Sleep-deprived healthy persons experience increased hunger. They also have increased blood levels of leptin and decreased levels of ghrelin (hormones that regulate satiety and hunger). These hormon...

Brief communication: Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite.

https://escholarship.org/content/qt1jq9h1jp/qt1jq9h1jp.pdf

Sleep Disturbance, Sleep Duration, and Inflammation: A Systematic Review and Meta-Analysis of Cohort Studies and Experimental Sleep Deprivation

Sleep plays an important role in energy homeostasis. The present study tests the hypothesis that circulating levels of leptin, a hormone that signals energy balance to the brain, are influenced by sleep duration. We also analyzed associations between leptin and sympathovagal balance, cortisol, TSH, glucose, and insulin under different bedtime conditions. Twenty-four-hour hormonal and glucose profiles were sampled at frequent intervals, and sympathovagal balance was estimated from heart rate variability in 11 subjects studied after 6 d of 4-h bedtimes (mean +/- sem of sleep duration during last 2 d: 3 h and 49 +/- 2 min) and after 6 d of 12-h bedtimes (sleep: 9 h and 03 +/- 15 min). A study with 8-h bedtimes was performed 1 yr later (sleep: 6 h and 52 +/- 10 min). Caloric intake and activity levels were carefully controlled in all studies. Mean levels, maximal levels, and rhythm amplitude of leptin were decreased (-19%, -26%, and -20%, respectively) during sleep restriction compared with sleep extension. The decrease in leptin levels was concomitant with an elevation of sympathovagal balance. The effects of sleep duration on leptin were quantitatively associated with alterations of the cortisol and TSH profiles and were accompanied by an elevation of postbreakfast homeostasis model assessment values. Measures of perceived stress were not increased during sleep restriction. During the study with 8-h bedtimes, hormonal and metabolic parameters were intermediate between those observed with 4-h and 12-h bedtimes. In conclusion, sleep modulates a major component of the neuroendocrine control of appetite.

https://sites.oxy.edu/clint/physio/article/leptinlevelsaredependentonsleepduration.pdf

Leptin Levels Are Dependent on Sleep Duration: Relationships with Sympathovagal Balance, Carbohydrate Regulation, Cortisol, and Thyrotropin

Results: The median sleep time was 7 hours per night, with 27.1% of subjects sleeping 6 hours or less per night. Compared with those sleeping 7 to 8 hours per night, subjects sleeping 5 hours or less and 6 hours per night had adjusted odds ratios for DM of 2.51 (95% confidence interval, 1.57-4.02) and 1.66 (95% confidence interval, 1.15-2.39), respectively. Adjusted odds ratios for IGT were 1.33 (95% confidence interval, 0.832.15) and 1.58 (95% confidence interval, 1.15-2.18), respectively. Subjects sleeping 9 hours or more per night also had increased odds ratios for DM and IGT. These associations persisted when subjects with insomnia symptoms were excluded. Conclusions: A sleep duration of 6 hours or less or 9 hours or more is associated with increased prevalence of DM and IGT. Because this effect was present in subjects without insomnia, voluntary sleep restriction may contribute to the large public health burden of DM. Arch Intern Med. 2005;165:863-868

/pdf/association-of-sleep-time-with-diabetes-mellitus-and-2136l1eor0.pdf

Association of sleep time with diabetes mellitus and impaired glucose tolerance.

Sleep plays a vital role in brain function and systemic physiology across many body systems Problems with sleep are widely prevalent and include deficits in quantity and quality of sleep; sleep problems that impact the continuity of sleep are collectively referred to as sleep disruptions Numerous factors contribute to sleep disruption, ranging from lifestyle and environmental factors to sleep disorders and other medical conditions Sleep disruptions have substantial adverse short- and long-term health consequences A literature search was conducted to provide a nonsystematic review of these health consequences (this review was designed to be nonsystematic to better focus on the topics of interest due to the myriad parameters affected by sleep) Sleep disruption is associated with increased activity of the sympathetic nervous system and hypothalamic-pituitary-adrenal axis, metabolic effects, changes in circadian rhythms, and proinflammatory responses In otherwise healthy adults, short-term consequences of sleep disruption include increased stress responsivity, somatic pain, reduced quality of life, emotional distress and mood disorders, and cognitive, memory, and performance deficits For adolescents, psychosocial health, school performance, and risk-taking behaviors are impacted by sleep disruption Behavioral problems and cognitive functioning are associated with sleep disruption in children Long-term consequences of sleep disruption in otherwise healthy individuals include hypertension, dyslipidemia, cardiovascular disease, weight-related issues, metabolic syndrome, type 2 diabetes mellitus, and colorectal cancer All-cause mortality is also increased in men with sleep disturbances For those with underlying medical conditions, sleep disruption may diminish the health-related quality of life of children and adolescents and may worsen the severity of common gastrointestinal disorders As a result of the potential consequences of sleep disruption, health care professionals should be cognizant of how managing underlying medical conditions may help to optimize sleep continuity and consider prescribing interventions that minimize sleep disruption

/pdf/short-and-long-term-health-consequences-of-sleep-disruption-13vmodjcjv.pdf

Short- and long-term health consequences of sleep disruption.

The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on catecholamine and interleukin-2 (IL-2) levels in humans. Circulating levels of catecholamines and IL-2 were sampled every 30 min during 2 nights: undisturbed, baseline sleep and partial sleep deprivation-late night (PSD-L; awake from 0300-0600 h) in 17 healthy male volunteers. Sleep was monitored somnopolygraphically. Sleep onset was associated with a significant (P < 0.05) decline of circulating concentrations of norepinephrine and epinephrine, with a nocturnal nadir that occurred 1 h after nocturnal sleep. On the PSD-L night, levels of norepinephrine and epinephrine significantly (P < 0.05) increased in association with nocturnal awakening. During stage 3-4 sleep, levels of norepinephrine, but not epinephrine, were significantly lower (P < 0.05) compared to average levels during the awake period, stages 1-2 sleep, and rapid eye movement sleep. Nocturnal levels of circulating IL-2 did not change with sleep onset or in relation to PSD-L or the various sleep stages. We conclude that sleep onset is associated with changes in levels of circulating catecholamines. Loss of sleep and disordered sleep with decreases in slow wave sleep may serve to elevate nocturnal catecholamine levels and contribute to cardiovascular disease.

/pdf/effects-of-sleep-and-sleep-deprivation-on-catecholamine-and-5gctiigfnr.pdf

Effects of sleep and sleep deprivation on catecholamine and interleukin-2 levels in humans: clinical implications.

Background: Disturbances of sleep EEG are prominent in alcoholic patients, persist into recovery, and recently have been found to predict those alcoholics who are most likely to relapse. Increasing evidence indicates that there are ethnic differences in sleep EEG and that African-Americans may be at elevated risk for disordered sleep.



Methods: This study compared polysomnographic and spectral sleep EEG measures in male primary alcoholic inpatients (n= 31) and age-matched comparison controls (n= 31) stratified by African-American and Euro-American ethnicity.



Results: African-American alcoholic patients showed more severe sleep abnormalities than Euro-American alcoholics, and the interaction between alcohol dependence and ethnicity uniquely contributed to prolonged sleep latency (p < 0.001), loss of delta sleep (p < 0.001), and short rapid eye movement (REM) latency (p < 0.001). Spectral EEG analyses confirmed polysomnographic findings of disordered sleep architecture in alcoholics. Compared with controls, alcoholics had lower delta (0.75–4.5 Hz) activity over the whole night (p < 0.05), reductions in mean spectral power (0.75–40 Hz, p < 0.05), and decreases of delta (p < 0.01) and theta (4.5–7.5 Hz, p= 0.05) activity during the first period of non-REM sleep, with African-American alcoholics having the lowest theta of the four groups.



Conclusions: In view of the possible connection between relapse and poor sleep and the role of sleep in the maintenance of health, these data have implications for treatment and morbidity outcomes in African-American alcoholics.

Polysomnographic and spectral sleep EEG in primary alcoholics: an interaction between alcohol dependence and African-American ethnicity.

Background: Epidemiological data indicate that among alcoholics African-American men have higher rates of infections compared with white alcoholics. Alcohol is thought to reduce natural killer (NK) cell responses and to alter cellular immunity by changing the relative balance of Thl versus Th2 cytokine response profiles. However, translation of these basic immunological observations into the clinical setting is limited, and what clinical data are available are contradictory, in part, because of heterogeneity within the alcoholic patient population. Whether ethnic characteristics contribute to variation in the immunological effects of alcohol is not known. Methods: This study compared NK activity, interleukin (IL)-2-stimulated NK activity, and concanavalin A-stimulated peripheral blood mononuclear cell production of Th1 (IL-12 and IL-2), Th2 (IL-10), and proinflammatory (IL-6) cytokines in 31 hospitalized chronic alcoholic patients and 31 age-matched controls who were stratified on the basis of ethnicity. Results: NK-cell responses were significantly different across the four groups, and African-American alcoholics showed the lowest levels of NK activity (F = 9.5; p < 0.001) and IL-2-stimulated NK activity (F = 2.9; p < 0.05). Compared with the other three groups, African-American alcoholics also showed lower levels of IL-6 (F = 7.2; p < 0.01) and higher levels of IL-10 (F = 4.9; p < 0.05). Stimulated production of IL-2 and IL-12 were similar in the four groups. Regression analyses showed that alcohol dependence and ethnicity predicted NK activity, whereas the interaction between alcohol dependence and ethnicity predicted levels of IL-6 and IL-10. Conclusions: In summary, the immunological effects of alcohol dependence are modified by ethnicity status, consistent with the increased health risks found in African-American alcoholics.

Decreased natural killer cell responses and altered interleukin-6 and interleukin-10 production in alcoholism: an interaction between alcohol dependence and African-American ethnicity.

Claudine Miller

Papers

Effects of sleep and sleep deprivation on catecholamine and interleukin-2 levels in humans: clinical implications.

Polysomnographic and spectral sleep EEG in primary alcoholics: an interaction between alcohol dependence and African-American ethnicity.

Decreased natural killer cell responses and altered interleukin-6 and interleukin-10 production in alcoholism: an interaction between alcohol dependence and African-American ethnicity.