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PubMed1992

Should caffeine abuse, dependence, or withdrawal be added to DSM-IV and ICD-10?

OBJECTIVE: The authors reviewed basic science and clinical data on caffeine abuse, dependence, and withdrawal in order to make a conclusion about whether these disorders exist and should be included in DSM-IV and ICD-10. METHOD: Studies were located through computerized searches, reference sections of published articles, and written requests. RESULTS: The studies show that abstinence from caffeine induces a withdrawal syndrome of headache, fatigue, and drowsiness which begins within 12-24 hours and lasts about 1 week. The syndrome can be severe and appears to be one reason for continued use of coffee. The prevalence of this caffeine withdrawal syndrome is unknown. Use of caffeine may aggravate some common behavioral and medical disorders. In double-blind tests, a subset of coffee and soda drinkers reliably self-administered caffeinated beverages in preference to uncaffeinated beverages. Clinical indicators of dependence, such as difficulty stopping use of caffeine and use despite harm, have not been documented. CONCLUSIONS: Caffeine withdrawal but not caffeine abuse or dependence should be included as a diagnosis in DSM-IV and ICD-10. Future research should focus on whether some caffeine users exhibit clinical indicators of drug dependence.

Caffeine↗

PubMed1995

Safety and efficacy of caffeine-augmented ECT in elderly depressives: a retrospective study.

Prior studies have shown that in younger depressives undergoing ECT whose seizure durations declined despite maximum settings on three different ECT devices, pretreatment with caffeine lengthened seizures and resulted in clinical improvement. Caffeine (half life, 140-270 minutes) was well tolerated even in patients with pre-existing cardiovascular disease. The purpose of this retrospective study was to determine the safety and efficacy of caffeine augmented ECT in elderly depressed patients. The charts of 14 elderly depressives (average age 75.6, range 59-83; 2 males, 12 females) who received caffeine-augmented ECT were reviewed. Patients pre- and post-ECT medications, blood pressure, pulse, and seizure times (cuff and EEG) for each ECT performed were noted. The following conclusions were drawn from our study: (1) Caffeine definitely increases the seizure length and was useful in our setting when the energy settings could not be increased anymore. (2) Caffeine augmentation inconsistently causes an increase in pulse rate, on average, in the elderly. (3) Caffeine inconsistently produces an increase in mean arterial pressure. (4) Caffeine did not consistently produce an increase in the maximum rate-pressure product. We conclude from this study that caffeine-augmented ECT is safe and effective in increasing seizure duration in the elderly. However, more research needs to be done to determine optimal dosing and tolerability.

Aged↗

PubMed1988

Caffeine induces uncoordinated expression of cell cycle functions after ultraviolet irradiation. Accelerated cycle transit, sister chromatid exchanges and premature chromosome condensation in a transformed Indian muntjac cell line.

Caffeine enhances the lethal effect of DNA-damaging agents. It also affects the timing of events in the cell cycle; the enhanced cytotoxicity may be partly due to caffeine's ability to overcome the protective damage-induced delay in S or G2 phase. When the effects of caffeine are compared in a normal Indian muntjac cell line and a simian virus 40 (SV40)-transformed, ultraviolet light (u.v.)-sensitive line in which u.v. induces many sister chromatid exchanges, different cell cycle sensitivities are seen. In the SV40-transformed line, caffeine over-rides the delay in DNA synthesis imposed by DNA damage; it initiates late cycle events after u.v. irradiation, and in some cases it induces S-phase premature chromosome condensation, apparently by inducing mitotic factors in cells where the chromatin is still replicating. Caffeine has been reported to induce similar premature chromosome condensation in cells arrested with DNA polymerase inhibitors; this is the first recognition that such events occur in response to caffeine treatment after DNA damage. Some apparent paradoxes of caffeine's action on irradiated cells can be thus explained. In the normal line, caffeine neither affects progression through the cycle nor induces premature chromosome condensation after irradiation. In both lines, caffeine increases killing and sister chromatid exchanges after u.v. irradiation; but these effects are more pronounced when exerted through the cell cycle-related mechanism.

Animals↗

PubMed2000

The effect of caffeine on p53-dependent radioresponses in undifferentiated mouse embryonal carcinoma cells after X-ray and UV-irradiations.

The effect of caffeine was studied on the radioresponses of undifferentiated mouse embryonal carcinoma cells (EC cells) with or without the functional p53. The radioresponses studied included radiosensitivity, the activation of p53, apoptosis with characteristic DNA ladder formation and cell cycle progression. An undifferentiated mouse EC cell line, ECA2, and a newly established p53-deficient EC cell line, p53 delta, were used in the present study. The status of the p53 gene did not significantly affect the colony survivals of undifferentiated EC cells to X-rays and UV. Although a post-irradiation treatment with caffeine sensitized both lines to X-rays marginally, the sensitization was prominent for UV regardless of the p53 status of the cells. The activation of a p53 responsible lacZ reporter construct was observed in stably transfected ECA2 cells after X-ray and UV irradiations. Caffeine suppressed the X-ray induced activation of the lacZ reporter, while it drastically enhanced the activation after UV irradiation. X-rays and UV readily triggered the apoptosis of ECA2 cells with the characteristic DNA ladder. Although UV-induced DNA ladder formation was enhanced by caffeine, that induced by X-rays was unaffected. Therefore, the effects of caffeine on the p53-dependent radioresponses were found to be agent specific: suppression for the X-ray induced and augmentation for the UV induced. In contrast to p53-proficient ECA2 cells, smear-like DNA degradation was observed for irradiated p53 delta cells, suggesting the presence of a mode of cell death without DNA ladder formation. UV induction of the smear-like DNA degradation was enhanced in the presence of caffeine. Regardless of the state of the p53 gene, G1/S arrest was not observed in X-ray and UV irradiated EC cells. X-ray induced G2/M arrest in both lines, which was abrogated by caffeine, while G2/M arrest after UV was unaffected by a caffeine treatment. These results indicate that the radioresponses of undifferentiated EC cells differ considerably from those of somatic cells, and that these radioresponses were modulated by a post-irradiation treatment with caffeine.

Animals↗

PubMed1986

Bronchodilator effects of caffeine in coffee. A dose-response study of asthmatic subjects.

Although caffeine is a universal drug and has multiple pharmacologic and physiologic actions in man, there are surprisingly few objective data about its effect on pulmonary function. We conducted a short-term, double-blind, randomized crossover study in nine asthmatic adults who ingested decaffeinated coffee containing varying amounts of added caffeine (mean of 0.2,2.5,5.6, and 7.2 mg/kg of body weight) on different days. The subjects also ingested decaffeinated coffee and aminophylline (200 mg) on a separate day of study. Baseline and post-drug determinations of serum levels of caffeine and theophylline, forced expired volume and flow, specific airway conductance (Gaw/VL), vital signs, and reported symptoms were obtained. Peak increases in serum caffeine concentrations (mean, 12.4 micrograms/ml +/- 1.5 micrograms/ml) occurred 45 minutes following the highest dose of caffeine (7.2 mg/kg), whereas the peak theophylline level (mean 3.8 micrograms/ml +/- 0.4 micrograms/ml) occurred 90 minutes following oral administration of aminophylline (mean theophylline, 2.6 mg/kg). Comparable peak increases in the forced expiratory volume in one second (FEV1), the forced expiratory flow during the middle half of the forced vital capacity (FEF25-75%), and Gaw/VL occurred at 120 minutes following aminophylline and the highest dose of caffeine, indicating that caffeine is an effective bronchodilator but is only 40 percent as active as an equivalent molar dose of theophylline. Regression analysis revealed statistically significant dose-response relationships between peak increases in serum caffeine concentrations and increases in FEV1, FEF25-75%, and Gaw/VL from baseline values. These findings have diagnostic and therapeutic implications regarding the use of caffeine prior to tests of pulmonary function and as a dietary agent, alone or in combination with theophylline.

Administration, Oral↗

PubMedDate not supplied

How many ryanodine binding sites are involved in caffeine induced calcium release from sarcoplasmic reticulum terminal cysternae vesicles?

The inhibition by ryanodine of caffeine induced calcium release from actively loaded heavy sarcoplasmic vesicles has been studied in order to analyse the relation between the occupancy of the vesicular calcium release channels by ryanodine and channel function. Ryanodine binding was monitored with [3H]ryanodine under ionic conditions favouring the establishment of binding equilibrium. Binding follows 1:1 stoichiometry yielding dissociations constants between 7-12 nM and 12-15 pmol ryanodine/mg vesicular protein as maximum number of ryanodine binding sites. When ryanodine labeling was monitored by measuring the decline of the amplitude of caffeine induced calcium release 50% inhibition occurred at a free ryanodine concentration of 1 nM. At this concentration less than 10% of the available ryanodine binding sites are occupied. Caffeine induced calcium release is completely abolished when 3 pmol ryanodine/mg have reacted. A corresponding divergence between ryanodine binding and its effect on caffeine induced calcium release was observed when the initial rate of ryanodine binding was measured either by labeling the vesicles with [3H]ryanodine or by following the decline with time of caffeine induced calcium release. Caffeine induced calcium release declines four times faster than the fraction of unoccupied ryanodine binding sites, k = 4.3 x 10(4) M-1 s-1 versus 1.2 x 10(4) M-1 s-1. The observed interrelation between the occupation of ryanodine binding sites and its effect on caffeine induced calcium release indicates that the caffeine sensitive calcium channel functions as an assembly of at least 4 ryanodine binding sites whereby the occupation of one site suffices to abolish calcium release. The stoichiometric composition appears to be not fixed but might change according to the size of the fraction of ryanodine receptors exhibiting caffeine sensitivity. The reported data were evaluated according to the algorithm derived by H. Asai and M. F. Morales, J. Biol. Chem. 4, 830-838 (1965) for the activity of a macromolecule and the extent of an inhibiting reaction.

Animals↗

PubMed2006

Estrogen prevents neuroprotection by caffeine in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of Parkinson's disease.

Epidemiological studies have strongly linked caffeine consumption with a reduced risk of developing Parkinson's disease (PD) in men. Interestingly, in women, this inverse association is present only in those who have not taken postmenopausal estrogens, suggesting an interaction between the influences of estrogen and caffeine use on the risk of PD. To explore a possible biological basis for this interaction, we systematically investigated how the neuroprotective effect of caffeine is influenced by gender, ovariectomy (OVX), and then exogenous estrogen in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of PD. (1) Caffeine treatment produced a dose-dependent attenuation of MPTP-induced striatal dopamine loss in both young and retired breeder (RB) male, but not female, mice. (2) In female mice (both young and RB), caffeine was less potent or altogether ineffective as a neuroprotectant after sham surgery compared to OVX or after OVX plus estrogen replacement compared to OVX plus placebo treatment. (3) Estrogen treatment also prevented the protection of caffeine against dopamine loss in young male mice. (4) Consistent with the putative protective effect of estrogen, female and OVX plus estrogen mice were relatively resistant to MPTP toxicity compared to male and OVX plus placebo mice, respectively. (5) There was no overall difference in brain levels of caffeine and its metabolites between OVX plus placebo and OVX plus estrogen mice. Together, these results suggest that estrogen can occlude and thereby prevent the neuroprotective effect of caffeine in a model of PD neurodegeneration, supporting a biological basis for the interaction between estrogen and caffeine in modifying the risk of PD.

3,4-Dihydroxyphenylacetic Acid↗

PubMed2003

Caffeine consumption and weekly sleep patterns in US seventh-, eighth-, and ninth-graders.

OBJECTIVE: To survey caffeine use by seventh-, eighth-, and ninth-graders and relate its use to age, sex, sleep characteristics, and day of week METHODS: Students kept a daily, 2-week diary of their sleep times and use of caffeine containing drinks and foods. Data were analyzed by fitted multiple regression models RESULTS: A total of 191 students participated. Caffeine intake ranged between 0 and 800 mg/d. Mean use over 2 weeks ranged up to 379.4 mg/d and averaged 62.7 mg/d (corrected for underrepresentation in our sample of boys, who consumed more caffeine). Higher caffeine intake in general was associated with shorter nocturnal sleep duration, increased wake time after sleep onset, and increased daytime sleep. SLEEP PATTERNS: Mean bedtime was 10:57 PM, and mean wake time was at 7:14 AM. Older children delayed bedtime longer on weekends, and younger ones had longer nightly sleep durations. Sleep duration lengthened on weekends, reflecting the combined effects of the circadian timing system and a mechanism that regulates the duration of sleep. Caffeine (soda) consumption also increased on weekends, for reasons that may be primarily social CONCLUSIONS: Regardless of whether caffeine use disturbed sleep or was consumed to counteract the daytime effect of interrupted sleep, caffeinated beverages had detectable pharmacologic effects. Limitation of the availability of caffeine to teenagers should therefore be considered.

Adolescent↗

PubMed2002

Caffeine induces TP53-independent G(1)-phase arrest and apoptosis in human lung tumor cells in a dose-dependent manner.

Caffeine is a model radiosensitizing agent that is thought to work by abrogating the radiation-induced G(2)-phase checkpoint. In this study, we examined the effect that various concentrations of caffeine had on cell cycle checkpoints and apoptosis in cells of a human lung carcinoma cell line and found that a concentration of 0.5 mM caffeine could abrogate the G(2)-phase arrest normally seen after exposure to ionizing radiation. Surprisingly, at a concentration of 5 mM, caffeine not only induced apoptosis by itself and acted synergistically to enhance radiation-induced apoptosis, but also induced a TP53-independent G(1)-phase arrest. Examination of the molecular mechanisms by which caffeine produced these effects revealed that caffeine had opposing effects on different cyclin-dependent kinases. CDK2 activity was suppressed by caffeine, whereas activity of CDC2 was enhanced by suppressing phosphorylation on Tyr15 and by interfering with 14-3-3 binding to CDC25C. These data indicate that the effect of caffeine on cell cycle checkpoints and apoptosis is dependent on dose and that caffeine acts through differential regulation of cyclin-dependent kinase activity.

Adenocarcinoma↗

PubMed1999

Combined effects of caffeine and prostaglandin E2 on the proliferation of osteoblast-like cells (UMR106-01).

BACKGROUND: The general public widely consumes caffeine (1,3,7-trimethylxanthine), which is contained in various foods, beverages and over-the-counter medications. We have shown previously that caffeine intake could affect bone metabolism in vivo. METHODS: Because prostaglandin E2 (PGE2) is shown to be elevated in the periodontally diseased site, the possible interaction between caffeine and PGE2 was investigated in the present study using UMR106-01 rat osteoblast-like cells in vitro. RESULTS: Although neither 0.1 mM caffeine nor 0.1 microg/ml of PGE2 alone showed any inhibitory effects on cell proliferation, the combination of caffeine and PGE2 showed significant inhibition. However, in order to have inhibitory effects, both caffeine and PGE2 had to be present at least 72 or 96 hours in the medium. Addition of the endogenous PGE2 synthesis inhibitor, indomethacin, showed no effects on cell proliferation. Neither cAMP-inducing agent IBMX (0.01 mM and 0.1 mM) nor forskolin (0.001 mM) inhibited cell proliferation, but combined with PGE2 these agents strongly inhibited proliferation as was observed with the combination of caffeine and PGE2, suggesting possibly that the increase of intracellular cAMP concentration plays an important role in the inhibitory effects of cell proliferation. CONCLUSIONS: The present data for the first time demonstrate the possible implication of routine caffeine intake in the acceleration of pathological conditions of periodontitis. Thus, we propose that chronic caffeine intake is one of the possible risk factors in the advancement of pathology in the periodontitis patient. Further research in this area is warranted.

1-Methyl-3-isobutylxanthine↗

PubMed1998

Caffeine and the elderly.

The most common source of dietary caffeine among the elderly is coffee, with consumption averaging about 200 mg/day. Because of the greater proportion of adipose tissue to lean body mass in older humans, and because caffeine is distributed essentially only through lean body mass, a dose of caffeine expressed as mg/kg total bodyweight may result in a higher plasma and tissue concentration in elderly compared with younger individuals. The metabolism of, and physiological responses to, caffeine is similar in elderly and younger individuals. However, there is a limited amount of evidence that responses to caffeine in some physiological systems may be greater in the elderly at doses in the 200 to 300 mg range. Although caffeine consumption increases urinary calcium levels similarly in both younger and older individuals, the preponderance of data suggest that caffeine has a greater impact on calcium metabolism and bone in older people. Evidence also suggests that increasing age is associated with increasing sensitivity to the pressor effects of caffeine. Caffeine appears to affect metabolic and neurological responses similarly in both young and elderly individuals, when differences in baseline performance are taken into account.

Aged↗

PubMed2001

Caffeine citrate: a review of its use in apnoea of prematurity.

UNLABELLED: Apnoea of prematurity is a common condition in neonates born at less than 37 weeks' gestational age; it affects approximately 90% of premature neonates weighing under 1000 g at birth, and 25% of infants with a birthweight of less than 2500 g. Caffeine, a methylxanthine which occurs naturally in many plants, has been used for over 20 years to treat apnoea of prematurity. In a recent double-blind, placebo-controlled trial, apnoea was eliminated or reduced by at least 50% in significantly more neonates receiving caffeine citrate as first-line treatment than those receiving placebo. In a nonblind trial, caffeine citrate was more effective at reducing apnoeic episodes when compared with neonates receiving no treatment. Caffeine as first-line treatment demonstrated similar efficacy to theophylline or aminophylline (theophylline ethylenediamine) in 4 small randomised studies. Caffeine citrate was generally well tolerated in short term clinical trials, with very few adverse events reported. Caffeine was associated with fewer adverse events than theophylline in randomised trials. No differences in the incidence of individual adverse events were reported between caffeine citrate and placebo in a double-blind, randomised trial. Long term tolerability data are not yet available. CONCLUSIONS: Caffeine citrate was generally well tolerated by neonates in clinical trials and it decreased the incidence of apnoea of prematurity compared with placebo. It has demonstrated similar efficacy to theophylline, but is generally better tolerated and has a wider therapeutic index. Caffeine citrate should, therefore, be considered the drug of choice when pharmacological treatment of apnoea of prematurity is required.

Apnea↗

PubMed1996

Illustrating caffeine's pharmacological and expectancy effects utilizing a balanced placebo design.

Caffeine consumption, a ubiquitous cultural phenomenon with significant health implications may be governed by some of the same principles which affect other drug use [1]. We hypothesized that pharmacological and expectancy effects may be two of those principles. A balanced placebo design was used with 100 male undergraduates to separate caffeine's active drug effects from the expectancy of having consumed caffeine on mood, performance, and physiological measures. The manipulation of expectancies was highly effective on subjects' judgments of caffeine dosage, regardless of actual caffeine content. As predicted, expectancy set and caffeine content appeared equally powerful, and worked additively, to affect subjects' ratings of how much the coffee influenced their mood and performance. Main effects on systolic and diastolic blood pressure, pulse rate, and a fatigue measure were found for caffeine vs. no caffeine groups only. Additional increases in diastolic blood pressure for smokers were noted within the caffeine-receiving conditions. Results are discussed with heuristic and health implications.

Adolescent↗

PubMed2002

Effects of caffeine on performance of low intensity tasks.

31 college age men and women who consume less than three caffeinated beverages per week agreed to participate as subjects in research on the effects of acute caffeine intake on low intensity task performance. All subjects performed two randomly administered test conditions: (1) caffeine (5 mg/kg) and (2) placebo on separate visits following an initial 1-hr. orientation visit. Subjects were administered the beverage 30 min. prior to performing 12 separate tests assessing basic mathematics, simple response, logical reasoning, hand-eye coordination, and spatial and assembly skills. The Spielberger State Anxiety test was administered immediately after consuming the test beverage and once again at posttest. Analysis showed that caffeine did not significantly affect performance on all tests with the exception of the peripheral awareness (hand-eye coordination) test on which performance was higher after ingesting caffeine. The placebo treatment produced no effect on state anxiety, which contrasted with a significant rise in anxiety after caffeine consumption. State anxiety values were significantly greater after caffeine treatment relative to the placebo at pretest, and this difference persisted at posttest. These results demonstrated that the dose of caffeine increased scores on state anxiety for individuals who consumed less than three caffeinated beverages weekly but had very little effect on performance of low intensity tasks, except for a hand-eye coordination test involving peripheral awareness. Perhaps longer continuous performance of more demanding tasks would be more sensitive.

Adult↗

PubMed1980

Influence of caffeine on blood creatine phosphokinase levels in swine.

Eight stress-susceptible and eight normal pigs weighing 35 to 50 kg were studied to determine if caffeine administration would trigger the stress syndrome and affect blood CPK levels. The pigs were littermates of Yorkshire descent. One gram of caffeine (dissolved in 10 ml of saline-sodium benzoate solution) was infused into the pigs through a jugular catheter at a rate of 1.0 ml/min. Blood samples were collected through the catheter before caffeine administration and at specific intervals up to 8 hr after the caffeine administration for the determination of blood creatine phosphokinase levels. The pigs were sacrificed approximately 48 hr after caffeine administration, and M. longissimus pH and reflectance values were obtained 45 min and 24 hr postmortem. Caffeine administration stimulated the development of the signs associated with the porcine stress syndrome in seven of the eight pigs genetically classified as stress-susceptible, and only one control pig exhibited an early sign of the stress syndrome, muscle tremors. Blood CPK levels did not differ significantly between the normal and stress-susceptible groups until visual signs of the stress syndrome were no longer observed (approximately 45 min after caffeine administration). Stress-susceptible pigs had significantly higher blood CPK levels than controls 45 min after the initial caffeine administration. Physical stress received by the pigs during transport and the stress from being held in a new environment resulted in a greater elevation of blood CPK than did the stress administered through the caffeine infusion.

Animals↗

PubMed1988

Prenatal caffeine causes long lasting behavioral and neurochemical changes.

The effects of prenatal exposure to caffeine were studied on later physical development, behavior and brain neurochemistry. Daily doses (150, 300 or 450 mg/L) of caffeine were given to rat dams during the last week of pregnancy. Prenatal caffeine exposure resulted in a number of behavioral and neurochemical changes in the offspring which were long lasting and dose related. The low dose (150 mg/L) of prenatal caffeine caused hyperactivity in an open-field. The high dose of caffeine caused learning disabilities in complex visual and auditory discrimination learning paradigms while simple motor learning or a spatial orientation task were not affected. Both male and female offspring showed some behavioral effects of caffeine exposure. The medium and high doses of caffeine resulted in weight gain that was observable as early as 35 days of age and increased progressively with age. This weight gain was associated with increased food intake. The neurochemical studies carried out at 2-3 months of age revealed an increase in choline uptake in hippocampus, mainly in the animals treated with the lower doses of caffeine and higher protein concentration (microgram/mg wet tissue) in the cortex or hippocampus of offspring exposed to the higher doses of caffeine. At 15 months of age, choline uptake in the frontal cortex was significantly reduced in the animals prenatally exposed to the 300 and 450 mg/L dose.

Animals↗

PubMed1982

Reduction in caffeine toxicity by acetaminophen.

A patient who allegedly consumed 100 tablets of an over-the-counter analgesic containing sodium acetylsalicylate, caffeine, and acetaminophen displayed no significant CNS stimulation despite the presence of 175 micrograms of caffeine per mL of serum. Because salicylates have been reported to augment the stimulatory effects of caffeine on the CNS, attention was focused on the possibility that the presence of acetaminophen (52 micrograms/mL) reduced the CNS toxicity of caffeine. Studies in DBA/2J mice showed that: 1) pretreatment with acetaminophen (100 mg/kg) increased the interval between the administration of caffeine (300 to 450 mg/kg IP) and the onset of fatal convulsions by a factor of about two; and 2) pretreatment with acetaminophen (75 mg/kg) reduced the incidence of audiogenic seizures produced in the presence of caffeine (12.5 to 75 mg/kg IP). The frequency of sound-induced seizures after 12.5 or 25 mg/kg caffeine was reduced from 50 to 5% by acetaminophen. In the absence of caffeine, acetaminophen (up to 300 mg/kg) did not modify the seizures induced by maximal electroshock and did not alter the convulsant dose of pentylenetetrezol in mice (tests performed by the Anticonvulsant Screening Project of NINCDS). Acetaminophen (up to 150 micrograms/mL) did not retard the incorporation of radioactive adenosine into ATP in slices of rat cerebral cortex. Thus the mechanism by which acetaminophen antagonizes the actions of caffeine in the CNS remains unknown.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗

PubMed2006

Beverage caffeine intakes in young children in Canada and the US.

PURPOSE: Throughout childhood there is a shift from predominantly milk-based beverage consumption to other types of beverages, including those containing caffeine. Although a variety of health effects in children and adults have been attributed to caffeine, few data exist on caffeine intake in children aged one to five years. METHODS: Because beverages provide about 80% of total caffeine consumed in children of this age group, beverage consumption patterns and caffeine intakes were evaluated from two beverage marketing surveys: the 2001 Canadian Facts study and the 1999 United States Share of Intake Panel study. RESULTS: Considerably fewer Canadian children than American children consume caffeinated beverages (36% versus 56%); Canadian children consume approximately half the amount of caffeine (7 versus 14 mg/day in American children). Differences were largely because of higher intakes of carbonated soft drinks in the US. CONCLUSIONS: Caffeine intakes from caffeinated beverages remain well within safe levels for consumption by young children.

Beverages↗