Increased Sleep Duration for Sleep Deprivation
Recruiting in Palo Alto (17 mi)
Age: 18 - 65
Sex: Any
Travel: May Be Covered
Time Reimbursement: Varies
Trial Phase: Academic
Recruiting
Sponsor: University of Utah
Must not be taking: Prescription medications
Disqualifiers: Unstable medical, psychiatric, sleep disorders, others
No Placebo Group
Trial Summary
What is the purpose of this trial?
This protocol will increase sleep duration in participants who maintain less than 6 hours sleep per night, to target the recommended 7 hours of sleep per night. The focus of this study is determine how increasing nightly sleep duration in these individuals who maintain less than 6 hours sleep per night changes their plasma metabolome and insulin sensitivity. The primary outcome will examine changes in branched-chain amino acids and the secondary outcome will examine changes in insulin sensitivity. The investigators will also determine if changes in plasma metabolites can be used as a biomarker to discriminate between adequate versus insufficient sleep.
Will I have to stop taking my current medications?
Yes, participants must stop taking prescription medications and supplements at least one month before the study and cannot use them during the study.
What data supports the effectiveness of the treatment Increased sleep duration for sleep deprivation?
Research shows that after sleep deprivation, longer sleep opportunities help improve alertness and performance. For example, after moderate sleep deprivation, a 9-hour sleep period helped people return to normal alertness and performance levels, while shorter sleep periods did not fully restore these functions.12345
Is increased sleep duration generally safe for humans?
How does increased sleep duration differ from other treatments for sleep deprivation?
Increased sleep duration is unique because it focuses on extending the amount of sleep to address sleep deprivation, unlike other treatments that often involve sleep restriction to improve sleep quality. This approach is based on the idea that many people are chronically sleep deprived and could benefit from simply getting more sleep, although the benefits to daytime alertness may be minor.1112131415
Research Team
CD
Christopher Depner
Principal Investigator
University of Utah
Eligibility Criteria
This trial is for adults aged 18-35 with a BMI of 18.5-24.9, who sleep less than 6 hours per night and have lived at high altitudes like Denver's for over 3 months. It excludes those with unstable medical conditions, psychiatric disorders, significant sleep disorders, recent medication use or need during the study, drug users including nicotine and herbal products within a month prior to the study.Inclusion Criteria
I am between 18 and 35 years old.
You have lived in a place as high as Denver or higher for at least 3 months.
Your BMI is between 18.5 and 24.9.
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Exclusion Criteria
I haven't used any drugs, medications, nicotine, or herbal products for a month.
You have worked night shifts in the past year or traveled across multiple time zones in the three weeks before the study.
Blood donation in the 30 days prior to inpatient study
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Trial Timeline
Screening
Participants are screened for eligibility to participate in the trial
2-4 weeks
Baseline Assessment
Participants sleep in the lab for one night based on their habitual insufficient sleep schedule. Plasma is collected for metabolomics analyses and an oral glucose tolerance test is conducted.
1 night
1 visit (in-person)
Increased Sleep Duration Intervention
Participants undergo a 4-week intervention to increase sleep duration to the recommended 7 hours per night.
4 weeks
Post-Intervention Assessment
Participants sleep in the lab for one night on their new sleep schedule. Plasma is collected for metabolomics analyses and an oral glucose tolerance test is conducted.
1 night
1 visit (in-person)
Follow-up
Participants are monitored for changes in plasma metabolites and insulin sensitivity after the intervention.
4 weeks
Treatment Details
Interventions
- Increased sleep duration (Behavioral Intervention)
Trial OverviewThe trial aims to increase participants' nightly sleep from under 6 hours to the recommended 7 hours to see how it affects blood markers related to metabolism and insulin sensitivity. The main focus is on changes in branched-chain amino acids as primary outcomes and insulin sensitivity as secondary outcomes.
Participant Groups
1Treatment groups
Experimental Treatment
Group I: Increased Sleep Duration InterventionExperimental Treatment1 Intervention
Following baseline assessments, participants will complete a 4-week increased sleep duration intervention followed by one night of sleep in the lab on this increased sleep duration schedule. In the morning, participants will have blood collected for metabolomics analyses and complete oral glucose tolerance testing
Find a Clinic Near You
Research Locations NearbySelect from list below to view details:
Sleep Wake Center--University of UtahSalt Lake City, UT
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Who Is Running the Clinical Trial?
University of Utah
Lead Sponsor
Trials
1169
Patients Recruited
1,623,000+
University of Colorado, Boulder
Collaborator
Trials
128
Patients Recruited
29,600+
References
[Quantitative study of desynchronized sleep recovery after short term total deprivation in the cat]. [2006]The results show that the cumulative hourly duration of desynchronized sleep during recovery is increased with respect to the control value of 40 +/- 4 sec per hour of total deprivation.
Risk-taking and other effects of sleep loss on brain function and behaviour. [2011]The sleep-deprivation paradigm remains a powerful approach in the study of the functions of sleep. When combined with the assessment of novel dependent measures or integration of multiple standard variables new insights may be obtained. This issue of the Journal of Sleep Research contains several studies that shed some new light on the effects of sleep deprivation and sleepiness. In addition, several papers emphasize the need to better characterize and understand the consequences of insomnia.
Sleep deprivation: outcome of controlled single case studies of depressed patients. [2019]Six drug-free depressed patients, each of whom acted as their own control, were studied for eleven consecutive days during which they were twice deprived of sleep for either 36 or 40 hours. The sequence of events was baseline (3 days), SD, recovery (3 days), SD, recovery (3 days). Blind ratings of clinical state were made on the basis of four-hourly interviews (standardized for each case), which were videotaped; sleep was monitored by conventional electrophysiological methods. Sleep deprivation had a beneficial, but transient, effect on four of the six patients studied. Changes in sleep were unrelated to changes in clinical state.
The characteristics of recovery sleep when recovery opportunity is restricted. [2019]The aim of this study was to investigate the recovery of sleep and waking functions following one night of total sleep deprivation, when recovery opportunity was either augmented or restricted.
The dynamics of neurobehavioural recovery following sleep loss. [2007]Rate of recovery of daytime performance and sleepiness following moderate and severe sleep deprivation (SD) was examined when recovery opportunity was either augmented or restricted. Thirty healthy non-smokers, aged 18-33 years, participated in one of three conditions: moderate SD with augmented (9-h) recovery opportunities, moderate SD with restricted (6-h) recovery opportunities, or severe SD with augmented recovery opportunities. Each participant attended the laboratory for 8-9 consecutive nights: an adaptation and baseline night (23:00-08:00 hours), one or two night(s) of wakefulness, and five consecutive recovery sleep opportunities (23:00-08:00 hours or 02:00-08:00 hours). On each experimental day, psychomotor vigilance performance (PVT) and subjective sleepiness (SSS) were assessed at two-hourly intervals, and MSLTs were performed at 1000 h. PSG data was collected for each sleep period. For all groups, PVT performance significantly deteriorated during the period of wakefulness, and sleepiness significantly increased. Significant differences were observed between the groups during the recovery phase. Following moderate SD, response speed, lapses and SSS returned to baseline after one 9-h sleep opportunity, while sleep latencies required two 9-h opportunities. When the recovery opportunity was restricted to six hours, neither PVT performance nor sleepiness recovered, but stabilised at below-baseline levels. Following severe SD, sleepiness recovered after one (SSS) or two (physiological) 9-h sleep opportunities, however PVT performance remained significantly below baseline for the entire recovery period. These results suggest that the mechanisms underlying the recovery process may be more complicated than previously thought, and that we may have underestimated the impact of sleep loss and/or the restorative value of subsequent sleep.
Alertness management strategies for operational contexts. [2008]This review addresses the problem of fatigue (on-the-job-sleepiness) attributable to sleep loss in modern society and the scientifically proven strategies useful for reducing fatigue-related risks. Fatigue has become pervasive because many people work non-standard schedules, and/or they consistently fail to obtain sufficient sleep. Sleep restriction, sleep deprivation, and circadian desynchronization produce a variety of decrements in cognitive performance as well as an array of occupational and health risks. A number of real-world mishaps have resulted from performance failures associated with operator sleepiness. In some cases, fatigue/sleepiness is unavoidable, at least temporarily, due to job-related or other factors, but in other cases, fatigue/sleepiness results from poor personal choices. Furthermore, some individuals are more vulnerable to the effects of sleep loss than others. Fortunately, fatigue-related risks can be mitigated with scientifically valid alertness-management strategies. Proper work/rest scheduling and good sleep hygiene are of primary importance. If sleep time is available but sleep is difficult to obtain, sleep-inducing medications and behavioral circadian-adjustment strategies are key. In fatiguing situations such as when sleep opportunities are temporarily inadequate, limiting time on tasks, strategic napping, and the potential use of alertness-enhancing compounds must be considered. To optimize any alertness-management program, everyone must first be educated about the nature of the problem and the manner in which accepted remedies should be implemented. In the near future, objective fatigue-detection technologies may contribute substantially to the alleviation of fatigue-related risks in real-world operations.
Sleep loss results in an elevation of cortisol levels the next evening. [2022]Sleep curtailment constitutes an increasingly common condition in industrialized societies and is thought to affect mood and performance rather than physiological functions. There is no evidence for prolonged or delayed effects of sleep loss on the hypothalamo-pituitary-adrenal (HPA) axis. We evaluated the effects of acute partial or total sleep deprivation on the nighttime and daytime profile of cortisol levels. Plasma cortisol profiles were determined during a 32-hour period (from 1800 hours on day 1 until 0200 hours on day 3) in normal young men submitted to three different protocols: normal sleep schedule (2300-0700 hours), partial sleep deprivation (0400-0800 hours), and total sleep deprivation. Alterations in cortisol levels could only be demonstrated in the evening following the night of sleep deprivation. After normal sleep, plasma cortisol levels over the 1800-2300-hour period were similar on days 1 and 2. After partial and total sleep deprivation, plasma cortisol levels over the 1800-2300-hour period were higher on day 2 than on day 1 (37 and 45% increases, p = 0.03 and 0.003, respectively), and the onset of the quiescent period of cortisol secretion was delayed by at least 1 hour. We conclude that even partial acute sleep loss delays the recovery of the HPA from early morning circadian stimulation and is thus likely to involve an alteration in negative glucocorticoid feedback regulation. Sleep loss could thus affect the resiliency of the stress response and may accelerate the development of metabolic and cognitive consequences of glucocorticoid excess.
Sleep deprivation therapy. [2019]This review reports, with as much detail as possible, on the literature relating to therapeutic sleep deprivation (or induced-wakefulness therapy) since it was first described in 1971. The antidepressive effect of sleep deprivation has been substantiated by numerous studies. A series of clinical predictors of response to sleep deprivation are also described. Partial sleep deprivation late in the night is equivalent to total sleep deprivation in terms of therapeutic value and--because of its simpler application--can be regarded today as the sleep deprivation method of choice. The status of sleep deprivation in the overall treatment schedule for depressive disorders is discussed in detail. Numerous findings, some of them contradictory, have been published on the effect of sleep deprivation on biological variables. To date, no unequivocal explanation has been found for the mechanism of action of sleep deprivation.
Uncovering residual effects of chronic sleep loss on human performance. [2022]Sleep loss leads to profound performance decrements. Yet many individuals believe they adapt to chronic sleep loss or that recovery requires only a single extended sleep episode. To evaluate this, we designed a protocol whereby the durations of sleep and wake episodes were increased to 10 and 32.85 hours, respectively, to yield a reduced sleep-to-wake ratio of 1:3.3. These sleep and wake episodes were distributed across all circadian phases, enabling measurement of the effects of acute and chronic sleep loss at different times of the circadian day and night. Despite recurrent acute and substantial chronic sleep loss, 10-hour sleep opportunities consistently restored vigilance task performance during the first several hours of wakefulness. However, chronic sleep loss markedly increased the rate of deterioration in performance across wakefulness, particularly during the circadian "night." Thus, extended wake during the circadian night reveals the cumulative detrimental effects of chronic sleep loss on performance, with potential adverse health and safety consequences.
Clamping Cortisol and Testosterone Mitigates the Development of Insulin Resistance during Sleep Restriction in Men. [2022]Sleep loss in men increases cortisol and decreases testosterone, and sleep restriction by 3 to 4 hours/night induces insulin resistance.
Should we be taking more sleep? [2015]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.
Effects of different sleep restriction protocols on sleep architecture and daytime vigilance in healthy men. [2021]Sleep is regulated by complex biological systems and environmental influences, neither of which is fully clarified. This study demonstrates differential effects of partial sleep deprivation (SD) on sleep architecture and psychomotor vigilance task (PVT) performance using two different protocols (sequentially) that each restricted daily sleep to 3 hours in healthy adult men. The protocols differed only in the period of sleep restriction; in one, sleep was restricted to a 3-hour block from 12:00 AM to 3:00 AM, and in the other, sleep was restricted to a block from 3:00 AM to 6:00 AM. Subjects in the earlier sleep restriction period showed a significantly lower percentage of rapid-eye-movement (REM) sleep after 4 days (17.0 vs. 25.7 %) and a longer latency to the onset of REM sleep (L-REM) after 1 day (78.8 vs. 45.5 min) than they did in the later sleep restriction period. Reaction times on PVT performance were also better (i.e. shorter) in the earlier SR period on day 4 (249.8 vs. 272 ms). These data support the view that earlier-night sleep may be more beneficial for daytime vigilance than later-night sleep. The study also showed that cumulative declines in daytime vigilance resulted from loss of total sleep time, rather than from specific stages, and underscored the reversibility of SR effects with greater amounts of sleep.
Long sleep and mortality: rationale for sleep restriction. [2022]Epidemiologic studies have consistently shown that sleeping >8 h per night is associated with increased mortality. Indeed, the most recent American Cancer Society data of 1.1 million respondents showed that sleeping longer than 7.5 h was associated with approximately 5% of the total mortality of the sample. The excess mortality was found even after controlling for 32 potentially confounding risk factors. Although epidemiologic data cannot prove that long sleep duration causes mortality, there is sufficient evidence to warrant future testing of the hypothesis that mild sleep restriction would decrease mortality in long sleepers. Sleep restriction might resemble dietary restriction as a potential aid to survival. Sleep restriction has several potential benefits besides possible enhanced survival. Acute sleep restriction can have dramatic antidepressant effects. Also, chronic sleep restriction is perhaps the most effective treatment for primary insomnia. Conversely, spending excessive time in bed can elicit daytime lethargy and exacerbate sleep fragmentation, resulting in a vicious cycle of further time in bed and further sleep fragmentation. Sleep restriction may be most beneficial for older adults, who tend to spend excessive time in bed and have more sleep fragmentation compared with young adults.
Adverse effects of modest sleep restriction on sleepiness, performance, and inflammatory cytokines. [2022]Total sleep restriction in humans is associated with increased daytime sleepiness, decreased performance, and hormonal/metabolic disturbances. The effects of mild chronic sleep restriction that mimic real life are not known. To assess the effects of modest sleep restriction from 8 to 6 h/night for 1 wk, 25 young, healthy, normal sleepers (12 men and 13 women) were studied for 12 consecutive nights in the sleep laboratory. After 1 wk of sleep restriction, although subjects' nighttime sleep was deeper, subjects were significantly sleepier (multiple sleep latency test) and performed worse in four primary variables of psychomotor vigilance test (both P
Impact of chronic sleep restriction on sleep continuity, sleep structure, and neurobehavioral performance. [2023]Chronic sleep restriction (CSR) has been associated with adverse effects including cognitive impairment and increased risk of diabetes and cardiovascular disease. Yet, sleep restriction therapy is an essential component of most behavioral treatments for insomnia. Moreover, little is known about the impact of CSR on sleep continuity and structure in healthy people whose need for sleep is satiated. We investigated the impact of CSR on sleep continuity and structure in nine healthy participants. They had 4 nights of sleep extension, 2 nights of post-extension sleep, 21 nights of CSR (5/5.6-hour time-in-bed), and 9 nights of recovery sleep. Compared to postextension sleep, during CSR sleep duration was reduced by 95.4 ± 21.2 min per night, Slow-Wave Activity was significantly increased, and sleep was more consolidated. During recovery, sleep duration was increased by 103.3 ± 23.8 min compared to CSR, and the CSR-induced increase in Slow-Wave Activity persisted, particularly after the 5-hour exposure. Yet, we found that sustained vigilant attention was not fully recovered even after nine nights of recovery sleep. Our results suggest that CSR improves traditional metrics of sleep quality and may have a persistent impact on sleep depth, which is consistent with the reported benefits on sleep continuity and structure of sleep restriction therapy. However, these improvements in traditional metrics of sleep quality were associated with deterioration rather than improvement in neurobehavioral performance, demonstrating that sleep duration should be included in assessments of sleep quality. These results have implications for the long-term use of sleep restriction in the behavioral treatment of insomnia. Clinical Trial Registration: Impact of Chronic Circadian Disruption vs. Chronic Sleep Restriction on Metabolism (https://clinicaltrials.gov/ct2/show/; #NCT02171273).