Caffeine and Naps as Countermeasures for Sleep Loss

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Insuffi cient sleep impacts nearly every aspect of human physiology including cognition and performance. Health consequences, including increased risk of systemic and neuropsychiatric disorders as well as safety issues involving driving and occupational accidents, have been detailed in several reports, including a recent detailed cost analysis .

Polls conducted by the National Sleep Foundation reveal striking selfreported statistics of sleep-related problems and driving: 60 % of adult drivers reported feeling drowsy while at the wheel and 20 % fell asleep while driving. Impaired performance is a major concern for work productivity from absenteeism, but perhaps more commonly, presenteeism problems. Sleep deprivation can be compared to alcohol consumption in terms of the impairments in performance and reaction time.

In a now classic study, the performance  decrement over 10–26 h of sustained wakefulness was similar to that obtained with alcohol ingestion, such that 17 h of wake was associated with performance impairment similar to that seen with a blood alcohol (BAC) level of 0.05 %, and after 24 h awake the impairment was similar to a 0.1 % BAC.

The goal of introducing countermeasures in those with sleep loss is to promote alertness and thus decrease the risk of sleep loss-related performance impairment. This can be accomplished in several ways, ranging from scheduling systems that facilitate adjustment of the circadian rhythm to atypical work schedules, to systemlevel safeguards designed to warn or prevent error occurrence associated with sleep loss and/ or shift work. At the individual level, three countermeasures have dominated the experimental literature regarding effectiveness for increasing alertness and/or performance: naps, caffeine, and prescription- stimulant use.
Here we review the literature evaluating the utility of caffeine and napping to promote improved objective performance under conditions of sleep deprivation and sleep restriction; stimulant use in sleep medicine has been reviewed recently .

The use of prescription-stimulant therapy is beyond the scope of this chapter and should be considered only in the context of a formal sleep disorders evaluation. Although countermeasures represent important consideration for those with sleepiness, it is important to recognize at the outset that symptoms often associated with sleep loss (sleepiness, fatigue, poor concentration) may be due to a primary sleep disorder or primary medical disorder, as well as insuffi cient sleep opportunity. It is critical in particular to recognize the medical possibilities so as not to mask the underlying problem and delay diagnosis and/or treatment by initiating countermeasures targeting only the symptom, thus allowing the root cause to persist unaddressed.

Overview of Caffeine:Coffee Consumption and Regulation

Caffeine is the most widely consumed psychoactive substance in the world . Among beverage formulations containing caffeine, the three most common types are coffee (71 %), soda (16 %), and tea (12 %)  . Common commercially available caffeine-containing products include soda, chocolate, ice cream, energy drinks, over-thecounter medications, and energy supplements. Natural sources of caffeine include over 60 plant species, the most common of which are coffee beans, tea leaves, kola nut, yerba mate, cacao, and guarana.

The caffeine content of coffee and tea sources varies greatly, and the beverages derived from them may have different caffeine contents depending on the type of plant and growing conditions, as well as the brewing and processing methods. In the USA, regulations by the Food and Drug Administration (FDA) for indicating on the food label the amount of caffeine depend on whether the source is natural (as in coffee beans), or added (as in colas) .

Interested readers are directed to one of many web sites cataloguing the caffeine content of food and beverages . In the USA, nearly 50 % adults drink coffee daily and 80 % of adults consume caffeine in some form. Published FDA analysis indicates that the average amount of caffeine consumed per day among adults over the age of 22 in the US was 300 mg in 2008. The US Army Medical Research and Material Command (USAMRC) recommends caffeine in daily doses <600 mg to improve cognitive performance and alertness among military personnel .

The amount of coffee consumed per capita, however, greatly differs around the world. For example, annual consumption in the US totals 4.2 kg of coffee per person, while in Finland it is 12 kg.

Basic Caffeine Pharmacology

The impact of caffeine on sleep-wake patterns can be understood in the context of current theories of sleep-wake regulation. Many of these theories are based on the two-process model of Borbely and Achermann, which invokes the dual infl uence of circadian rhythms and sleep homeostasis. Recent work implicates adenosine as an important mediator of the sleep homeostatic process, whereby the drive for sleep increases with the duration of preceding time awake and decreases during sleep.

Within this simplifi ed construct, caffeine is postulated to counteract sleep drive associated with the homeostatic buildup of central nervous system adenosine through its actions as an adenosine receptor antagonist . However, experimental evidence does not uniformly support this. For example, basal forebrain lesions in rodents that interrupted the homeostatic buildup of brain adenosine did not alter homeostatic recovery sleep after deprivation, or the behavioral response to an adenosine antagonist. Pharmacological manipulation of adenosine A 1 receptors modulated sleep in rodents in a manner consistent with a role in sleep physiology. However, mice engineered to lack adenosine A 1 receptors showed normal sleep and normal response to deprivation in one study , and a dissociation between impaired EEG-based slow wave activity (a marker of sleep drive) and intact recovery sleep duration after experimental sleep deprivation. Thus, it may be that sleep homeostasis involves adenosine but also depends on other factors.

In vitro studies suggest that caffeine is an antagonist of the A 1 and A 2A adenosine receptors. Adenosine receptors are present in the brain and nonneuronal tissues, which would explain the multisystem impact of caffeine consumption.

Adenosine receptor signaling is itself diverse and serves many central nervous system functions through a variety of second messenger pathways.

Caffeine has “off-target” activity, for example, directly modulating potassium channels, consistent with the increasing general evidence for molecular promiscuity. Adenosine receptors also show promiscuity at the protein assembly level, as the A 1 and A 2A receptors form heteromeric complexes with dopamine D 1 and D 2 receptors . In addition, coffee contains other bioactive compounds and recent studies linking caffeine to lower mortality found similar effects with caffeinated and decaffeinated coffee consumption, although decaffeinated coffee still has some caffeine content. Together with the behavioral sleep experiments above, it is apparent that adenosine signaling, and by inference caffeine’s actions in the adenosine system, are complex and require further elucidation

Caffeine, Absorption, Distribution, Metabolism, Excretion

Caffeine pharmacokinetics is an important topic contributing to inter-individual differences in caffeine bioactivity . Caffeine is readily absorbed after oral intake. In the serum, the protein- binding portion is 36 % in adults and lower in children.

Cerebrospinal fl uid (CSF) levels are similar to serum levels and tissue distribution is similar throughout the body. The main hepatic source of caffeine metabolism is CYP1A2 (which also is weakly inhibited by caffeine), with minor contributions by CYP2C9, CYP2D6, CYP2E1, and CYP3A4. Caffeine and its metabolites, theophylline, theobromine, and paraxanthine, are excreted in the urine. The average time for caffeine to reach peak plasma levels is 30–120 min and the elimination half-life is 4–5 h. The formulation (e.g., immediate versus sustained release) also impacts pharmacokinetics.

Clearance rate is increased by >50 % in smokers. The half-life of caffeine nearly triples during pregnancy and doubles in those taking oral contraceptives possibly attributed to estradiol/progesterone effects on the CYP1A enzymes. Fetal risks of caffeine are not likely to occur at routine consumption levels, but caffeine does cross the placenta and caffeine has a level C pregnancy risk classifi cation. Although caffeine binds to the fat in breast milk, according to the American Academy of Pediatrics, caffeine is not associated with risk at levels of 1–2 cups of coffee per day while breastfeeding

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