Chronic Sleep Curtailment Research Articles

Melatonin ameliorates chronic sleep deprivation against memory encoding vulnerability: Involvement of synapse regulation via the mitochondrial-dependent redox homeostasis-induced autophagy inhibition

Voluntary sleep curtailment is increasingly more rampant in modern society and compromises healthy cognition, including memory, to varying degrees. However, whether memory encoding is impaired after chronic sleep deprivation (CSD) and the underlying molecular mechanisms involved remain unclear. Here, using the mice, we tested the impact of CSD on the encoding abilities of social recognition-dependent memory and object recognition-dependent memory. We found that memory encoding was indeed vulnerable to CSD, while memory retrieval remained unaffected. The hippocampal neurons of mice with memory encoding deficits exhibited significant synapse damage and hyperactive autophagy, which dissipates during regular sleep cycles. This excessive autophagy appeared to be triggered by damage to mitochondrial DNA (mtDNA), resulting from oxidative stress within the mitochondria. The relief at the behavioral and molecular biological levels can be achieved with intraperitoneal injections of the antioxidant compound melatonin. Moreover, our in vitro experiments using HT-22 cells demonstrated that oxidative stress induced by hydrogen peroxide led to oxidative damage, including mtDNA damage, and activation of autophagy. Melatonin treatment effectively countered these effects, restoring redox homeostasis and reducing excessive autophagic activity. Notably, this protective effect was not observed when melatonin was administered as a pre-treatment. Together, our findings reveal the vulnerability of memory encoding during chronic sleep curtailment, which is caused by oxidative stress and consequent enhancement of autophagy, suggest a potential therapeutic strategy for addressing these effects following prolonged wakefulness through melatonin intervention, and reiterate the significance of adequate sleep for memory formation and retention.

The Impact of Delayed School Start Times During COVID-19 on Academic Performance: A Longitudinal Naturalistic Study in Italian High Schools.

Delaying school start times has been proposed as a potential solution to address chronic sleep curtailment among adolescents and its negative consequences on their physical and mental well-being. This study investigates the impact of delayed school start times due to the COVID-19 pandemic on academic achievement. Two separate observational studies were conducted involving high school students from the first/second year (n=232) (Study 1) and from the final year (n=39) (Study 2). Multivariate Analyses of Covariance were performed to assess for statistical differences in academic performance (ie, global, humanistic, and scientific performance) and absenteeism (ie, number of school absences). Two main factors were considered: "school start time" (ie, standard-8:00 AM vs late-9:40 AM) and "time interval" (ie, first academic semester vs second academic semester), controlling for the school year (Study 1) and circadian preference (Study 2). Delaying school start times was positively associated with better academic performance in scientific subjects among first/second-year students (F1,229=6.083, p=0.026) and global academic performance among last-year students (F1,35=4.522, p=0.041). Furthermore, first/second-year students significantly increased their school achievement (F1,229>29.423, p<0.001) and school absences (F1,229=66.160, p<0.001) during the second semester of the academic year. No significant effect of "school start time" on school attendance was observed. Additionally, circadian preference was found to be a significant covariate among last-year students, with early chronotypes exhibiting better academic performance (r>0.369, p<0.025). These findings confirm past evidence about the beneficial effects of delayed school start times on academic outcomes, with the additional advantage of observing them within a natural context that emerged during the pandemic. Further research is needed to explore the phenomenon more systematically and take into account the broader implications of implementing this change.

Association of night-time sleep and day napping with the prevalence of MOSH in young obese men.

Obesity in men is also shown to be associated with reduced reproductive potential, and this particular subtype was described as male obesity-associated secondary hypogonadism (MOSH). Recent studies showing the influence of sleep disorders on testosterone levels suggested a potential role of sleep disorders in determining the development of MOSH. To assess the association between night-time sleep duration and day napping and the prevalence of MOSH. In this cross-sectional study, 226 obese male participants aged 18-30 years were enrolled. Daytime napping and night-time sleep duration data were collected using a standardized self-reported Chinese-language questionnaire. MOSH was defined as obese men (BMI ≥ 30kg/m2 ) with hypogonadal symptoms and decreased total testosterone level and/or free testosterone level, excluding other causes of hypogonadism. The overall prevalence of MOSH was 48.2% in this study. An inverse association was observed between night sleep duration and the risk of prevalent MOSH. Men who reported fewer than 6h of night-time sleep had reduced total testosterone and free testosterone levels and an increased risk of MOSH. Further regression analysis revealed that after adjustment for potential confounders, the odds ratio of MOSH for the short night-time sleep group (<6 h vs. 6-8 h) was 6.17 (p=0.040). No significant association was observed between day napping status and prevalence of MOSH. Short night sleep duration was associated with an increased risk of MOSH in the young obese Chinese population. Chronic sleep curtailment has a negative effect on obese men's health in terms of hypogonadism.

Acute and chronic sleep deprivation in residents: Cognition and stress biomarkers.

Insufficient sleep affects circadian hormonal profiles and inflammatory markers and may modulate attention, executive functioning and decision-making. Medical professionals and specifically resident physicians, who are involved in long-term nightshift schedules during their post-graduate training, are prone to acute and chronic sleep deprivation and disruption, putting them at risk for making medical errors. The aim of the study was to evaluate the impact of chronic and acute-on-chronic sleep deprivation and disruption among residents on selected physiological and cognitive measures. Thirty-three medical and surgical residents were evaluated twice - at baseline and after a 26-hour shift. Eighteen young attending physicians who did not engage in nightshift schedules served as controls and were evaluated once. Measures included morning cortisol and high-sensitivity C-reactive protein (hs-CRP), computerised tests of attention and behaviour, the Behaviour Rating Inventory of Executive Function, a risk-taking questionnaire and the Pittsburgh Sleep Quality Index. Residents, but not attendings, reported chronic sleep disruption and deprivation. Residents at baseline exhibited reduced morning cortisol levels and elevated hs-CRP levels, compared to attendings. Residents at baseline had impaired global executive function compared to attendings. A nightshift with acute sleep deprivation further reduced residents' executive function. Residents at baseline and after a nightshift demonstrated increased impulsivity and slower processing time than attendings. Residents and attendings did not differ in risk-taking tendencies which were assessed in a separate cohort. In a real-life setting, resident physicians exhibit increased low-grade systemic inflammation (hs-CRP) and impaired HPA-axis function. Their chronic sleep curtailment is associated with greater impulsivity, slower cognitive processing, and impaired executive function. Future research is warranted to understand how improving working schedule by increasing sleep duration may minimise the short-term and potential long-term risks to physicians in training.

Chronic sleep curtailment, even without extended (>16-h) wakefulness, degrades human vigilance performance

Millions of individuals routinely remain awake for more than 18 h daily, which causes performance decrements. It is unknown if these functional impairments are the result of that extended wakefulness or from the associated shortened sleep durations. We therefore examined changes in objective reaction time performance and subjective alertness in a 32-d inpatient protocol in which participants were scheduled to wakefulness durations below 16 h while on a 20-h "day," with randomization into standard sleep:wake ratio (1:2) or chronic sleep restriction (CSR) ratio (1:3.3) conditions. This protocol allowed determination of the contribution of sleep deficiency independent of extended wakefulness, since individual episodes of wakefulness in the CSR condition were only 15.33 h in duration (less than the usual 16 h of wakefulness in a 24-h day) and sleep episodes were 4.67 h in duration each cycle. We found that chronic short sleep duration, even without extended wakefulness, doubled neurobehavioral reaction time performance and increased lapses of attention fivefold, yet did not uniformly decrease self-reported alertness. Further, these impairments in neurobehavioral performance were worsened during the circadian night and were not recovered during the circadian day, indicating that the deleterious effect from the homeostatic buildup of CSR is expressed even during the circadian promotion of daytime arousal. These findings reveal a fundamental aspect of human biology: Chronic insufficient sleep duration equivalent to 5.6 h of sleep opportunity per 24 h impairs neurobehavioral performance and self-assessment of alertness, even without extended wakefulness.

Racial/Ethnic and Socio-Contextual Correlates of Chronic Sleep Curtailment in Childhood.

To examine the association between race/ethnicity and sleep curtailment from infancy to mid-childhood, and to determine the extent to which socioeconomic and contextual factors both explain racial/ethnic differences and are independently associated with sleep curtailment. We studied 1,288 children longitudinally in Project Viva, a pre-birth cohort study, from 6 months to 7 years of age. The main exposure was the child's race/ethnicity. The main outcome was a sleep curtailment score from 6 months to 7 years. The score ranged from 0-13, where 0 indicated maximal sleep curtailment and 13 indicated never having curtailed sleep. The mean (standard deviation) sleep curtailment score was 10.2 (2.7) points. In adjusted models (β [95% CI]), black (-1.92, [-2.39, -1.45] points), Hispanic (-1.58, [-2.43, -0.72] points), and Asian (-1.71, [-2.55, -0.86] points) children had lower sleep scores than white children. Adjustment for sociodemographic covariates attenuated racial/ethnic differences in sleep scores for black (by 24%) and Hispanic children (by 32%) but strengthened the differences for Asian children by 14%. Further adjustment for environmental and behavioral variables did not substantially change these differences. Independently, low maternal education, living in households with incomes < $70,000, viewing more TV, and having a TV in the child's bedroom were associated with lower sleep scores. Chronic sleep curtailment from infancy to mid-childhood was more prevalent among black, Hispanic, and Asian children. These differences were partially but not entirely explained by socio-contextual variables. Independently, children from lower socioeconomic status and those with greater exposures to TV also had greater sleep curtailment.

Sleep restriction acutely impairs glucose tolerance in rats.

Chronic sleep curtailment in humans has been related to impairment of glucose metabolism. To better understand the underlying mechanisms, the purpose of the present study was to investigate the effect of acute sleep deprivation on glucose tolerance in rats. A group of rats was challenged by 4‐h sleep deprivation in the early rest period, leading to prolonged (16 h) wakefulness. Another group of rats was allowed to sleep during the first 4 h of the light period and sleep deprived in the next 4 h. During treatment, food was withdrawn to avoid a postmeal rise in plasma glucose. An intravenous glucose tolerance test (IVGTT) was performed immediately after the sleep deprivation period. Sleep deprivation at both times of the day similarly impaired glucose tolerance and reduced the early‐phase insulin responses to a glucose challenge. Basal concentrations of plasma glucose, insulin, and corticosterone remained unchanged after sleep deprivation. Throughout IVGTTs, plasma corticosterone concentrations were not different between the control and sleep‐deprived group. Together, these results demonstrate that independent of time of day and sleep pressure, short sleep deprivation during the resting phase favors glucose intolerance in rats by attenuating the first‐phase insulin response to a glucose load. In conclusion, this study highlights the acute adverse effects of only a short sleep restriction on glucose homeostasis.

Prevalence of sleep deficiency and use of hypnotic drugs in astronauts before, during, and after spaceflight: an observational study

Sleep deprivation and fatigue are common subjective complaints among astronauts. Previous studies of sleep and hypnotic drug use in space have been limited to post-flight subjective survey data or in-flight objective data collection from a small number of crew members. We aimed to characterise representative sleep patterns of astronauts on both short-duration and long-duration spaceflight missions. For this observational study, we recruited crew members assigned to Space Transportation System shuttle flights with in-flight experiments between July 12, 2001, and July 21, 2011, or assigned to International Space Station (ISS) expeditions between Sept 18, 2006, and March 16, 2011. We assessed sleep-wake timing objectively via wrist actigraphy, and subjective sleep characteristics and hypnotic drug use via daily logs, in-flight and during Earth-based data-collection intervals: for 2 weeks scheduled about 3 months before launch, 11 days before launch until launch day, and for 7 days upon return to Earth. We collected data from 64 astronauts on 80 space shuttle missions (26 flights, 1063 in-flight days) and 21 astronauts on 13 ISS missions (3248 in-flight days), with ground-based data from all astronauts (4014 days). Crew members attempted and obtained significantly less sleep per night as estimated by actigraphy during space shuttle missions (7·35 h [SD 0·47] attempted, 5·96 h [0·56] obtained), in the 11 days before spaceflight (7·35 h [0·51], 6·04 h [0·72]), and about 3 months before spaceflight (7·40 h [0·59], 6·29 h [0·67]) compared with the first week post-mission (8·01 h [0·78], 6·74 h [0·91]; p<0·0001 for both measures). Crew members on ISS missions obtained significantly less sleep during spaceflight (6·09 h [0·67]), in the 11 days before spaceflight (5·86 h [0·94]), and during the 2-week interval scheduled about 3 months before spaceflight (6·41 h [SD 0·65]) compared with in the first week post-mission (6·95 h [1·04]; p<0·0001). 61 (78%) of 78 shuttle-mission crew members reported taking a dose of sleep-promoting drug on 500 (52%) of 963 nights; 12 (75%) of 16 ISS crew members reported using sleep-promoting drugs. Sleep deficiency in astronauts was prevalent not only during space shuttle and ISS missions, but also throughout a 3 month preflight training interval. Despite chronic sleep curtailment, use of sleep-promoting drugs was pervasive during spaceflight. Because chronic sleep loss leads to performance decrements, our findings emphasise the need for development of effective countermeasures to promote sleep. The National Aeronautics and Space Administration.

Chronic Sleep Curtailment and Adiposity

To examine the extent to which chronic sleep curtailment from infancy to mid-childhood is associated with total and central adiposity. We studied 1046 children participating in a prospective cohort study. At age 6 months and yearly from age 1 to 7 years, mothers reported their children's sleep duration in a usual 24-hour period. The main exposure was a sleep curtailment score from age 6 months to 7 years. The range of the total score was 0 to 13, where 0 indicated the maximal sleep curtailment and 13 indicated never having curtailed sleep. Outcomes in mid-childhood were BMI z score, dual X-ray absorptiometry total and trunk fat mass index (kg/m(2)), and waist and hip circumferences (cm). The mean (SD) sleep score was 10.2 (2.7); 4.4% scored a 0 to 4, indicating multiple exposures to sleep curtailment between age 6 months to 7 years, 12.3% scored 5 to 7, 14.1% scored 8 to 9, 28.8% scored 10 to 11, and 40.3% scored 12 to 13. In multivariable models, children who had a sleep score of 0 to 4 had a BMI z score that was 0.48 U (95% confidence interval, 0.13 to 0.83) higher than those who had a sleep score of 12 to 13. We observed similar associations of higher total and trunk fat mass index and waist and hip circumferences, and higher odds of obesity (odds ratio, 2.62; 95% confidence interval, 0.99 to 6.97) among children who had a score of 0 to 4 vs 12 to 13. Chronic sleep curtailment from infancy to school age was associated with higher overall and central adiposity in mid-childhood.

The effects of sleep restriction on neurobiological parameters

In modern 24-h society, the increasing work demands and lifestyle changes have resulted in the adults sleeping during the weeknights considerably less than the eight hours per night which is considered to be necessary to sustain optimal daytime functioning. Epidemiological studies have shown the association of short sleep duration and the increased risk of obesity, diabetes, cardiovascular diseases and cancer. Furthermore, laboratory studies in healthy, young adults have consistently demonstrated that chronic sleep restriction results in a number of abnormal physiologic changes including increased inflammatory markers and impaired blood glucose regulation suggesting the potential mechanisms whereby chronic sleep curtailment may affect health and longevity. Also, chronic sleep restriction results in a significant decrease of neurobehavioral performance (measured by Psychomotor Vigilance Task) as well as an increase in objective sleepiness levels (measured by Multiple Sleep Latency Test) which may lead to serious adverse effects in public safety.

Individual variation in sleep behaviour in blue tits Cyanistes caeruleus: assortative mating and associations with fitness‐related traits

Sleep is ubiquitous in animals, but there is great inter‐ and intraspecific variation in the daily amount of sleep that is needed. Chronic sleep curtailment or experimental sleep deprivation are known to impair health and performance of individuals, but not much is known about the fitness consequences of naturally occurring variation in sleep behaviour. Here we test for assortative mating in sleep behaviour and for correlations between sleep phenotypes and reproductive success and survival in a free‐living blue tit population. We found that partners of a social breeding pair were mated assortatively in regard to standardized awakening time, i.e. awakening time relative to that of other birds of the same sex in the population. We found no evidence for assortative mating for other sleep parameters. In female blue tits no sleep parameter that we measured was significantly correlated with lay date or clutch size. Females that had extra‐pair young in their brood did not differ in awakening time, or in any other sleep parameter, compared to females without extra‐pair young. In males, the probability of siring extra‐pair young was related to sleep onset and sleep duration, but not as predicted. Males that began to sleep earlier and slept longer were more likely to sire extra‐pair offspring. None of the sleep parameters were significantly correlated with local survival of first‐year birds. Our results suggest that there is no strong effect of variation in sleep behaviour on fitness in blue tits, at least under natural conditions. Such a relationship might only become evident when natural sleep patterns are experimentally disturbed, or when sleep quality is affected by anthropogenic noise or light pollution.

Sleep Curtailment and Workers' Productivity

To the Editor: In their landmark study, Dr Kowlessar et al concluded, “Modifiable health risks are associated with higher employer costs. Targeted programs that address these risks are expected to yield substantial savings.”1 In the current financially challenging period, these researchers have provided a practical, timely, and novel idea to improve the employers' bottom line. To the 11 Mayo-Clinic health risks Dr Kowlessar evaluated, we recommend adding one more: the growing public health problem of “chronic sleep curtailment.” Sleep deprivation is endemic in modern society. At least 15% of the US working population gets less than 5 hours sleep per night.2 Late night activities are pervasive parts of our life. We use sleep time as “safety net” time for unfinished daytime business. Naively, we extend an activity into the sleep-time, since our calendar contains nothing else scheduled there! Sleep restriction reduces testosterone levels in young healthy men, with consequent adverse effect on mental concentration at work, vigor, libido, muscle mass, bone density, and adiposity.3 The sleep-wake cycle is regulated by melatonin, a hormone secreted only in the dark. Melatonin promotes sleep by chemically causing drowsiness and lowering the body temperature. Melatonin is a powerful antioxidant, protects DNA, and may have beneficial effects on learning and memory.4When people sleep less, they spend less time in darkness, and therefore may develop hypomelatoninemia. Most importantly, sleep loss directly contributes to the causation of all of the 11 health risks Dr Kowlessar studied, namely obesity, hypertension, diabetes mellitus, hypercholesterolemia, inadequate exercise, poor nutrition, poor emotional health, hypertriglyceridemia, poor safety practices, smoking, and alcohol abuse.5,6 Several factors deprive people of a good 7 to 8 hours sleep. One striking example is the 7 PM or later start of many athletic and entertainment events. The situation may be worse on the US east coast where some games start at 9 PM local time to catch the west coast television audiences. By the time the event ends, and one navigates the traffic, it would be past midnight for retiring to sleep. How can there be time left for adequate sleep if one has to work at 7 AM the next morning? Likewise, many college classes are held in the late evening, with students staying over past midnight in the laboratories to finish assignments. Other common causes of sleep deprivation are late night TV watching and Internet use, and widespread caffeine abuse. Sleep is not a waste of time.6 To curb sleep deprivation, we need to make major changes in our lifestyle. For a start, sporting events should begin at 6 PM local time. West coast viewers could use TiVo-DVR (TiVo Inc, Alviso, CA) to record a Yankees home game! Academic coursework could be planned such that more use is made of the daylight hours. The American public is quite flexible in adjusting to a genuine need. For example, we readily adapt to an abrupt change from standard to daylight time and vice versa. A good night's sleep should reduce the prevalence and severity of the 11 health risks by primary prevention, and thereby improve the workers' general health and productivity. Since the vast majority of Americans are employed, the employment setting is the ideal venue, and as trusted Occupational Medicine specialists, we are the most suited professionals to bring about this sea change. Ghan-Shyam Lohiya, MD, MS, FACOEM Consultant, Occupational Medicine & Toxicology Royal Medical Group Santa Ana, Calif Eileene Humerez Student, Riverside Community College Norco, Calif Pavan Lohia Student, University High School Irvine, Calif

Effect of 1 Week of Sleep Restriction on Testosterone Levels in Young Healthy Men

To the Editor: Chronic sleep curtailment is endemic in modern societies. The majority of the daily testosterone release in men occurs during sleep.1 Sleep fragmentation and obstructive sleep apnea are associated with reduced testosterone levels.2 In older men, morning testosterone levels are partly predicted by total sleep time.3 Testosterone is critical in male sexual behavior and reproduction, but also has important beneficial effects on muscle mass and strength, adiposity, bone density, and vigor and well-being.4 We investigated the effect of 1 week of sleep restriction on testosterone levels in young healthy men.

Acute sleep deprivation reduces energy expenditure in healthy men

Epidemiologic evidence indicates that chronic sleep curtailment increases risk of developing obesity, but the mechanisms behind this relation are largely unknown. We examined the influence of a single night of total sleep deprivation on morning energy expenditures and food intakes in healthy humans. According to a balanced crossover design, we examined 14 normal-weight male subjects on 2 occasions during a regular 24-h sleep-wake cycle (including 8 h of nocturnal sleep) and a 24-h period of continuous wakefulness. On the morning after regular sleep and total sleep deprivation, resting and postprandial energy expenditures were assessed by indirect calorimetry, and the free-choice food intake from an opulent buffet was tested in the late afternoon at the end of the experiment. Circulating concentrations of ghrelin, leptin, norepinephrine, cortisol, thyreotropin, glucose, and insulin were repeatedly measured over the entire 24-h session. In comparison with normal sleep, resting and postprandial energy expenditures assessed on the subsequent morning were significantly reduced after sleep deprivation by ≈5% and 20%, respectively (P < 0.05 and P < 0.0001). Nocturnal wakefulness increased morning plasma ghrelin concentrations (P < 0.02) and nocturnal and daytime circulating concentrations of thyreotropin, cortisol, and norepinephrine (P < 0.05) as well as morning postprandial plasma glucose concentrations (P < 0.05). Changes in food intakes were variable, and no differences between wake and sleep conditions were detected. Our findings show that one night of sleep deprivation acutely reduces energy expenditure in healthy men, which suggests that sleep contributes to the acute regulation of daytime energy expenditure in humans.

Chronic sleep curtailment impairs the flexible implementation of task goals in new parents

Chronic sleep curtailment is a major concern for health in Western societies. Yet, research on potential consequences of long-term sleep curtailment on cognitive functions is still scarce. The present study investigated the link between chronic sleep limitation and executive functions that enable adaptation to changing environmental demands, i.e. the ability to flexibly implement task goals. To address the effects of chronic sleep restriction under real-life conditions, we considered a sample of adults who often suffer from reduced sleep durations over many months. One-hundred and six new parents (infant's age: 6-18months) were assigned to a sleep-curtailed group (<7h of nighttime sleep) and a non-sleep-curtailed group (≥7h of nighttime sleep), respectively, based on their self-reported average nighttime sleep duration over the preceding 6months. The ability to implement task goals was addressed applying a task-switching paradigm in which participants randomly switched between two tasks. While the two groups did not differ with regard to overall performance level, number of nighttime awakenings, naps during the day, daytime sleepiness, mood, chronic stress level and subjectively perceived cognitive capability, sleep-curtailed new parents showed higher costs for switching between tasks compared with repeating a task than non-sleep-curtailed new parents. This finding on the group level was further substantiated by a negative correlation between nighttime sleep duration and switch costs. With this study, we provide the first evidence for an impairment of the ability to flexibly implement task goals in chronically sleep-deprived new parents and, thus, for a link between chronic sleep curtailment and executive functions.

The metabolic consequences of sleep deprivation

The prevalence of diabetes and obesity is increasing at an alarming rate worldwide, and the causes of this pandemic are not fully understood. Chronic sleep curtailment is a behavior that has developed over the past 2-3 decades. Laboratory and epidemiological studies suggest that sleep loss may play a role in the increased prevalence of diabetes and/or obesity. Current data suggest the relationship between sleep restriction, weight gain and diabetes risk may involve at least three pathways: (1) alterations in glucose metabolism; (2) upregulation of appetite; and (3) decreased energy expenditure. The present article reviews the current evidence in support of these three mechanisms that might link short sleep and increased obesity and diabetes risk.