Sleep Medicine Reviews (2008) 12, 153–162 aSleep Disorders and Research Center, Henry Ford Hospital, 2799 W Grand Blvd, CFP-3, Detroit,MI 48202, USAbDepartment of Psychiatry and Behavioral Neuroscience, School of Medicine, Wayne State University,Detroit, MI, USA Caffeine is one of the most widely consumed psychoactive substances and it has profound effects on sleep and wake function. Laboratory studies have documented its sleep-disruptive effects. It clearly enhances alertness and performance in studies with explicit sleep deprivation, restriction, or circadian sleep schedule reversals. But, under conditions of habitual sleep the evidence indicates that caffeine, rather then enhancing performance, is merely restoringperformance degraded by sleepiness. The sleepiness and degraded function may bedue to basal sleep insufficiency, circadian sleep schedule reversals, reboundsleepiness, and/or a withdrawal syndrome after the acute, over-night, caffeinediscontinuation typical of most studies. Studies have shown that caffeinedependence develops at relatively low daily doses and after short periods of regulardaily use. Large sample and population-based studies indicate that regular dailydietary caffeine intake is associated with disturbed sleep and associated daytimesleepiness. Further, children and adolescents, while reporting lower daily, weight-corrected caffeine intake, similarly experience sleep disturbance and daytimesleepiness associated with their caffeine use. The risks to sleep and alertness ofregular caffeine use are greatly underestimated by both the general population andphysicians.
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coca, candy bars, and soft drinks. It also is aningredient in various over-the-counter drugs (OTCs) Caffeine is one of the most commonly consumed including headache, cold, allergy, pain relief, and psychoactive substances in the world. It is available alerting drugs. The caffeine content of some of the in a variety of dietary sources such as coffee, tea, various beverages, foods, and OTCs is provided in. The table is not to be consideredexhaustive. The caffeine content of foods, com- ÃCorresponding author. Sleep Disorders and Research Center, mercially prepared beverages, and OTCs is constant Henry Ford Hospital, 2799 W Grand Blvd, CFP-3, Detroit, and documented, but the caffeine content of MI 48202, USA. Tel./fax: +1 313 916 5177.
brewed beverages can vary depending on the bean 1087-0792/$ - see front matter & 2007 Elsevier Ltd. All rights reserved.
doi: pharmacology of caffeine and the well-documented Caffeine content of drinks and foods.
sleep disruptive effects of caffeine and studies suggesting that caffeine’s performance-enhancingeffects are for the most part restoring performance degraded by sleepiness, this review will evaluate the degree to which caffeine dependence interacts with its sleep–wake effects. Finally, evidence from population-based studies on the role of daily dietary caffeine in disturbed sleep and impaired daytime function will be assessed and the risks ofcaffeine associated sleep disruption and daytime sleepiness in children and adolescents will be Orally ingested caffeine is absorbed rapidly, reach- estimated that 80% of plasma caffeine levels arepresent in human brain, based on animal studies that have compared plasma to brain concentra- tion.Caffeine is metabolized to paraxanthine (80%) and to theobromine and theophylline (16%).
With higher caffeine doses, and the repeated consumption typical of regular caffeine users, the plasma levels of paraxanthine accumulate and this paraxanthine accumulation reduces caffeine clear- ance. Paraxanthine shares many of the effects of caffeine and consequently regular caffeine con-sumption leads to both accumulated caffeine andparaxanthine levels, both of which are biologically used and the method of brewing. This variability active. The half-life of single dose caffeine is 3–7 h, requires that investigators estimate the caffeine but with higher levels of intake the duration of content of brewed beverages when assessing self- action is extended, likely due to the accumulated reported caffeine consumption and introduces paraxanthine and retarded caffeine clearance.
error variance when relating caffeine doses to any Caffeine’s primary mode of action is adenosine receptor blockade. The A1 and A2A adenosine Caffeine’s effects on laboratory assessed sleep in receptors are those primarily involved in caffeine’s double-blind placebo controlled studies have been central effects. A1 receptors are distributed widely well documented. Laboratory studies have also throughout the brain including hippocampus, cere- documented its alerting and performance-enhan- bral and cerebellar cortex, and thalamus, while A2A cing effects. However, the extent to which regular receptors are located in striatum, nucleus accum- dietary caffeine intake affects sleep and daytime bens and olfactory tubercle. Adenosine receptors function in the population is not fully known. Such are also present in blood vessels, kidneys, heart information is important since there is evidence and the GI tract. Adenosine decreases neural firing suggesting the use of caffeine in society is expand- rate and inhibits most neurotransmitter release.
ing, both in terms of increased daily dosages and The mechanism(s) by which adenosine inhibits earlier ages for the initiation of regular daily neurotransmitter release have not been resolved.
The putative role of adenosine in sleep homeostasis To understand the effects of caffeine and its discontinuation on sleep and daytime alertness and postulated mechanism for adenosine’s role in sleep its tolerance and dependence liability we will first homeostasis is inhibition of cholinergic neurons in review its pharmacology. After reviewing the the basal forebrain which normally produce arousal.
Thus, adenosine promotes sleep and caffeine regarding dietary caffeine intake and cardiovascu- blocks adenosine’s sleep promoting effects.
lar health.Peripheral pressor responses to caf- The extent of tolerance development to caf- feine were assessed in the cortisol study cited feine’s effects is controversial and not clearly above using the same caffeine administration methodologyCaffeine elevated blood pressure due to methodological limitations. Studies compare relative to placebo and the blood pressure response caffeine naı¨ve to habitual caffeine consumers, or was not abolished after 5 days of 600 mg daily. The habitual consumers before and after caffeine sympathetic nervous system has an important role abstinence. Given that 80% or more of the popula- in regulating blood pressure. A study assessed tion report regular use of caffeine, non-caffeine sympathetic nerve activity and blood pressure in consumers are a very self-selected, atypical sub- habitual and non-habitual caffeine drinkers.Re- population. Response differences may merely re- lative to placebo, caffeine (250 mg) increased flect genetic or other trait differences between blood pressure in the non-habitual drinkers, but non-caffeine and habitual consumers, or an atypi- not the habitual drinkers. In contrast, sympathetic cal response to caffeine that led to the non- system activity was similarly increased in both consumer’s caffeine avoidance. Very few studies groups. Importantly, plasma caffeine concentra- have directly administered caffeine repeatedly tions did not differ between the two groups. Thus, with parallel placebo controls. The available data tolerance to the peripheral effects of caffeine may do suggest that caffeine tolerance development is be differential, depending on the response system partial and may differ with regard to caffeine’s assessed, but appears to be less consistent than the As to central effects, a study measured human brain metabolic response to caffeine using rapidproton echo-planar spectroscopic imaging in reg-ular caffeine useBrain lactate during 1 h following caffeine (10 mg/kg) was elevated in caffeine naive relative to regular caffeine users.
In the regular caffeine users after a 4–8 weeks A number of polysomnographic studies have as- abstinence, caffeine re-exposure raised brain lac- sessed the sleep effects of caffeine administered tate to a level similar to that of the caffeine naı¨ve within 1 h of sleep. An early study administered subjects. A study of caffeine (400 mg administered 0, 1.1, 2.3, or 4.6 mg/kg (77–322 mg for a 70 kg three times a day) effects on nocturnal sleep and person) caffeine 30 min before sleep to healthy daytime alertness attempted to model the physio- normals with a reported average daily 3-cup logical arousal of chronic insomnia in healthy caffeine consumption history.Caffeine reduced normals.The caffeine was administered for 7 days total sleep time, increased latency to sleep, and and over the 7 days partial tolerance to the sleep reduced percent stage 3–4 sleep in a dose-related disruptive and daytime alerting effects of caffeine was observed. It is possible that more clearly In a study of the hypnotic effects of temazepam, defined pharmacological tolerance occurred, but methylphenidate (10 mg) and caffeine (150 mg) that was offset by the increase in homeostatic drive were used to model insomnTo establish the resulting from the nightly sleep disruption. The insomnia model, healthy young adults with an hypothalamic-pituitary-adrenocortical axis (HPA) is unspecified caffeine history received each drug activated by caffeine administration and cortisol alone 30 min before sleep. Compared to placebo secretion has been used to mark this HPA activa- both drugs prolonged sleep onset and reduced total tion. Salivary cortisol response to a caffeine sleep time, but did not affect sleep stages.
challenge (250 mg) was assessed before and after Caffeine 150 mg had a greater effect on sleep 5 days of 0, 300, or 600 mg daily caffeOn day 1 latency and total sleep time than methylphenidate relative to placebo cortisol was elevated in a dose- related manner. By day 5 partial tolerance devel- Another study of young adults (21–31 yr) with an oped in the daily 300 mg group and complete unspecified caffeine drinking history compared the tolerance in the daily 600 mg group. Thus, most of effects of 000, 100, 200, and 300 mg of caffeine the evidence suggests either complete or partial taken at ‘‘lights-out’’.In a dose-related manner tolerance to caffeine’s central effects.
all caffeine doses reduced total sleep time and The peripheral effects of caffeine and possible percentage of stage 3+4 sleep. Sleep onset was not tolerance development to its peripheral effects affected, probably because of the ‘‘lights-out’’ have received more attention because of concerns drug administration used in the study and caffeine’s 30–70 min time to plasma peak. In a second stimulants, and are consistent with its mechanism study, done with the same participants, the sleep of action, adenosine blockade. Stage 3–4 sleep is effects of caffeine 300 mg were compared to decreased and EEG slow wave activity is suppressed methylphenidate 10 and 20 mg and pemoline 20 by caffeine. In contrast, the psychomotor stimu- lants are more likely to suppress REM sleep.
methylphenidate and pemoline reduced total sleeptime relative to placebo, with no differences intotal sleep time among the drugs. Sleep onsetand percent stage 3+4 sleep were not affected by any of the drugs. The high dose of methylphe- nidate prolonged REM latency and reduced REMpercent, which was not found with caffeine or Laboratory studies of the effects of caffeine on performance and mood have a long history dating A study attempting to model the physiological to the late nineteenth century. The acknowledged arousal of insomnia in healthy young men adminis- first placebo controlled study was published in tered 400 mg caffeine three times a day (800, 1600, 1907.The investigators reported that 500 mg and 2300 h) for 7 consecutive days.Relative to caffeine improved finger muscle strength. The baseline, total sleep time was reduced and sleep classic review article of Weis and Laties summar- latency was increased. The percentage of stage 4 ized the pre-1960s literature and concluded that sleep was reduced, but the percentage and latency the evidence clearly indicates that caffeine en- of REM sleep was not affected. As cited above, this hances a wide range of performance with the study showed partial tolerance development over exception of ‘‘intellectual’’ Weis and Laties then raised the critical question whether caffeine is Given adenosine’s putative role in sleep home- actually producing superior performance or merely ostasis several studies have assessed EEG slow wave restoring performance ‘‘degraded by fatigue, bore- activity during sleep after caffeine administration.
Caffeine (100 mg) or placebo was administered to The post-1960s literature provides additional young men with a caffeine drinking history of 1–3 information regarding the two issues raised by cups daily.Caffeine or placebo was administered Weis and Laties: does caffeine affect ‘‘intellec- at bedtime and relative to placebo it prolonged tual’’ performance and does caffeine restore or sleep latency and reduced sleep efficiency and improve performance. First, as to whether ‘‘in- visually scored stage 4 sleep. EEG spectral power tellectual’’ performance is improved, Weis and density in the 0.75–4.5 Hz band was reduced.
Laties were probably referring to what is currently Salivary caffeine was 7.5 mmol/l and declined to described as cognitive performance, which includes 3.5 mmol/l by the seventh hour of sleep. A parallel various types of memory and problem solving study administered placebo or caffeine 200 mg at performance. A recent review of the effects of 0700 h and assessed its effect on the subsequent caffeine on human behavior included a review of night of sleep (2300–0700 Immediately prior to the effects of caffeine on cognitive performanc sleep at 2300 h salivary caffeine levels were The literature supporting a positive effect of 3.1 mmol/l and relative to placebo sleep efficiency caffeine on complex cognitive processes is not as was reduced and EEG spectral power density in the strong as that for attention and psychomotor 0.75–4.5 Hz band was suppressed. As degree of performance. Methodological issues, discussed in sleep fragmentation was not quantified in any of more detail below, may explain some of the negative these studies it is difficult to determine if the results. Without completely reviewing this litera- decrease in stage 3–4 sleep and slow wave activity ture, several illustrative studies can be cited.
is a direct pharmacological effect as seen with A recent study in non-consumers and habitual drugs like the benzodiazepines, or is secondary to consumers, reporting 218 mg per day on average, the sleep disruptive effects of caffeine as seen in administered 0, 75, and 150 mg caffeine.In addition to improving attention and reaction time In summary, the sleep disruptive effects of performance, the caffeine also improved numeric caffeine, even at doses equivalent to a single working memory and sentence verification accu- cup of coffee, have been well documented.
racy performance. The magnitude of caffeine- Both sleep onset (i.e., when taken early enough associated improvements did not differ between before sleep to allow adequate absorption) and consumers and non-consumers. Another study sleep time are adversely affected. The sleep stage administered a larger caffeine dose (4 mg/kg– effects are unique, when compared to other 280 mg for a 70 kg participant) to young adults with an unspecified caffeine drinking history.Caffeine population-based study (n ¼ 259) of adults aged improved performance on semantic memory, logi- 21–65 yr, 15% of the sample had a daily average cal reasoning, free recall and recognition recall sleep latency of 6 min or less and 20% had an performance. In summary, while there are a Epworth Sleepiness Scale score of 11 or greater, a number of negative studies, studies with positive score generally considered pathological.A effects of caffeine on complex cognitive function complete caffeine intake history was not done in are available. Negative studies have to be cau- this study and a daily caffeine intake is not tiously interpreted because of the various metho- available for these participants. A study compared the psychomotor performance of sleepy young The second issue raised by Weis and Laties is adults, defined as a MSLT of 6 min or less, with whether caffeine is restoring or improving perfor- their alert counterparts, defined as a MSLT of 16 min mance. There is no question that caffeine acutely or greater, who did not differ in daily caffeine restores performance and mood under explicit intake (i.e., p200 The sleepy individuals conditions of sleep restriction, sleep deprivation, showed degraded performance relative to the alert and sleep phase reversals as seen in shift work, individuals. Finally, an extended bedtime of 10 h where prior performance impairment is clear. The nightly for 6 consecutive nights improved the literature assessing the use of stimulants, including performance of the sleepy individIn fact, caffeine, to improve performance during periods even 8 h in bed across several nights produced of extended wakefulness was recently reviewed an increase in alertness in healthy volunteers, who by a Task Force of the American Academy of Sleep Medicine.Similarly, a large number of the evidence suggests that in the typical caffeine laboratory and field studies have documented study there could be increased sleepiness (i.e.
performance impairment associated with night reduced alertness) and degraded performance work and have shown that caffeine can minimize among ‘‘normal volunteer’’ study participants.
the performance impairment that is associated The increased sleepiness and degraded perfor- mance in such individuals is likely due to a chronic But, what of performance under conditions of sleep insufficiency relative to that individual’s habitual sleep without explicit sleep loss or circadian disruption? Is there evidence that there Other important considerations are the time-of- is fatigue and degraded performance in the typical day and the homeostatic sleep load (i.e., the level caffeine study of normal healthy volunteers? And if of sleepiness) at which the caffeine is administered so, what is the cause of the sleepiness and and its effect assessed. Under conditions of degraded performance? Identification of the prob- habitual sleep, a circadian rhythm of sleepiness able causal factor(s) is necessary to determine has been described with increased sleepiness over whether or not performance is degraded. The the midday as the homeostatic sleep drive has factors that might be considered and discussed increased as a function of the accumulated time are: (1) a high rate of basal sleepiness in the typical awake. Studies have found that the sedative study participants (i.e., young adults specifically effects of alcohol differ as a function of time-of- and the general population more broadly), (2) a day and under differing basal levels of sleepiness at rebound sleepiness following acute discontinuation the same time-of-day; the effects are greater with of caffeine as required in most studies, and/or (3) a greater sleepiness and over the midday than in the withdrawal syndrome associated with caffeine evening. The same may be the case with the alerting effects of caffeine (i.e. they are clearly A high rate of basal sleepiness, and potentially present over the midday, but less so in the degraded performance, in the typical study parti- cipants is an important consideration. An early It is unlikely that basal sleepiness alone explains study assessed the level of sleepiness in a large degraded performance in studies of caffeine’s sample (n ¼ 129) of young adult volunteers for performance enhancing effects. In the large sample studies of the effects of caffeine, alcohol, and studies cited above approximately 20% of the benzodiazepines.These volunteers reported an sample had excessive sleepiness. The latter two average 7.2 h of nightly sleep, no daytime sleepi- factors mentioned above, rebound sleepiness and/ ness, and habitual daily caffeine intake of 200 mg or a withdrawal syndrome, appearing as a result or less. Yet 20% of these young adults had a daily of the caffeine discontinuation required in almost average sleep latency on the Multiple Sleep all caffeine studies, must be discussed. These Latency Test (MSLT) of 6 min or less, which is two factors suggest the possibility of caffeine considered a pathological level of sleepiness. In a drowsiness-sleepiness, decreased contentedness,depressed mood, difficulty concentrating, irritabil- Caffeine dependence is evident by the signs of ity, and fogginess. In addition, flu-like symptoms, behavioral and physiological dependence.These nausea and vomiting, and painful joints and two dependences often co-exist, but can be stiffness were also considered as probable valid differentiated. Physiological dependence is a state symptom classes. While this review did not differ- induced by repeated drug use that results in a entiate rebound sleepiness (i.e., an isolated symp- withdrawal syndrome when the drug is discontin- tom) from a withdrawal syndrome, drowsiness- ued or an antagonist is administered. Among sleepiness was found in 78% of studies, second only discontinuation effects, withdrawal should be to headache. The symptoms appeared after 12–24 h differentiated from rebound phenomenon. With- of abstinence and after as little as 100 mg of drawal is a collection of signs and symptoms that differs from rebound phenomenon in that there are As to whether degraded performance is asso- multiple signs and symptoms and the signs and ciated with the caffeine discontinuation, the symptoms are new, not present prior to drug standard practice in most placebo controlled administration. Rebound is the expression of a caffeine studies is to require discontinuation of single sign or symptom that is the reverse of the caffeine use the evening prior to entrance to the drug effect (i.e., for caffeine, rebound sleepiness) laboratory and the next-day caffeine or placebo and with intensity beyond the basal state. Rebound administration. Given the half-life of caffeine (i.e., can occur after single administrations of high drug 3–7 h) and the previously cited time-course for the doses, while withdrawal typically requires re- appearance of withdrawal symptoms (12–24 h), in peated drug administration and can occur with most studies that employ an over-night abstinence moderate or low drug doses.Behavioral depen- placebo or caffeine is being administered in the dence is a pattern of behavior characterized by midst of a potential withdrawal or at the very least repetitive and compulsive drug seeking and con- a rebound sleepiness. It has been argued by James sumption. The drug acts as a reinforcer either by and Rogers that caffeine’s effects on performance reversing an ‘‘aversive’’ state or producing a ‘‘positive’’ state. Behavioral dependence can be James and Rogers argue that the most definitive studied by assessing the likelihood of self-adminis- method to assess caffeine effects is to require a tering the drug and concurrently measuring its prior long-term abstinence before assessment.To make their point, they compared placebo con- What then is the evidence for rebound sleepiness trolled caffeine effects after a long-term absti- and withdrawal during caffeine discontinuation, for sleepiness/withdrawal associated degraded abstinence.The young adult study participants performance, and then for continued caffeine reported 400 mg daily caffeine intake on average.
self-administration to reverse the sleepiness and Relative to the long-term abstinence, the overnight performance impairment? A critical review of the abstinence was associated with degraded perfor- literature regarding caffeine withdrawal was re- mance including cognitive performance. Caffeine cently conducted.A total of 57 experimental and in a 1.2 mg/kg dose improved performance relative 9 survey studies could be identified. The experi- to placebo in the overnight abstinence condition mental studies were conducted as double-blind only. After the chronic abstinence no performance placebo controlled studies. To assess the presence enhancement was found. Therefore, the Weiss and and nature of the various withdrawal symptoms, Laties hypothesis that performance is impaired the studies employed several common methodolo- during caffeine discontinuation due to withdrawal gies and comparisons including: (1) acute absti- related sleepiness and that caffeine restores the nence versus preceding caffeine baseline, (2) acute performance impairment is directly supported by abstinence versus caffeine, (3) acute abstinence in caffeine consumers versus non-consumers, or (4) The final question raised is whether reversal of caffeine withdrawal or rebound sleepiness en- The symptoms and signs that were reported in hances the likelihood of self-administering caf- the comparisons (i.e., acute abstinence versus feine. Early caffeine self-administration studies preceding caffeine baseline) of the 57 studies were reported that 25–50% of participants reliably self- then classified and a given class was considered as administered caffeThese studies suggested valid if it appeared in six or more studies. The that caffeine functioned as a reinforcer for some symptom classes considered valid were headache, individuals, but not others. The variable suggested fatigue, decreased energy, decreased alertness, to explain these individual differences was caffeine withdrawal. A study examined caffeine’s with- 280 mg for a 70 kg person) caffeine per day from all drawal effects in moderate caffeine consumers (379 mg/day on average) and assessed choice Using the values of 85 mg/5 oz cup of coffee, between money and capsules that contained 40 mg/5 oz cup of tea, and 40 mg/12 oz cup of soda, a survey of caffeine intake in Vermont reported caffeine rather than $0.38 on caffeine days, but that 83% of respondents currently used one or more forfeited $2.51 to avoid the capsule on placebo caffeinated beverages weekly and the average days, suggesting that avoidance of withdrawal daily intake was 186 Forty-one percent of promotes caffeine choices. The implication of this respondents had stopped use of at least one type of study is that the primary reinforcing function of beverage and 14% stopped all caffeine use.
caffeine is reversal of a negative state rather than Insomnia was among the health concerns leading the production of a positive state. A final study in to cessation or reduction of use. A survey of a this series of studies directly manipulated caffeine Southern California community found that among lifetime coffee-drinkers, women were more likely (300 mg/70 kg per day) and placebo in counter- to curtail caffeine use than men and did so because balanced study phases of 9–12 days. After the of sleep problems.A recent survey of seven caffeine phase they chose caffeine two times as European countries evaluated factors contributing frequently as after the placebo phase. These to reports of nonrestorative sleep.Daily caffeine studies suggest that caffeine functions as a nega- intake contributed to nonrestorative sleep as a tive reinforcer by reversing caffeine withdrawal. It bivariate, but not an independent predictor. How- should be noted that these effects were seen in ever, the assessment of caffeine intake in this moderate caffeine consumers with a daily caffeine survey merely consisted of a yes/no response to a intake similar to the mean intake seen in popula- question regarding daily use of caffeine. Yet, these tion-based studies as reviewed below.
limited data suggest that in the general population The major problem with all of the laboratory sleep problems are associated with caffeine use.
studies of caffeine and caffeine discontinuation is However it is important to remember that the that the study participants are volunteers. Caffeine relation can be bi-directional. Disturbed sleep study volunteers may represent a highly select leads to sleepiness and hence increased caffeine sample of individuals who have various biases and consumption. Similarly, as previously discussed expectancies regarding caffeine effects relative to caffeine consumption can, as well, lead to dis- their own level of daily caffeine intake. The critical turbed sleep. Thus, it is not difficult to imagine that question is whether in the general population daily in some individuals this can be a vicious circle dietary caffeine intake is associated with nocturnal leading to elevated caffeine consumption.
sleep and/or daytime sleepiness problems.
Several population-based studies have also sug- gested that high caffeine use is associated withdaytime sleepiness. A representative sample of theBritish population assessed daytime sleepiness and Dietary caffeine in the population: sleep associated factors.Those with the most severe sleepiness, meaning daily sleepiness for a month orgreater, reported high daily caffeine consumption Accurate survey data on caffeine consumption in defined as 7 or more cups of tea or coffee per day.
the general population are difficult to collect due The prevalence of severe sleepiness was 5.9% in to the variety of caffeine sources and the varia- moderate caffeine users, while it was 10.6% in the bility of caffeine content in various beverages.
high caffeine consumers. A questionnaire and A survey of the caffeine content reported by diary-based study assessed sleep habits and caf- various authors found a range of 64–124 mg feine use of workers in the French National Gas and reported in a 150 ml (5 oz) cup of brewed coffe Electricity Company.Time-in-bed was associated This variability is a problem in attempting to with caffeine use such that, as caffeine use associate caffeine consumption with indices of increased time-in-bed decreased. The association sleep and daytime alertness and requires that suggests caffeine is shortening sleep and/or is being investigators assign a caffeine content value to a used to counter the sleepiness associated with reported cup of coffee. The value suggested by short time-in-bed. The latter explanation is the Barone and Roberts is 85 mg per 150 ml for brewed more likely since caffeine use was not associated coffee and they also provided values for other Sleep problems and sleepiness associated with adults in the US daily consumed 4 mg/kg (i.e., caffeine use is also found in children and adolescents as reported in multiple studies. Several surveys found among some children. Even at the lower from the 1980s reported children and adolescents, caffeine daily intake levels, and without clear aged 5–18 yr, consumed 37 mg or 0.9 mg/kg caf- indications of dependence, an association of sleep feine daily.The majority of the caffeine intake disturbance and daytime sleepiness with caffeine was derived from soda, chocolate, and tea and between 75% and 98% of respondents consumedcaffeine. Caffeine intake in children and adoles- cents was estimated to be about 1.0 mg/kg daily inSome smaller sample studies of teenagers 1. Assessment of patients’ caffeine intake have reported much higher daily caffeine intakes and have found caffeine dependence, defined as the observation of withdrawal signs and symptoms 26–40% of participants showing dependence, daily 2. Regular use of even low caffeine doses can caffeine intake was 2.4–3.2 mg/kg. Among the more common withdrawal signs in these teenagers 3. Sleepiness is a common discontinuation The US National Institute of Child Health and effect of caffeine and could be a factor in Human Development conducted a US survey in 1998 of children in grades 6–10.Sixty-eight percent drank one or more soda or coffee drinks per day.
4. Caffeine use should be considered in asses- After adjusting for socio-demographic factors those sing sleep disturbance or daytime sleepi- reporting high caffeine intake were 1.9 times more likely to report difficulty sleeping and 1.8 5. Persistent caffeine use and inability to times more likely to be tired in the morning.
Two-week sleep diaries were collected in a large sample of 7–9 grade students from Columbus, gradual reduction of caffeine intake.
6. Discontinuation of caffeine within a day or consumed daily and 20% of the sample averaged contributing factor in patients complaining study did not correct for body weight and thus these data cannot be compared to the earlierstudies. The data clearly show high caffeine intakewas associated with increased wakefulness duringthe sleep period and with a shortened bedtime.
The authors speculate that the caffeine is being used to counter sleepiness associated with the 1. Further study of the disruptive effects of shortened sleep and bedtime. A survey of Italian high school students specifically assessed daytime alertness in the population is important.
sleepiness and found high use of caffeine was 2. Further study of the extent of sleep and associated with increased daytime sleepiness.
daytime alertness problems associated with However, the association was only found in evening caffeine use in children and adolescents is types, as defined by the Morningness–Eveningness scale adapted for children.In other studies it has 3. Studies determining the degree to which been shown that evening types sleep less than sleep restriction or restriction of time in To summarize, population and large sample 4. Further studies are needed to determine studies find an association between daily dietary caffeine intake and sleep problems and daytime sleepiness. The levels of daily caffeine intake in adult population studies are comparable to the 5. Studies investigating the alerting-perfor- caffeine doses administered in laboratory studies showing caffeine is disruptive of sleep. In children differing basal levels of sleepiness–alert- and adolescents the levels of caffeine intake, ness, ranging from a sleep satiated state to corrected for body weight, are lower than that during sleep loss: a review by the sleep deprivation andstimulant task force of the American Academy of SleepMedicine. Sleep 2005;28:1163–87.
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In the tribunal of the pension funds adjudicator

IN THE TRIBUNAL OF THE PENSION FUNDS ADJUDICATOR PRELIMINARY RULING IN TERMS OF SECTION 30J OF THE PENSION FUNDS ACT OF 1956 This is a complaint lodged with the Pension Funds Adjudicator in terms ofsection 30A of the Pension Funds Act relating to the fund’s refusal to admit thecomplainant’s claim for a disability benefit. No hearings were conducted andtherefore in determining this mat


Abstracts of the 3rd International Congress on Prediabetes and the Metabolic Syndrome DETERMINATION OF BODY COMPOSITION IN PATIENTS min PG (r=0.7), indicating an inverse relationship between prevailing PG WITH METABOLIC SYNDROME, BY BIO-IMPEDANCE and the presence of edema. Therefore, paradoxically, the risk of BC-L appears to be inversely related to the patients' measured insulin sensitivity.

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