Sleep duration

Figure 8.1 The duration of NREM sleep and delta activity during NREM sleep following saline (open circles) or 0.5mg/kg MK-801 (filled circles), administered 6h after the start of the dark period. MK-801 initially produced a period of wakefulness approximately 3 h long. In the subsequent light period, NREM sleep duration (A), total integrated amplitude (TIA, a period amplitude measure similar to power) of NREM sleep delta (B), and NREM sleep delta integrated amplitude per minute (IA/min) (C) were all significantly increased above control levels.

Taheri, S., Lin, L., Austin, D., Young, T. 8r Mignot, E. (2004). Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index. PLoS Med. 1, e62. 

Having observed a decrease in appetite and thirst when testing BZ, we decided to measured caloric and fluid intake more precisely in the EA 3443 series. At the incapacitating dose, calories ingested and fluid consumed both dropped by about 40%. Sleep duration, also measured, increased at the lower doses but seemed to drop precipitously at the incapacitating dose. This seeming insomnia, however, was illusory. Delirious subjects appeared physically awake, but were asleep in terms of brain electrical activity - the so-called pseudowakeful state. ... 

Number of Subjects Dose (mcg/kg) Food Intake (cal.) mean S.E. Fluid Intake (ml) mean S.E. Sleep Duration (h) S.E. 

Table 8 EA 3443 Dose-related differences in caloric intake, fluid intake and sleep duration.

In general, caloric and fluid intake both tend to decrease as the dose of EA 3443 is increased (Table 8). Sleep duration per 24 hours increases at lower doses (reflecting its sedative effect) but then declines as delirium takes over. The apparent insomnia during delirium often referred to as the pseudowakeftil state, in which the subject is active and seems to be awake, but is actually asleep in terms of EEG activity. 

Results of the study on impact of the Complex on thiopental sleep duration in rats are presented in Table 4. 

All these drugs reduce sleep duration, decrease SWS and REM sleep, increase sleep latency and increase sleep fragmentation. They can cause a dose-related insomnia during use, and hypersomnia with increased dreaming and nightmares on withdrawal after chronic use. 

Sleep polveram WASO, unrest [ Sleep duration T No effect No effect... 

Sleq> WASO, unrest Sleep duration REM sleep J Sleep unrest ... 

Sleep polygram WASO and unrest f, stage 2 and sleep duration f, REM sleep f No data... 

Sleeo oolveram Sleep unrest sleep duration, Sleep unrest f, sleep... 

Some short-acting BZDs (e.g., midazolam and triazolam) are ultrarapidly eliminated and their effect on sleep duration may be so short that patients may awaken earlier then they desire. Brotizolam, in contrast, has a half-life of around 5 hours that places it in the middle of the range of activity of the rapidly eliminated hypnotics. Thus, brotizolam may not only induce sleep quickly but also sustain sleep without residual effects the next day and without accumulation on repeated ingestion. 

There are several double-blind studies that support melatonin administration. For example, rapid deployment aviation groups sent to the Middle East demonstrated longer sleep duration and better test performance on melatonin than did the placebo group ( 174, 175). Arendt (173), who has had extensive experience with both controlled and uncontrolled studies, summarized the overall experience in 386 subjects, showing a 60% reduction in jet lag for eastern travel and a 40% reduction for western travel. 

Clinical studies in patients with sleep disorders have shown that oral melatonin supplementation may alter sleep architecture. Subjective improvements in sleep quality and improvements in sleep onset and sleep duration have been reported. However, the significance of these findings is impaired by many study limitations. 

Jewett ME, Dijk DJ, Kronauer RE, Dinges DF. Dose-response relationship between sleep duration and human psychomotor vigilance and subjective alertness. Sleep 1999 22 171-179. 

Despite the co-occurrence of sleep disturbances with virtually all infectious diseases, relatively few studies have looked at the exact nature of sleep changes associated with infection. Reports of sleep during rhinovirus 23 infection (the cold virus) have included a decrease in sleep duration and sleep efficiency, with an associated reduction in neurobehavioral performance (vigilance) and a trend for reduced subjective vigor (Profile of Mood States, POMS) (190). 

A. Developmental Changes and Individual Differences in Sleep Duration... 

The average newborn sleeps about 16 out of every 24 hr in bouts of 1 4 hr (7). Sleep decreases to about 13 hr at 1 year and consists of nocturnal sleep plus two daytime naps. By 4-5 years old, most children have given up naps and spend at least 10 hr asleep at night (8). We believe that older children and adolescents need at least 9 hr of sleep, although most obtain far less than that amount. These familiar generalizations about changes in sleep duration across age are based on studies in both naturalistic settings and the laboratory. Rarely, however, is the construct of sleep need addressed directly and we must be careful not to confuse usual sleep duration with sleep need. 

V. Sleep Duration and Schedules Sleep as an Independent Variable... 

Iglowstein I, lenni OG, Molinari L, Largo RH. Sleep duration from infancy to adolescence reference values and generational trends. Pediatrics 2003 111 302-307. 

In this discussion, we will present a reanalysis of the CPSII data, to further explore the influence of comorbid risk factors on the mortality associated with sleep duration. The risks associated with insomnia, shift work, and sleeping pills will also be examined. 

The question arises whether the association of sleep duration with mortality hazard could be an artifact of comorbidities, since so many diseases, disorders, and discomforts are associated with disturbed sleep. In our prior analysis of CPSII, we controlled as far as possible for the major risk factor data available from the CPSII questionnaires, to see if such extensive control for comorbidities would eliminate the significant associations of mortality hazard with sleep duration. 

Figure 1 The relative 6-year mortality hazard ratios are shown for reported usual sleep hr from 2-3 hr/night to 10 or more hr/night, relative to 1.0 assigned to the hazard for 7 hr/night as the reference standard. The solid line with 95% confidence interval bars shows results from a 32-covariate Cox proportional hazards survival model, as reported previously (3). The dotted lines show data from models that excluded subjects who were not initially healthy, i.e., who died within the first year or whose questionnaires reported any cancer, heart disease, stroke, chronic bronchitis, emphysema, asthma, or current illness (a yes answer to the question are you sick at the present time ). The dot-dash lines with X symbols show models controlling only for age, insomnia, and use of sleeping pills. Data were from 635,317 women and 478,619 men. The thin solid lines with diamonds show the percent of subjects with each reported sleep duration (right axis).

We are not certain which comorbid risk factors cause mortality independent of sleep effects, and therefore, we cannot be certain whether we controlled too much or too little for comorbidities. For example, since short sleep or long sleep may cause a person to be sick at present or to get little exercise or to have heart disease (17), diabetes (18), etc., controlling for these possible mediating variables may have incorrectly minimized the hazards associated with sleep durations. This would be overcontrol. The hazard ratios for participants who were rather healthy at the time of the initial questionnaires were unlikely to be overcontrolled for initial illness. Since the 32-covariate models and the hazard ratios for initially healthy participants were similar, this similarity reduced concern that the 32-covariate models were overcontrolled. On the other hand, there may have been residual confounding processes that caused both short or long sleep and early death that we could not adequately control in the CPSII data set, either because available control variables did not adequately measure the confound or because the disease did not yet manifest itself. Depression, sleep apnea, and dysregulation of cytokines are plausible confounders that were not adequately controlled. It may be impossible to be confident that all conceivable confounds are adequately controlled in epidemiological studies of sleep. 

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