The effects on subsequent sleep of an acute restriction of sleep length.
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BACKGROUND: This research examined the association between sleep duration and new-onset chronic kidney disease (CKD) among community-dwelling middle-aged and elderly individuals in Korea. METHODS: This prospective cohort study utilized data from the Korean Genome and Epidemiology Study (KoGES) from 2001-2002 (baseline) to 2019-2020 (tenth follow-up visit). New-onset CKD was the primary outcome, defined as an estimated glomerular filtration rate <60 mL/min/1.73 m2 or the proteinuria. Study populations were classified into six self-reported sleep length categories: <5h, 5h ≤ to <6h, 6h ≤ to <7h, 7h ≤ to ≤8h, 8h < to <9h, and 9h/day ≤. Cox proportional hazards models were used to ascertain the hazard ratios (HRs) and 95% confidence intervals (CIs) for CKD incidence across these categories. RESULTS: Over a median follow-up duration of 17.41 years, CKD was identified in 551 (14.4%) of 3835 participants (mean age 48.7 ± 7.5 years). After adjusting for confounding variables, a U-shaped relationship between sleep lengths and CKD was identified. Participants with insufficient (<5h) and excessive (9h ≤) sleep length exhibited HRs for CKD incidence of 1.44 (1.09-1.89) and 1.85 (1.04-3.27), respectively, compared to individuals with normal sleep length (7h ≤ to ≤8h). Age and sex differences were observed in the association between sleep length and CKD incidence. The association between sleep duration and new-onset CKD was significant only in participants aged 40 to 64 years, with no significant association observed in individuals aged 65 years and older. CONCLUSIONS: This research identified a relationship between the amount of sleep and CKD in Korean adults. Maintaining an appropriate sleep duration of 7-8 h/day is important for preventing new-onset CKD.
In this research, a quantitative study of the EEG from 5 subjects permitted a detailed analysis of the effect of 30 mg of flurazepam administered over 7 nights. Four placebo baseline nights and 3 placebo withdrawal nights were also recorded. For 4 of the subjects, a nondrug and nonplacebo follow-up record was obtained 4 to 6 weeks later. The subjects were 4 females, 1 male, age range 23-42. All complained of either sleep onset greater than 45 min, sleep length of less than 6 h, or two or more sleep awakenings. Compressed spectral analysis yielded a computer-generated somnogram on each of the 15 nights of sleep, and an automated spindle detector was used to count and measure the duration of spindle bursts with frequencies of 12.25-15.5 c/sec on baseline nights 3 and 4, drug nights 1, 2, 3 and 7, on the 3rd withdrawal night, and on the 4-6 week followup record. K-complexes were scored visually on the 4th baseline and 7th drug nights. There were no significant differences in spindle rate per minute among baseline nights and the follow-up record. By the 2nd drug night, spindle rate had significantly increased over the baseline rate. Linear contrast analysis indicated there was a significant increase of spindle rate over drug nights. All 5 subjects showed this pattern of increase. In contrast to the increase in spindle activity, the rate per minute of K-complexes significantly decreased during drug administration.
Studied psychological correlates of irregularity in chronic sleep routines. The California Psychological Inventory (CPI) and Cornell Medical Index (CMI) were administered to two groups of 18 male university students who were categorized as either irregular sleepers or control Ss. The control group was composed of persons who habitually slept from 12-8:00 A.M. Irregular sleepers were defined as those whose retiring and awakening times continuously varied by about 2 to 4 hours. Control Ss scored significantly higher than the irregular group on the CPI scales of Do (dominance), Sy (sociability), Sa (self-acceptance), Sc (self-control), Ac (achievement via conformance), and Ie (intellectual efficiency), but lower on the Fx (flexibility) scale. There were no significant differences between the groups in scores on the CMI or average sleep length recorded over 2 weeks. The present findings indicate that in young adults, personality functioning is related more closely to the regularity of nocturnal sleep routines than to differences in chronic sleep duration. It is postulated that stable or irregular sleeping patterns are largely dependent factors not only of the psychological characteristics that distinguished the groups, but as yet unspecified constitutional and sociocultural antecedents of the human sleep response.
A 20 min period of diffuse brain stimulation (DBS), administered just before sleep onset in 16 human subjects, appeared to alter significantly the first sleep cycle of the succeeding sleep. The length of the first sleep cycle and the amount of REM sleep increased, whereas a shift from deep to more superficial NREM sleep occurred. This effect of DBS on sleep is discussed with respect to data from the literature on the effect of narcotic DBS and on that of local brain stimulation in animals.
Five young rats, age 152--175 days, and six old rats, age 782--801 days, all of the F-344 strain, were compared by electronic methods for amplitude of slow wave activity during sleep and for other sleep parameters. Unlike humans, who show a pronounced loss of slow wave activity with advanced age, no significant difference in delta activity could be detected between young and old rats. Several hypotheses about the species difference were reviewed. Young and old rats, however, did show several differences in other sleep parameters which parallel those observed in humans. These age-related changes were a moderate decrease in the percent of total sleep time spent in paradoxical sleep, a decrease in the length of sleep bouts, an increase in the number of sleep bouts, and a decrease in the amplitude of the diurnal rhythm of sleep.
One male cat was adapted to different schedules of restricted sleep. The cat was allowed to go to sleep during a certain number of hours per day. During the rest of the 24 h period, wakefulness was enforced by means of a treadmill. The following schedules of restricted sleep were run: 12 h sleep--12 h treadmill (12S--12T), 8S--16T, 4S--20T. The cat was also adapted to a 36 h day: 12S--24T. The sleep was investigated after at least 2 weeks on each schedule and compared to ad lib. sleep (24S--0T). As available sleep time bacame shorter, the composition of the sleep changed. LSWS (in % of available sleep time) decreased, while DSWS % and REM sleep % increased. The length of the DSWS and REM sleep episodes increased with decreasing sleep time, as did sleep cycle length.
The relation between reduced nutritional intake, with consequent weight loss, and sleep disturbance was studied by comparing certain sleep encephalogram patterns in a group of inpatients with anorexia nervosa before, during, and after a regimen of refeeding with a normal diet to a matched population mean weight. At low body weights patients had less sleep and more restlessness, especially in the last four hours of the night. During refeeding and weight gain slow-wave sleep initially increased and then tended to decrease during the final stage of restoration of weight back to matched population mean levels. With the overall weight gain, however, there was a significant increase in length of sleep and rapid eye movement sleep, the latter increasing especially during the later stages of weight gain. These results reaffirm that insomnia, and especially early morning waking, is associated with low body weight in anorexia nervosa, and their implications are discussed with particular reference to a hypothetical association between various anabolic profiles and the need for differing components of sleep.
The sleep state characteristics of infant sleep apnea were studied in 36 twins examined by polygraphy at 40, 44, and 52 weeks after conception. The definition of sleep apnea is dependent upon the length of apnea, sleep state, and post-conceptional age. None of the infants had apnea longer than 20 seconds and apnea of 10 seconds or longer was uncommon. The attack rates for apneas 2 to 4.9 seconds long were highest in REM and lowest in qliet sleep. The attack rates for apneas 5 to 9.9 seconds long were equal in REM and indeterminate and lowest in quiet sleep. The percentage of infants with apnea of 10 seconds or longer at 40 weeks was highest in REM (27%) and indeterminate sleep (42%) and lowest in quiet sleep (12%). At 52 weeks, apnea 10 seconds or longer during REM decreased to 0%. The effect of maturation on apnea varies with sleep state. Over the period from 40 to 52 weeks, quiet sleep apnea was unchanged and indeterminate sleep apnea decreased only between 40 and 44 weeks. Although REM apnea 2 to 4.9 seconds long was unchanged, REM apnea 5 to 9.9 seconds long decreased between 40 and 44 weeks, and REM apnea of 10 seconds or longer decreased from 27% at 40 weeks to 0% at 52 weeks. This suggests that semi-independent apnea turn-on and turn-off mechanism operate during REM sleep. A correlation between brief apneas and the longer apneas was seen only during REM sleep. For all sleep states, there was no correlation between the levels of apnea of 5 seconds or longer at 40, 44, and 52 weeks.
Seven-hr sleep recordings were performed on rats following intraperitoneal injection of saline or one of four doses of ethanol (1.1, 1.5, 2.0 or 2.5 g/kg). Total minutes of REM sleep and percentage REM sleep were decreased in a dose-dependent manner. Percentage nonREM sleep increased with progressively higher doses. The decrease in REM sleep appeared to be related to a decrease in the number of REM sleep episodes and an increase in the length of the REM-nonREM cycle. Other variables such as mean length of REM sleep episodes and REM sleep efficiency were unchanged. An analysis of the first and second 3.5 hr of the recording showed that ethanol continued to have marked effects on REM and nonREM sleep during the second 3.5 hr, when blood levels were declining. Ethanol produced decreases in sleep latency, but total sleep time was unchanged.
Twenty-six normal children (age range range 4-68 months) were studied during Stage 2 sleep which occurred within 20 min preceding or following the first three REM periods of the night. Sleep spindles were measured in Fp1T3. The number, length, and percent of sleep spindle activity were found to be maximal at 46 months of age. Beyond 6 months spindle activity decreased to reach minimal values by 27 months, remained fairly constant to 54 months, then rose again to higher values in the oldest subjects. The mean spindle-wave frequency was 1314 c/sec in subjects younger than 40 months, but was 12-13 c/sec in older subjects. Spindle onsets in Fp1T3 and Fp2T4 were more often concurrent in older as compared to younger subjects. Auditory stimulation (binaural clicks, 60 dB above hearing threshold) affected neither the incidence nor the length of spindles during sleep. Because sizable changes in sleep spindle activity are found between 3 months and 5 years of age, and because such changes are relatively consistent between subjects, it is concluded that sleep spindles recorded between frontal and temporal areas may serve as a useful index of neural maturation in the human subject.
In four consecutive weekly sessions 12 subjects, aged 20--25 years, listened to a sentence stimulus before the onset of sleep and were asked to reproduce it after an awakening provoked during stage 2 or REM sleep of the first cycle. Recall of the sentence stimuli heard before sleep was affected by their semantic acceptability, but was unaffected by the sleep type (REM/NREM) or by the length of waking preceding sleep. The differing retention intervals involved for the recall tests after REM and NREM sleep may, however, have masked any effect of the former on recall.
The first cycle of sleep was studied in different situations: normal night sleep, naps, diurnal sleep after night shifts (3 x 8 shift workers). Results show two types of first cycle: some started with SWS (normal cycles), others with REM (sleep onset REM periods: SOREMPs). (1) Normal cycles: the length of SWS in the first cycle was positively correlated with prior wakefulness; conversely, the latency of SWS decreased as prior wakefulness increased; the decrease was due to the decrease in the length of the previous stage II or of the sleep onset latency (SOL). Length of sleep onset (SO) showed only few variations. The structure of the first cycle of shift workers' sleep probably reflects an important sleep loss. (2) SOREMPs occcurred during diurnal sleep. Some hypotheses about these cycles are discussed including REM 'pressures' (circadian, sleep loss) and inter-individual variations.
The sleep E.E.G. of the child under 3 years old is characteristic from several points of view: Drowsiness: The hypersynchrony is always observed. It is more continuous in younger children, than in the older one, where only bursts of hypersynchrony are seen. The fast rhythms of low amplitude may exist, during stage 2 sleep, but they are rare. Calm Sleep (C.S.): The vertex humps are more and more acute and sharper from 18 months. The sleep spindles are of high amplitude and frequent at 6 and 8 months. They diminish later. It may be for that reason that III and IV sleep stages seem to be more important after 12 months than before. From 21 months, we have observed an unusual pattern during C.S.: rhythmic and diffuse thêta rhythms of about 6 c/s. Paradoxal sleep (P.S.): If it is possible to observe P.S. during day-naps 8 or 9 months, it is rare later and for recording P.S., it is necessary to record E.E.G.s at night. The E.E.Gs are either a little like stage I E.E.G, or consistent of high and monomorphic delta waves. If it is possible to observe at least 3 complete sleep cycles, the proportion of P.S. is about 20 p. 100 of the total length of the sleep. At least, it is very important, even in medical practice, to record not only E.E.G. but also polygraphic leads: breathing, electro-myogram, electrocardiogram, and to notice also the rapid eyes movements.
The 24-hr electrographic patterns (EEG, EOG, EMG) of six normal pointer dogs were recorded in a laboratory setting. Two states of sleep (slow-wave and rapid eye movement) and wakefulness (alert and drowsy) were identified. The total recording period comprised 44% of alert wakefulness, 21% of the drowsy state, while slow-wave sleep occupied 23% and REM sleep 12% of the time. The mean length of a REM sleep episode averaged 6 min and the mean REM sleep cycle was 20 min. The mean polycyclic sleep-wake cycle was 83 min. Sleep episodes averaged 45 min and the mean waking episode was 38 min. There was an average of two REM sleep episodes per sleep-wake cycle. The dog has a propensity to sleep over a 16-hr interval from 1300 to 0500 but the most sleep occurred between 2100 and 0400 hr during darkness.
11 healthy children were repeatedly studied during 2 sleep cycles in 2 sessions at 2,6, 12 and 20 wk of life. Three acoustic stimuli, light and tactile stimulus were applied in a randomized order in intervals ranging randomly from 30 to 120 sec. Continuous polygraphic recordings were made of respiration, REMs, EEG and EMG of biceps and triceps brachii. The effect of stimuli on the length of paradoxical sleep, REMs and EMG was assessed. There were age-related changes in the number of REMs after stimuli. At 2 and 6 wk no stimulus elicited any change. At 12 wk the children responded with an increased number of rapid eye movements to acoustic stimuli, at 20 wk they responded to acoustic stimuli and light. The conclusion is that, as far as REMs are concerned, responsiveness during paradoxical sleep changes with age. There was a difference in the incidence of EOG responses and EMG responses. These findings show that it is not possible to assess responsiveness in infants during PS by one measure only.
Several studies indicate that ethanol may depress the central nervous system by altering neurotransmitter release. Evidence obtained from the peripheral nervous system suggests that prostaglandins act as negative feedback inhibitors of transmitter release. If a similar process occurs in the brain, then perhaps ethanol affects transmitter release via a mechanism involving prostaglandins. Prostaglandin synthetase inhibitors were administered to adult HS/Ibg male mice prior to intraperitoneal injection of a hypnotic dose of either ethanol, propanol, or t-butanol. A significant decrease in the length of alcohol sleep time was found: in the ethanol study, this was coupled with a significant increase in waking blood alcohol levels. These results indicate that inhibition of prostaglandin synthesis alters CNS sensitivity to the depressant effects of alcohol. When the same inhibitors were administered prior to other sedative hypnotics, i.e., pentobarbital and chloral hydrate, no effect was found. This suggests that prostaglandins may be specifically involved in the biochemical mechanism of alcohol depression.
Individual differences in sleep duration have been reported, and genetic components of sleep duration have been identified showing various heritability. To identify genetic variants that contribute to sleep duration, we conducted a human genome-wide identification on sleep duration and performed confirmatory experiments using a Drosophila model. Genome-wide association study in human was analyzed to determine the association of the genetic variants with self-aware sleep duration from two community-based cohort, Ansan (cohort 1, n = 4635) and Ansung (cohort 2, n = 4205), recruited from the Korean Genome and Epidemiology Study. Individual single nucleotide variants (rs16948804 and rs4887991) in the WW domain containing oxidoreductase (WWOX) gene were associated with self-aware sleep duration in human (p-values, 1.11 × 10- 7 and 2.05 × 10- 7, retrospectively). To examine the functional relevance of the WWOX gene identified in the genome-wide association study, we analyzed the sleep duration of Drosophila loss-of-function mutants. The deletion of Wwox in flies reduced sleep duration and quality with average bout length during daytime and increased night-time sleep duration (all of p-values < 0.01). Our findings suggested that WWOX expression is associated with sleep duration in both humans and Drosophila and genetic factors play a role in inter-individual variability in sleep characteristics.