Plamen D. Penev

Bio: Plamen D. Penev is an academic researcher from University of Chicago. The author has contributed to research in topics: Sleep deprivation & Sleep restriction. The author has an hindex of 19, co-authored 24 publications receiving 4037 citations. Previous affiliations of Plamen D. Penev include University of Wisconsin-Madison.

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

Abstract: 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.

Impact of Sleep and Sleep Loss on Neuroendocrine and Metabolic Function

Abstract: Background: Sleep exerts important modulatory effects on neuroendocrine function and glucose regulation. During the past few decades, sleep curtailment has become a very common behavior in industrialized countries. This trend toward shorter sleep times has occurred over the same time period as the dramatic increases in the prevalence of obesity and diabetes. Aims: This article will review rapidly accumulating laboratory and epidemiologic evidence indicating that chronic partial sleep loss could play a role in the current epidemics of obesity and diabetes. Conclusions: Laboratory studies in healthy young volunteers have shown that experimental sleep restriction is associated with a dysregulation of the neuroendocrine control of appetite consistent with increased hunger and with alterations in parameters of glucose tolerance suggestive of an increased risk of diabetes. Epidemiologic findings in both children and adults are consistent with the laboratory data.

Insufficient Sleep Undermines Dietary Efforts to Reduce Adiposity

Abstract: Decreased sleep time has been suggested to contribute to obesity. This study assigned 10 healthy adults to sleep either 5.5 hours or 8.5 hours each night in conjunction with moderate caloric restri...

Short Sleep Duration Is Associated with Reduced Leptin, Elevated Ghrelin, and Increased Body Mass Index

Abstract: Background Sleep duration may be an important regulator of body weight and metabolism. An association between short habitual sleep time and increased body mass index (BMI) has been reported in large population samples. The potential role of metabolic hormones in this association is unknown. Methods and Findings Study participants were 1,024 volunteers from the Wisconsin Sleep Cohort Study, a population-based longitudinal study of sleep disorders. Participants underwent nocturnal polysomnography and reported on their sleep habits through questionnaires and sleep diaries. Following polysomnography, morning, fasted blood samples were evaluated for serum leptin and ghrelin (two key opposing hormones in appetite regulation), adiponectin, insulin, glucose, and lipid profile. Relationships among these measures, BMI, and sleep duration (habitual and immediately prior to blood sampling) were examined using multiple variable regressions with control for confounding factors. A U-shaped curvilinear association between sleep duration and BMI was observed. In persons sleeping less than 8 h (74.4% of the sample), increased BMI was proportional to decreased sleep. Short sleep was associated with low leptin (p for slope = 0.01), with a predicted 15.5% lower leptin for habitual sleep of 5 h versus 8 h, and high ghrelin (p for slope = 0.008), with a predicted 14.9% higher ghrelin for nocturnal (polysomnographic) sleep of 5 h versus 8 h, independent of BMI.

About sleep's role in memory

Abstract: Over more than a century of research has established the fact that sleep benefits the retention of memory. In this review we aim to comprehensively cover the field of "sleep and memory" research by providing a historical perspective on concepts and a discussion of more recent key findings. Whereas initial theories posed a passive role for sleep enhancing memories by protecting them from interfering stimuli, current theories highlight an active role for sleep in which memories undergo a process of system consolidation during sleep. Whereas older research concentrated on the role of rapid-eye-movement (REM) sleep, recent work has revealed the importance of slow-wave sleep (SWS) for memory consolidation and also enlightened some of the underlying electrophysiological, neurochemical, and genetic mechanisms, as well as developmental aspects in these processes. Specifically, newer findings characterize sleep as a brain state optimizing memory consolidation, in opposition to the waking brain being optimized for encoding of memories. Consolidation originates from reactivation of recently encoded neuronal memory representations, which occur during SWS and transform respective representations for integration into long-term memory. Ensuing REM sleep may stabilize transformed memories. While elaborated with respect to hippocampus-dependent memories, the concept of an active redistribution of memory representations from networks serving as temporary store into long-term stores might hold also for non-hippocampus-dependent memory, and even for nonneuronal, i.e., immunological memories, giving rise to the idea that the offline consolidation of memory during sleep represents a principle of long-term memory formation established in quite different physiological systems.

Adverse metabolic and cardiovascular consequences of circadian misalignment

Abstract: Effects of Behavioral Cycle. The effects of the behavioral cycle, independent of the circadian cycle, on leptin, glucose, insulin, epinephrine, norepinephrine, and cortisol are shown in Fig. 2, Left panels. Leptin varied significantly across the behavioral cycle, with a trough around breakfast and a peak after the last meal, coinciding with the onset of the scheduled sleep episode (P 0.001, peak-to-trough 44%). Also, both glucose and insulin varied significantly across the behavioral cycle (glucose: P 0.001, peak-to-trough 26%; insulin: P 0.001, peak-to-trough 158%), presumably the result of the timing of meals. Both epinephrine and norepinephrine varied significantly across the behavioral cycle with peaks during the wake episode and troughs during the sleep episode (epinephrine: P 0.001, peak-totrough 83%; norepinephrine: P 0.001, peak-to-trough 72%). Cortisol varied significantly across the behavioral cycle, peaking after awakening and with a trough at the onset of the scheduled sleep episode (P 0.001, peak-to-trough 38%). Effect of Circadian Cycle. The effects of the circadian cycle, independent of the behavioral cycle, on leptin, glucose, insulin, epinephrine, norepinephrine, and cortisol, are shown in Fig. 2, Right panels. Glucose had a significant endogenous circadian rhythm (P 0.018, peak-to-trough 4%), with a peak during the biological night (circadian bin 300° and 0°; equivalent to22:30– 06:30 in these subjects). Epinephrine exhibited a significant endogenous circadian rhythm (P 0.001, peak-to-trough 53%), with a peak during the biological day (circadian bin 180°; equivalent to 14:30–18:30). Cortisol had a significant endogenous circadian rhythm (P 0.001, peak-to-trough 113%), with a peak at the end of the biological night (60°; close to habitual wake time). There were no significant circadian rhythms in leptin, insulin, or norepinephrine.

Meta-Analysis of Short Sleep Duration and Obesity in Children and Adults

Abstract: IN THE LAST FEW DECADES THERE HAS BEEN A SIGNIFICANT INCREASE IN THE PREVALENCE OF OBESITY WORLDWIDE AND THE WORLD HEALTH organization has declared it a global epidemic.1 Obesity in childhood is a cause of psychosocial problems including low self esteem,2 and frequently continues into adulthood3 where it is a cause of major morbidity and mortality including cardiovascular disease and type 2 diabetes. At the same time there has been a reduction in sleep time. National surveys in USA have shown a decline in self-reported sleep duration over the past 50 years by 1.5 to 2 hours.4 This sleep curtailment has been attributed to lifestyle changes. Several studies have reported associations between duration of sleep (short as well as long) and ill-health, including relationships with self-reported well-being,5 morbidity and mortality,6–12 and with chronic conditions including type 2 diabetes, respiratory disorders, hypertension, and obesity.13–18 The associations between short duration of sleep and obesity, in particular, have stimulated a debate given the potential implications for children19,20 as well as adults.21,22 However, given the variety of studies and the large differences in the target populations, it is difficult to draw immediate conclusions on the consistency of the association, the direction of causality and the likely mechanisms involved. The aims of this article are to (i) systematically review published population-based studies, (ii) to carry out a meta-analysis to assess whether the evidence supports the presence of a relationship between short sleep duration and obesity at different ages, and (iii) to obtain a quantitative estimate of the risk in order to assess the consistency and potential public health relevance

Sleep Duration and All-Cause Mortality: A Systematic Review and Meta-Analysis of Prospective Studies

Abstract: Background: Increasing evidence suggests an association between both short and long duration of habitual sleep with adverse health outcomes. Objectives: To assess whether the population longitudinal evidence supports the presence of a relationship between duration of sleep and all-cause mortality, to investigate both short and long sleep duration and to obtain an estimate of the risk. Methods: We performed a systematic search of publications using MEDLINE (1966-2009), EMBASE (from 1980), the Cochrane Library, and manual searches without language restrictions. We included studies if they were prospective, had follow-up >3 years, had duration of sleep at baseline, and all-cause mortality prospectively. We extracted relative risks (RR) and 95% confidence intervals (CI) and pooled them using a random effect model. We carried out sensitivity analyses and assessed heterogeneity and publication bias. Results: Overall, the 16 studies analyzed provided 27 independent cohort samples. They included 1,382,999 male and female participants (follow-up range 4 to 25 years), and 112,566 deaths. Sleep duration was assessed by questionnaire and outcome through death certification. In the pooled analysis, short duration of sleep was associated with a greater risk of death (RR: 1.12; 95% CI 1.06 to 1.18; P <0.01) with no evidence of publication bias (P = 0.74) but heterogeneity between studies (P = 0.02). Long duration of sleep was also associated with a greater risk of death (1.30; [1.22 to 1.38]; P < 0.0001) with no evidence of publication bias (P = 0.18) but significant heterogeneity between studies (P < 0.0001). Conclusion: Both short and long duration of sleep are significant predictors of death in prospective population studies.