Caffeine is the most widely consumed behaviorally active substance in the world. Almost all caffeine comes from dietary sources (beverages and food), most of it from coffee and tea. Acute and, especially, chronic caffeine intake appear to have only minor negative consequences on health. For this

Actions of Caffeine in the Brain with Special Reference to Factors That Contribute to Its Widespread Use

International classification of sleep disorders-third edition: highlights and modifications.

Human behavior shows large interindividual variation in temporal organization. Extreme "larks" wake up when extreme "owls" fall asleep. These chronotypes are attributed to differences in the circadian clock, and in animals, the genetic basis of similar phenotypic differences is well established. To better understand the genetic basis of temporal organization in humans, the authors developed a questionnaire to document individual sleep times, self-reported light exposure, and self-assessed chronotype, considering work and free days separately. This report summarizes the results of 500 questionnaires completed inapilotstudy.Individualsleeptimesshowlargedifferencesbetweenworkand freedays,exceptforextremeearlytypes.Duringtheworkweek,latechronotypes

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Life between clocks: daily temporal patterns of human chronotypes.

Sleep function and synaptic homeostasis.

Deficits in daytime performance due to sleep loss are experienced universally and associated with a significant social, financial, and human cost. Microsleeps, sleep attacks, and lapses in cognition increase with sleep loss as a function of state instability. Sleep deprivation studies repeatedly show a variable (negative) impact on mood, cognitive performance, and motor function due to an increasing sleep propensity and destabilization of the wake state. Specific neurocognitive domains including executive attention, working memory, and divergent higher cognitive functions are particularly vulnerable to sleep loss. In humans, functional metabolic and neurophysiological studies demonstrate that neural systems involved in executive function (i.e., prefrontal cortex) are more susceptible to sleep deprivation in some individuals than others. Recent chronic partial sleep deprivation experiments, which more closely replicate sleep loss in society, demonstrate that profound neurocognitive deficits accumulate over time in the face of subjective adaptation to the sensation of sleepiness. Sleep deprivation associated with disease-related sleep fragmentation (i.e., sleep apnea and restless legs syndrome) also results in neurocognitive performance decrements similar to those seen in sleep restriction studies. Performance deficits associated with sleep disorders are often viewed as a simple function of disease severity; however, recent experiments suggest that individual vulnerability to sleep loss may play a more critical role than previously thought.

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Neurocognitive Consequences of Sleep Deprivation

Hyperarousal and insomnia: state of the science.

Groups of 10 objectively defined insomniacs and age-, sex- and weight-matched normal sleepers were evaluated on sleep, performance, mood, personality and metabolic measures over a 36-hour sleep laboratory stay. Insomniacs were defined to have increased wake time during the night but also had decreased stage 2 and rapid eye movement sleep. As expected insomniacs reported increased confusion, tension and depression and decreased vigor on the profile of mood states mood scale throughout the evaluation period as compared to the normals. Insomniacs also had decreased memory ability on the short-term memory test and the MAST. These performance and mood differences were not secondary to sleepiness because the insomniacs also had significantly increased multiple sleep latency test (MSLT) values throughout the evaluation period. In conjunction with the consistent mood, performance and MSLT differences during the day and the sleep differences at night, whole body VO2, measured at intervals across the day and throughout one night of sleep, was consistently elevated at all measurement points in the insomniacs as compared to the normals. The nocturnal increase in metabolic rate remained even after metabolic values from periods during the night containing wake time or arousals were eliminated from the data set. It was concluded that patients who report chronic insomnia may suffer from a more general disorder of hyperarousal (as measured here by a 24-hour increase in metabolic rate) that may be responsible for both the daytime symptoms and the nocturnal poor sleep. Future studies need to explore 24-hour insomnia treatment strategies that decrease hyperarousal.

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24-Hour metabolic rate in insomniacs and matched normal sleepers.

Summary: Data from recent laboratory studies indicate that nocturnal sleep periods reduced by as little as 1.3 to 1.5 hours for 1 night result in reduction of daytime alertness by as much as 32% as measured by the Multiple Sleep Latency Test (MSLT). Other data document that 1) 170/0--57% of normal young adults have MSLT latencies of ::;5.5 minutes, whereas ::;50% have MSLT values of ~ 10 minutes and 2) 28°/0--29% of young adults reported normally sleeping ::;6.5 hours on each weeknight. More extensive reduction of daily sleep amount is seen in night­ shift workers. A minimum of 2%-4% of middle-aged adults have hypersomnolence associated with sleep apnea. Together, these data show that significant sleep loss exists in one-third or more of normal adults, that the effects are large and replicable and that similar effects can be produced in just I night in the laboratory. In light of the magnitude of this sleep debt, it is not surprising that fatigue is a factor in 57% of accidents leading to the death of a truck driver and in 10% of fatal car accidents and results in costs of up to 56 billion dollars per year. A recent sleep extension study suggests that the average underlying sleep tendency in young adults is about 8.5 hours per night. By comparison, the average reported sleep length of 7.2-7.4 hours is deficient, and common sleep lengths of ::;6.5 hours can be disastrous. We must recognize the alertness function of sleep and the increasing consequences of sleepiness with the same vigor that we have come to recognize the societal impact of alcohol. Key Words: Sleep deprivation-Sleepiness-Sleep disorders- Work schedule tolerance. Weare in the midst of a golden age of discovery of the intricate interrelationship between our nocturnal sleep process and our level of daytime function. Fueled by the discovery of the tremendous incidence of sleep apnea and periodic leg movements in the population, the relationship between fragmented sleep and residual sleepiness, as well as the increased ability to measure the level of objective sleepiness with an objective test [the Multiple Sleep Latency Test (MSLT)] and in am­ bulatory environments, the pervasive role of excessive sleepiness in our society is becoming apparent. Much literature documents the negative effects of sleep deprivation on a wide range of psychomotor per­ formance tasks and mood variables. For the sake of simplicity, the primary outcome measure reported in this paper will be MSL T. However, the MSL T findings reported are consistent with similar changes in a broad range of abilities, including reaction time, short-term memory, vigilance and mood (1). Many empirical and applied studies have provided evidence for our national sleep debt. The degree of our

We are chronically sleep deprived

Objective It was hypothesized that psychophysiological insomniacs, who have been shown to have elevated heart rate, body temperature, and whole body metabolic rate, would also have increased low frequency and decreased high frequency power in the spectral analysis of their heart period data. Method Groups of 12 objectively defined insomniacs and age-, sex-, and weight-matched controls with normal sleep were evaluated on sleep and EKG measures over a 36-hour sleep laboratory stay. Results Heart period was decreased (ie, heart rate was increased) and its SD was decreased in all stages of sleep in the insomniacs compared with the controls. Spectral analysis revealed significantly increased low frequency power and decreased high frequency power in insomniacs compared with controls across all stages of sleep. Conclusions Because increased low frequency spectral power is an indicator of increased sympathetic nervous system activity, these data imply that chronic insomniacs could be at increased risk for the development of disorders, such as coronary artery disease, that are related to increased sympathetic nervous system activity.

Donna L. Arand

Papers

Hyperarousal and insomnia: state of the science.

24-Hour metabolic rate in insomniacs and matched normal sleepers.

We are chronically sleep deprived

Heart Rate Variability in Insomniacs and Matched Normal Sleepers

Clinical effects of sleep fragmentation versus sleep deprivation