TL;DR: Most people are not chronically sleep deprived but have the capacity to take more sleep, in the same way that the authors eat and drink in excess of physiological needs.
Abstract: Reports of reduced daytime sleepiness following extended nighttime sleep in normal, regular sleepers suggest that they (and perhaps much of the general population) are chronically sleep deprived. However, 1) the social and environmental contexts of sleep allow for much intraindividual variation in sleep duration and structure; 2) animal studies show that when there is opportunity for sleep and few incentives to remain awake, sleep occurs for reasons other than in response to a physiological requirement, i.e. sleep satiation may precede actual awakening, 3) accounts of increased sleep duration earlier this century are flawed and 4) because increased sleep onset latency and wake after sleep onset are features of extended sleep, it would be difficult to persuade people to sleep longer for the small benefits to daytime alertness. Laboratory studies show that 1) following extended sleep the improvements in daytime alertness are minor, even by the Multiple Sleep Latency Test (MSLT), and could be achieved equally successfully and with less disruption to habitual daily patterns by taking a short nap; 2) normal subjects extend sleep at night not necessarily because they are chronically sleepy, because there may be no prior MSLT signs of daytime sleepiness; 3) mood effects of extended sleep are confounded by earlier bedtimes; and 4) extended sleep does not necessarily make subjects feel well rested immediately on waking. In sum, most people are not chronically sleep deprived but have the capacity to take more sleep, in the same way that we eat and drink in excess of physiological needs.
TL;DR: Seasonal affective disorder (SAD) is characterised by recurrent episodes in autumn and winter of depression, hypersomnia, augmented appetite with carbohydrate craving, and weight gain, and can be successfully treated with bright light.
Abstract: Seasonal affective disorder (SAD) is characterised by recurrent episodes in autumn and winter of depression, hypersomnia, augmented appetite with carbohydrate craving, and weight gain, and can be successfully treated with bright light. Circadian rhythm hypotheses (summarized in) have stimulated research into the pathophysiology of SAD, postulating that: 1.The illness is a consequence of delayed phase position, 2.It is correlated with diminished circadian amplitude, or 3.It results from changes in the nocturnal duration between dusk and dawn e.g. of low core body temperature or melatonin secretion. Light is considered to act directly on the circadian pacemaker ('Process C') and not on sleep dependent processes ('Process S'). Thus successful treatment of SAD must act via mechanisms within known retinohypothalamic pathways. Conversely, emergence of SAD symptoms may reflect inappropriate neurobiological response to decreasing daylength.
TL;DR: Experiments have provided new insights in the role of the endogenous circadian pacemaker in this consolidation of sleep and wakefulness and showed that during sleep deprivation both processes change simultaneously and their relative contribution to alertness and sleep propensity cannot be assessed under these conditions.
Abstract: The adult human typically exhibits a monophasic sleep-wake cycle, i.e., remains awake and alert for approximately 16 hours and then sleeps for 8 hours. Recent experiments have provided new insights in the role of the endogenous circadian pacemaker in this consolidation of sleep and wakefulness. Sleep deprivation studies had shown previously that sleepiness and alertness are co-determined by a process which keeps track of the history of sleep and wakefulness and the circadian pacemaker, which keeps track of time. During every day life and during sleep deprivation both processes change simultaneously and their relative contribution to alertness and sleep propensity cannot be assessed under these conditions.