of a litter. Postimplantation fetuses were collected on gestational day 12 or allowed to go to term. RESULTS: Preconceptual caffeine exposure significantly reduced maternal fertility by the failure of a proportion of the litters to implant, rather than curtailing preimplantation development or postimplantation losses. Postnatal mortality between weeks 0 and 1 was elevated and the weekly incremental growth rate of the pups from week 3 through week 7 was significantly reduced in the preconceptually caffeine-treated offspring. Experimental females reached puberty at the same age as the controls but at a significantly lower body weight. Gestation length, hirthweight, litter size, sex ratio, and anogenital distance (a measure of prenatal androgenization) were not affected by preconceptual caffeine treatment. CONCLUSIONS: It was concluded that the reduced fertility rate in preconceptually caffeine-exposed rats was due to the failure of litters to implant rather than to a reduced fertilization rate, which was normal. It was further concluded that the growth rate over the neonatal and prepubertal periods of surviving pups in the caffeine-treated group was subnormal.

Animals↗
PubMed1979

Caffeine metabolism in the newborn.

The concentrations of caffeine and metabolites in urine have been examined as a function of age to explore the remarkably slow elimination of caffeine by human infants. Urine samples were obtained from 3 adults and 10 infants aged 8 days to 8 months during therapeutic treatment with caffeine. A high-performance liquid chromatographic (HPLC) procedure involving reversed-phase partition chromatography was developed to separate caffeine and 13 of its metabolites. During the first month of life, caffeine accounted for more than 85% of the identifiable products in urine. Caffeine remained the predominant component for the first 3 months, but its percentage decreased gradually to the adult value of less than 2% by the age of 7 to 9 months. This change reflected increasing metabolite production, not decreasing urinary caffeine concentration. The adult metabolite pattern of partially demethylated xanthines and urates was attained by 7 to 9 months. The data indicate that the 4-day plasma t1/2 of caffeine characteristic of the newborn depends in large part on slow urinary excretion of unchanged drug since there is little or no metabolism. Subsequent decrease in the t1/2 to about 4 hr by the age of 8 months correlates closely with the rise in metabolite production.

Adult↗
PubMed2005

Effects of caffeine on linear and nonlinear measures of heart rate variability before and after exercise.

Caffeine intake is associated with an increase in heart rate (HR) variability. This study sought to examine the effects of caffeine on HR variability measures before and during progressive exercise in 11 healthy volunteers in a double-blind randomized and counterbalanced placebo-controlled paradigm. As expected, there were significant increases in HR and decreases in HR variability after exercise during both placebo and caffeine conditions; however, pre-exercise caffeine condition was associated with a significant increase of HR variability, especially in the high-frequency range (0.15-0.5 Hz), and also approximate entropy (APEN), which is usually attributed to cardiac vagal function. But during progressive exercise, caffeine intake resulted in a greater decrease of HF power as well as HR APEN. Caffeine also was associated with significantly higher LF power during exercise compared to the placebo condition. These results suggest that caffeine may have different effects on HR variability at rest, compared to exercise. These findings may have implications for patients with cardiac illness and anxiety, depression, and psychotic disorders who use beverages containing excessive caffeine.

Adolescent↗
PubMed2005

Determination of caffeine and its metabolites in urine by capillary electrophoresis-mass spectrometry.

The caffeine content of foods and beverages varies considerably, interfering with our ability to obtain valid interpretations in many human studies with regard to the mechanism of action(s) of caffeine and/or its metabolites. The rate of metabolism of caffeine and other xanthine drugs also varies greatly from one individual to another. Therefore, it is extremely important to develop accurate, reliable analytical methods to quantify caffeine and its metabolites in simple and complex matrixes. A simple method is described for the separation and characterization of caffeine and its major metabolites employing capillary electrophoresis (CE) coupled to ultraviolet-absorption and mass spectrometry (MS) detection. After optimization of the electrophoresis separation conditions, a reliable separation of caffeine and 11 of its major metabolites was achieved in 50 mM ammonium carbonate buffer, pH 11.0. The volatile aqueous electrolyte system used with a normal electroosmotic flow polarity also provided an optimal separation condition for the characterization of the analytes by MS. The CE method achieved baseline resolution for all 12 compounds in less than 30 min. The CE-MS method is suitable for use as a routine procedure for the rapid separation and characterization of caffeine and its metabolites. The usefulness of this method was demonstrated by the extraction, separation, and identification of caffeine and its 11 metabolites from normal urine samples. The urine specimens were first acidified to obtain optimum binding efficiency to the sorbents of the off-line, solid-phase extraction procedure employed here, and an acidified eluent solvent was employed for the desorption step to maximize the recovery of the bound analytes.

Buffers↗
PubMed1982

Variations among species and cell types in the effects of caffeine on mutagen-induced cytotoxicity and postreplication repair of DNA.

The influence of caffeine on cytotoxicity and postreplication repair of DNA was examined following exposure of several cell types to physical and chemical agents known to damage DNA. The cell types used in this study were normal human fibroblasts (HS-WP), human xeroderma pigmentosum fibroblasts (SGL), Chinese hamster V79 cells, mouse BALB/c-3T3 cells, and secondary Syrian hamster embryo cells. The DNA damaging agents were ultraviolet light (UV), N-2-acetoxy-fluorenylacetamide (AFAA), nitroquinoline-N-oxide (NQO) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). Induction of cytotoxicity in Chinese hamster V79 cells due to ultraviolet light or AFAA exposure was enhanced by caffeine at a concentration of 1.0 mM in the culture medium, but not at 0.2 or 0.05 mM. Caffeine also inhibited postreplication repair in these cells at the same concentrations. In contrast, postreplication repair was not affected by caffeine at concentrations up to 1.0 mM in normal human fibroblasts (HS-WP), human xeroderma pigmentosum fibroblasts (SGL), secondary Syrian hamster embryo cells, and mouse BALB/c-3T3 cells following treatment with ultraviolet light, AFAA, NQO, or MNNG. Cytotoxicity in BALB/c-3T3 cells following exposure to ultraviolet light or AFAA was enhanced in the presence of caffeine at 1.0 or 0.2 mM, although these concentrations of caffeine had no effect on postreplication repair in these cells. The inhibitory effect of caffeine on postreplication repair was found only in Chinese hamster V79 cells among the five cell types used in this study. Both normal and xeroderma pigmentosum human cells repaired mutagen-induced DNA damage equally well in the absence or presence of caffeine at concentrations of 1.0 mM or less.

2-Acetylaminofluorene↗
PubMed2007

Caffeine attenuates practice effects in word stem completion as measured by fMRI BOLD signal.

Caffeine ingestion results in increased brain cell metabolism (Nehlig et al. [1992] Brain Res Brain Res Rev 17:139-170) and decreased cerebral blood flow (Field et al. [2003] Radiology 227:129-135; Mulderink et al. [2002] Neuroimage 15:37-44). The current study investigated the effect of caffeine in a word stem completion task using only novel word stems (no repeated stimuli). Resting perfusion was measured with arterial spin labeled perfusion MRI, along with blood oxygenation level-dependent (BOLD) signal before and after ingestion of regular coffee, decaffeinated coffee, and water. Based on previous research (Laurienti et al. [2002] Neuroimage 17:751-757; Mulderink et al. [2002] Neuroimage 15:37-44), we hypothesized that caffeine would result in increased BOLD signal intensity and extent of BOLD activation. As expected, caffeine resulted in a significant decrease in cerebral perfusion. However, both the control and caffeine groups showed an increase in BOLD signal amplitude across two sets of novel word stems. Additionally, the control group showed a 50% reduction in the extent of BOLD activation, while the caffeine group showed no change in activation extent. Neither group showed changes in BOLD baseline signal over time, which had been suggested to mediate caffeine-related BOLD signal changes. The results suggest that caffeine may attenuate general task practice effects that have been described in recent functional MRI studies of word stem completion (Buckner et al. [2000] Brain 123:620-640).

Adolescent↗
PubMed2004

Effects of dietary caffeine on mood when rested and sleep restricted.

Prolonged use of caffeine can lead to physical dependence evidenced by characteristic withdrawal symptoms during abstinence. Debate exists as to whether mood enhancement by caffeine represents a net effect or merely the restoration of abstinence-induced mood decrements. One aim of this study was to determine the net effects on mood of dietary caffeine compared with prolonged abstinence. In addition, the study aimed to determine whether caffeine restores mood degraded by a non-caffeine source, namely, sleep restriction. A double-blind placebo-controlled cross-over design was employed in which 48 male and female volunteers alternated weekly between ingesting placebo and caffeine (1.75 mg/kg) three times daily for 4 consecutive weeks, while being either rested or sleep restricted. Mood was assessed using a computerized version of the profile of mood states (POMS), giving scores for overall mood and six mood dimensions. Gender had small effects on mood, whereas all mood dimensions were markedly adversely affected by sleep restriction. Caffeine had no significant net enhancing effects on mood when participants were rested, and produced no net restorative effects when mood was degraded by sleep restriction. On the contrary, caffeine-induced decrements in mood were observed during both conditions of rest and sleep restriction.

Adolescent↗
PubMed2005

Effects of caffeine in non-withdrawn volunteers.

RATIONALE: Evidence for the behavioural effects of caffeine is prevalent in the literature. It is associated with increased subjective alertness, improved reaction time and enhanced encoding of new information. However, there is an on-going debate as to whether such changes are in fact improvements or merely a reversal of the negative effects of caffeine withdrawal. Using participants who had consumed their normal daily quota of caffeine this study alleviated this potential confound as all participants were not withdrawn at the time of testing. OBJECTIVES: To determine whether caffeine influenced the mood and performance of non-withdrawn volunteers. METHODS: Sixty eight volunteers, all of whom were regular caffeine consumers, consumed their normal amount of caffeine over the course of the day. Baseline measures of mood and performance were then carried out followed by double-blind administration of caffeine (2 mg/kg) or placebo. The test battery was repeated again 30 min after ingestion of the drink. RESULTS: Our findings showed improvements comparable to previous research. Mood was improved and performance on a number of cognitive measures was improved. The findings are discussed in relation to both noradrenergic and cholinergic neurotransmitter systems. CONCLUSIONS: This study provided evidence against the argument that behavioural changes due to caffeine are merely the reversal of negative withdrawal effects.

Activity Cycles↗
PubMed1991

Effect of caffeine on parameters of osteoblast growth and differentiation of a mineralized extracellular matrix in vitro.

The effects of caffeine exposure on bone formation were examined using a chick osteoblast culture system. Secondary cultures of normal diploid osteoblasts were exposed to chronic doses of 0, 0.1, 0.2, or 0.4 mM caffeine beginning on day 0 through day 28. Neither the rate of cell proliferation nor cell number, as measured by total DNA, was decreased for any of the doses examined. In contrast, osteocalcin levels, alkaline phosphatase activity, and total calcium levels showed a dose-related decrease in cultures treated with caffeine. These parameters were significantly decreased at the highest dose of 0.4 mM. The reduction in total protein levels ranged from 29 to 66% of control values and was independent of dose. In contrast, total collagen levels were more affected by the dose of caffeine used. Inhibition of collagen levels was most apparent on days 17 and 21, time points during the period of active formation of the matrix immediately preceding the deposition of mineral. By day 28 collagen levels in cultures exposed to the lower doses of caffeine had returned to control levels, and only the cultures exposed to the highest dose (0.4 mM) remained significantly inhibited with respect to both collagen and mineral. Histochemically, alkaline phosphatase and mineral staining of day 28 cultures mirrored the biochemical events with the 0.4 mM caffeine exposure. The results indicate that one of the effects of caffeine on bone development is to inhibit the formation of a competent extracellular matrix during the osteoblast differentiation sequence, which results in the inhibition of mineralization analogous to the delayed ossification observed in fetal animals after prenatal caffeine exposure.

Alkaline Phosphatase↗
PubMed1991

Caffeine potentiation of mefenamic acid-induced lesions in the rat renal medulla.

The effect of caffeine given in combination with mefenamic acid on the renal medulla was examined. Sprague-Dawley rats were divided into four groups and gavage fed either vehicle suspension (control), mefenamic acid, mefenamic acid+caffeine or caffeine only for 4 months. Renal tissue taken from the corticomedullary junction was processed for electron microscopy. Ultrathin sections were cut after identification of vasa rectae on survey sections. On subsequent morphometric analysis, percentage interstitial tissue was calculated from the total area of vasa recta less the non-interstitial tissue. The median percentage of interstitial tissue in the mefenamic acid and caffeine group was 41 (range 33-50; n = 15) compared with 34 (20-48; n = 20) in mefenamic acid (P less than 0.01), 29 (15-42; n = 15) in caffeine only (P less than 0.001) and 32 (20-46; n = 18) in vehicle-treated animals (P less than 0.001). There were no significant differences between mefenamic acid alone and vehicle or caffeine-only groups or between caffeine-only and vehicle-treated controls. This suggests that caffeine potentiates the effect of the non-steroidal anti-inflammatory drug, mefenamic acid, on the rat renal medulla, resulting in a quantitative increase in the interstitial tissue between adjacent afferent and efferent vasa recta.

Animals↗
PubMed1989

Transplacentally acquired caffeine and the occurrence of apnea, bradycardia, and periodic breathing in preterm infants: preliminary communication.

Cord blood caffeine concentrations were measured by high-pressure liquid chromatography in 79 preterm infants. Eleven infants (14%) had detectable caffeine concentrations ranging from 1.1 to 3.7 micrograms/mL (means +/- SD = 2.5 +/- 0.8), and 68 infants had no measurable caffeine. Seven infants with detectable caffeine (group 1) had impedance pneumograms recorded before 2 weeks of age. Each infant in group 1 was matched with two infants without detectable caffeine by birthweight, gestational age, and chronologic age at pneumogram recording to yield a control group (group 2) of 14 infants. Comparison of the groups using quantitative measures of apnea, bradycardia, and periodic breathing obtained from pneumogram analysis and the incidence of monitor alarms on bedside nursing records showed no significant differences. Thus, caffeine was present infrequently and at low concentrations at birth in 79 preterm infants. The amount of apnea, bradycardia, and periodic breathing experienced before 2 weeks of age in 7 preterm infants with detectable cord blood caffeine was not different from that in 14 similar infants without caffeine. Future studies are planned to examine the relationship between postnatal changes in transplacentally acquired methylxanthine concentrations and quantitative measures of apnea, bradycardia, and periodic breathing in a larger number of preterm infants without cardiorespiratory disease.

Apnea↗
PubMed2001

Acute and chronic caffeine administration differentially alters striatal gene expression in wild-type and adenosine A(2A) receptor-deficient mice.

In order to assess for the respective involvement of adenosine A(1) and A(2A) receptors (A(2A)-R) in the consequences of short- and long-term caffeine exposure on gene expression, the effects of acute caffeine administration on striatal, cortical, and hippocampal expression of immediate early genes (IEG), zif-268 and arc, and the effects of long-term caffeine or 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) exposure (once daily for 15 days) on striatal gene expression of substance P, enkephalin, and glutamic acid decarboxylase isoforms, GAD65 and GAD67, were evaluated in wild-type and A(2A)-R-deficient (A(2A)-R(-/-)) mice. In situ hybridization histochemistry was performed using oligonucleotides followed by quantitative image analysis. Our results demonstrated that a biphasic response of IEG expression to acute caffeine observed in the wild-type striatum was resumed in a monophasic response in the mutant striatum. In the cerebral cortex and hippocampus, the effect of caffeine was weak in wild-type, whereas in mutant mice it induced a 2-3-fold increase in the IEG expression to restore a level similar to the wild-type basal expression. Chronic caffeine and DPCPX-mediated regulation in neuropeptide and GADs striatal gene expression typically showed the mimicking of alterations resulting from the A(2A)-R genetic deficiency in 25 mg/kg caffeine-treated wild-type mice as well as the dose-dependent normalization of substance P and enkephalin expression in A(2A)-R(-/-) mice. These results indicate that, depending on the dose, the blockade of A(2A)-R or A(1) receptors by caffeine is preferentially revealed leading to highly differential alterations in striatal gene expression and they also suggested the central role of these two receptors on the control of dopaminergic functions.

Animals↗
PubMed1994

In utero exposure to caffeine causes delayed neural tube closure in rat embryos.

We have investigated the effect of caffeine on embryo growth and development. Caffeine (25 mg/kg) was administered on gestation day (g.d.) 8-9 and the embryos examined histologically 24 h after the final dose. The crown-rump length of caffeine treated embryos (1.92 +/- 0.08 mm) was significantly smaller (P < 0.001) than the controls (2.91 +/- 0.26 mm) as was the circumferential length (caffeine vs. controls, 3.79 +/- 0.16 mm vs. 6.03 +/- 0.61 mm; P < 0.001). Additional measures, such as development of the heart, eye, and limb buds, were also reduced in the caffeine treated embryos. The most striking difference between the control and caffeine treated embryos was the larger proportion of treated embryos with regions of open neural tube. This was most marked in the caudal region of the embryos where 91% of treated embryos had regions of open neural tube compared with 14% of controls. The amount of open neural tube in any individual caffeine treated embryo did not relate to the crown-rump or circumferential length of that embryo nor was the effect restricted to particular litters. These results indicate that caffeine had a significant effects on embryonic growth and development.

Animals↗
PubMed1986

Pulmonary stenosis with ventricular septal defect, common aorticopulmonary trunk, and dextroposition of the aorta: morphologic and qualitative physiologic effects in caffeine-treated chick embryos.

Effects of caffeine administration to Hamburger-Hamilton stage 19 chick embryos (3 days of incubation) were investigated. A morphologic study of the effect of caffeine on cardiogenesis showed that caffeine produced total cardiac malformations in the chick in a dose-related fashion. A maximum frequency of 70.6% was observed with 4.7 mg caffeine. Major malformations included common aorticopulmonary trunk and dextroposition of the aorta accompanied by ventricular septal defect with/without pulmonary stenosis. Qualitative analysis of cinegraphs following exposure of embryos to a single teratogenic dose of caffeine (3.5 mg/egg) produced marked alterations in cardiac function when compared with chick Ringer's controls. Within 3 minutes after exposure to caffeine, dilation of the common ventricle and weak ventricular contractility were observed and persisted for 1 hour. Dose-response data and microcinematographic observations suggest that caffeine induced cardiac anomalies by a direct toxic effect on the embryo rather than by altering cardiac cell function. Our data also suggest that pathophysiologic changes in cardiac function may play an important role in the pathogenesis of caffeine-induced cardiac anomalies in the chick embryo.

Abnormalities, Drug-Induced↗
PubMed1986

Caffeine effects on cyclic AMP levels in the mouse embryonic limb and palate in vitro.

Caffeine is a teratogen that causes limb and palate malformations in rodents. Since the ability to raise cyclic nucleotide levels is a known biological action of caffeine, cyclic AMP levels were measured in CD-1 mouse embryonic forelimb from whole embryo culture and embryonic limb and palate cells grown in primary culture following treatment with various concentrations of caffeine (0, 1, 3, or 10 mM). In forelimb buds from whole embryo culture, a dose-dependent response was observed. Caffeine at 1 mM concentration stimulated cyclic AMP levels to 151% of control value at 60 min. Even greater stimulation of cyclic AMP occurred at higher caffeine concentrations. A dose-dependent response was seen in both limb and palate cell culture. In limb cell culture, all caffeine concentrations significantly stimulated cyclic AMP after 10 min compared to control. In palate cell culture, there was a twofold increase in cyclic AMP at the 1-mM caffeine concentration. At higher caffeine concentrations, cyclic AMP was significantly increased after 60 min. In addition, stimulation of cyclic AMP in cultured limb and palate cells by isoproterenol, a beta-adrenergic agonist, was used as a positive control. Isoproterenol stimulated a 2.5-fold greater response in the palate cells than in the limb bud cells at isoproterenol levels of 10(-5) or 10(-4) M. The increase of cyclic AMP may be influential in the process of abnormal limb or palate development.

Animals↗