Energy balance and sleep quality -
digestive, oral, and skin physiology. Eating behavior. Energy Metabolism - physiology. Environmental health. Feeding Behavior - physiology. Feeding Behavior - psychology.
Fundamental and applied biological sciences. Internal medicine. Medical sciences. Metabolic diseases. Obesity - etiology. Obesity - psychology. Sleep - physiology. Sleep in non-human animals. Short sleep duration, poor sleep quality, and later bedtimes are all associated with increased food intake, poor diet quality, and excess body weight.
Insufficient sleep seems to facilitate the ingestion of calories when exposed to the modern obesogenic environment of readily accessible food. Lack of sleep has been shown to increase snacking, the number of meals consumed per day, and the preference for energy-rich foods.
Proposed mechanisms by which insufficient sleep may increase caloric consumption include: 1 more time and opportunities for eating, 2 psychological distress, 3 greater sensitivity to food reward, 4 disinhibited eating, 5 more energy needed to sustain extended wakefulness, and 6 changes in appetite hormones.
Globally, excess energy intake associated with not getting adequate sleep seems to be preferentially driven by hedonic rather than homeostatic factors. Moreover, the consumption of certain types of foods which impact the availability of tryptophan as well as the synthesis of serotonin and melatonin may aid in promoting sleep.
In summary, multiple connections exist between sleep patterns, eating behavior and energy balance. Sleep should not be overlooked in obesity research and should be included as part of the lifestyle package that traditionally has focused on diet and physical activity. Abstract There is increasing evidence showing that sleep has an influence on eating behaviors.
Amsterdam: Elsevier Inc. Elsevier ScienceDirect College Edition Collection - Health and Life Sciences eJournals. ISSN: EISSN: X. DOI: Dickson, I. Sadaf Farooqi, Sebastian M. The rise in obesity has been paralleled by a decline in sleep duration in epidemiological studies.
Sleep architecture, duration of sleep stages, and sleep-associated respiratory parameters were measured by polysomnography. Two days of caloric restriction significantly increased the duration of deep stage 4 sleep These findings provide a mechanistic framework for investigating the association between sleep duration and obesity risk.
Our results are in line with a study in the early s in which the duration of slow wave sleep increased after 4 days of complete starvation associated with weight loss. Taken together, these studies and previous studies of sleep deprivation provide a mechanistic framework for investigating the well-recognized associations between obesity and sleep disorders and between sleep debt and obesity risk.
The rising prevalence of obesity and associated disorders such as type 2 diabetes is associated with significant morbidity and mortality and represents a major public health concern. Reduced levels of physical activity and the increased consumption of highly palatable energy dense foods are major contributors to the rise in body mass index BMI.
Another factor that has been associated with an increased risk of obesity is an increase in sleep debt. CR was followed by a period of free feeding FF to allow for energy homeostasis to be reset. We measured ad libitum food intake to quantify changes in energy balance during this experimental paradigm.
We assessed sleep architecture and sleep-associated respiratory parameters in the baseline state, after CR, and upon FF using polysomnography PSG , which combines overnight electroencephalographic recording with measurements of chest wall movements, eye movements, and peripheral oxygen saturation.
In response to physiological stresses such as CR, hypothalamic pathways activate autonomic, neuroendocrine, and behavioral responses to maintain homeostasis. Therefore, we measured heart rate autonomic nervous system activity , the overnight pulsatile secretion of thyroid-stimulating hormone TSH , growth hormone GH , and cortisol release, as well as cognitive parameters and mood-related symptom scores.
The study was approved by the Cambridge local research ethics committee and was conducted in accordance with the principles of the Declaration of Helsinki. Written informed consent was received from each participant prior to inclusion in the study.
All clinical studies were conducted at the NIHR-Wellcome Trust Clinical Research Facility, Adden-brooke's Hospital, Cambridge, United Kingdom.
Participants were residents on the Clinical Research Facility for the duration of the study under direct observation. They were invited to eat freely; food consumption was covertly measured.
Seven volunteers continued to an additional day of FF Figure S1 in the supplemental material. We performed PSG and measured metabolic, neuroendocrine, autonomic, and cognitive parameters at baseline, after CR, and FF, as detailed in the following paragraphs. PSG for the assessment of sleep was performed during all nights using a SomnoScreen Plus device SOMNOmedics GmbH, Randesacker, Germany.
Electrodes were attached to the scalp Cz, C3, C4, O1, O2, A1, A2, Gnd for electroencephalographic EEG recordings, above, below, and beside the eyes for horizontal and vertical electrooculogram, and on the chin for electromyogram.
Recordings were scored offline by one investigator S. according to standard criteria by Rechtschaffen and Kales, 11 and independently assessed by a second sleep laboratory analyst unaware of the study design and hypothesis.
The following sleep parameters were determined: sleep period time SPT, i. All participants attended a prestudy overnight recording session with PSG to ensure that they had normal sleep architecture.
Plasma glucose, insulin, leptin, serum lipids, TSH, free thyroxin, GH, and cortisol, as well as routine biochemical and hematological assays were performed using standard commercially available assays. Concentrations of both total ghrelin and plasma orexin A were assessed using commercially available enzyme-linked immunosorbent assay kits for humans EZGRTK; Millipore, Billerica, MA and Uscn Life Science Inc.
For overnight pulsatility analysis, we collected serum samples every 10 min from to , via a long line running from the participants to the adjacent room to avoid any interference with their sleep. Cluster analysis was used for the detection of discrete TSH, GH, and cortisol peaks.
For the current analysis a 2 × 1 test cluster configuration was used, two data points for the test nadir and one for the test peak, and a t -statistic of 2. The locations and widths of all significant concentration peaks were identified, the total number of peaks was counted, and the mean peak interval was calculated in minutes as well as peak height, width, and area.
In addition, valley mean and nadir, area under the curve, and total average value were calculated. Blood pressure was measured using a wrist-type blood pressure monitor OMRON Healthcare, Hamburg, Germany.
Heart rate was measured continuously using a wireless sensor applied to the chest wall Actiheart, CamNtech Ltd, Cambridge, UK. This digitalizes the electrocardiogram signal and stores the R-R interval time-series from which heart rate can be calculated.
Heart rate data was exported to a spreadsheet via Actiheart software version 4. Sleep data collected by the PSG device was examined to determine a window of time min between and during which each participant was asleep.
Average heart rate while sleeping and on waking was calculated, and the difference between average asleep and average waking heart rate for each participant on each day was recorded.
Using validated questionnaires we collected data on neuroglycopenia and autonomic symptoms, 13 mood, 14 and sleepiness. We measured alertness by reaction times and error rates in a computer-based vigilance performance test during the three study phases.
Unless specified otherwise, data are expressed as mean and SEM. Data were tested for normality using graphical and numerical methods Shapiro-Wilk test. Data were compared by analysis of variance ANOVA with repeated measures to test for within-subjects changes.
The within-subjects P value was adjusted using the Greenhouse-Geisser correction factor for lack of sphericity. Pairwise comparisons of the study phases were performed by two-sided Student t -test when appropriate. by multiplying the uncorrected P value by the number of comparisons. For analyses of correlation between fasting hormones and sleep parameters, the nonparametric Spearman correlation test was used and repeated in sensitivity analyses excluding outliers.
Data were analyzed using Stata software package version Twelve adult males mean age Blood pressure, body composition, baseline biochemical and hematological parameters, and self-reported quality of sleep scores were within normal ranges Table S1 in the supplemental material.
However, those individuals provided with ad libitum meals for a third day continued to overeat, eating 2, kcal in excess on the third day Figure 1A. Barcharts of changes in the duration of sleep stages at baseline, during caloric restriction, and free feeding; and scatterplots of overnight pulsatile secretion of thyroid-stimulating hormone, growth hormone, and cortisol.
Durations of all sleep stages were analyzed using analysis of variance ANOVA with repeated measures to test for within-subject changes. Pairwise comparisons of the three study phases were performed by two-sided Student t -test when appropriate. A P value of 0. D—F Pulsatile secretion of thyroid-stimulating hormone D , growth hormone E and cortisol secretion F was measured in blood samples taken every 10 min from midnight until at baseline, after 2 days of caloric restriction and after 2 days of free feeding.
PSG recordings were performed at baseline, after CR and FF, and were visually scored by investigators blinded to the study design.
TST and sustained sleep efficiency were not affected by changes in energy balance Table 1. Disordered sleep has been associated with impaired memory retention. Alertness, as measured by reaction times and error rates in a vigilance performance test, did not change during the study data not shown.
Sleep-dependent consolidation of procedural and declarative memory tested by a standard finger tapping task and paired associate word learning task were preserved during all study phases Figure S2 in the supplemental material and not modified by changes in energy balance.
There was a discrete improvement in overall mood score as assessed by the Profile Of Mood States POMS questionnaire immediately upon FF compared to CR, but no significant changes in mood subdomains Table S2 in the supplemental material.
Changes in energy balance can affect the hypothalamic regulation of pituitary hormone synthesis and secretion, which may in turn influence sleep architecture. We measured serum TSH, GH, and cortisol release a marker of hypothalamopituitary adrenal axis activation every 10 min for 6 h overnight when participants were asleep as confirmed by PSG recordings.
Mean hormone concentrations and parameters of pulsatile secretion were analyzed at baseline, after CR and FF using the pulse detection cluster algorithm Table 2 ; Table S3 in the supplemental material.
There were no differences in the number of pulses and pulse width. There was no change in the pulsatile secretion of GH from baseline to CR, whereas FF was associated with a decrease in mean GH concentrations and integrated total AUC compared to baseline and CR values Figure 1E ; Table 2.
In conjunction, the interval between peaks was longer during FF compared to baseline. No differences in cortisol secretion were seen as result of changes in energy balance Figure 1F ; Table S3 in the supplemental material.
Analysis of pulsatile thyroid-stimulating hormone and growth hormone secretion. To examine activation of the autonomic nervous system, we measured heart rate continuously throughout the study.
The mean sleeping heart rate predominantly influenced by para-sympathetic tone was unchanged after CR but increased by 5. The increase in heart rate on waking sleeping-to-waking heart rate increment; predominantly due to sympathetic nervous system activation increased from 5.
Autonomic symptoms predominantly adrenergic were more prominent upon CR and decreased in FF Table S4 in the supplemental material. Barcharts of changes in heart rate at baseline, during caloric restriction, and free feeding. Mean sleeping heart rate A and the sleeping-to-waking heart rate increment B were measured every night in all 12 participants at baseline, during caloric restriction and free feeding.
Vertical bars represent the standard error of the mean. Measurements were compared using analysis of variance ANOVA with repeated measures to test for within-subject changes. Fasting plasma glucose decreased by 1.
Plasma ghrelin levels exhibit diurnal variation, act as a short-term hunger signal peaking before meal initiation, and are affected by sleep restriction. Barcharts of changes in peripheral hormones and orexin at baseline, during caloric restriction, and free feeding. Hormone levels were compared using analysis of variance ANOVA with repeated measures to test for within-subject changes.
We hypothesized that changes in peripheral hormones or in orexin might mediate the change in duration of stage 4 sleep seen with CR. Although there was no correlation between fasting leptin, insulin, or total ghrelin and the duration of stage 4 sleep in CR data not shown , plasma orexin levels correlated with specific sleep parameters after 48 h of CR Figure 4A.
Scatterplots of correlation of plasma orexin A levels with sleep parameters after 48 h of caloric restriction CR among nine participants. The duration of stage 4 sleep correlated positively with orexin level in CR A , as well as orexin decline from baseline to CR B.
There was no correlation between the number of awakenings and the absolute level of orexin in CR C. The number of awakenings in CR correlated negatively with orexin decline from baseline to CR D.
In this study we found that acute CR for 2 days significantly increased the duration of the deepest stage of sleep, stage 4 sleep. The effect of CR on stage 4 sleep was normalized with FF, which restored energy balance. Our findings align with a study from the s that observed an increased duration of SWS stages 3 and 4 together and reduced REM sleep in males studied before and after four days of complete starvation associated with weight loss, with reversal of these changes in refeeding characterized by weight regain.
One possibility is that increasing the time spent in the deepest stage of sleep may allow for the conservation of energy resources in response to acute CR. To date, very little is known about sleep architecture in rare severely obese patients with congenital leptin deficiency, a disorder that is often complicated by marked central and obstructive sleep apneas own observations.
We found that the decline in plasma orexin from baseline to CR was positively correlated with the duration of stage 4 sleep in CR and inversely correlated with the number of awakenings.
This finding is intriguing but will require further investigation. We do not know whether, or how far, plasma orexin levels reflect orexin-mediated signaling in the brain. However, Strawn et al. These observations in healthy volunteers are entirely consistent with studies in patients with genetic disruption of leptin signaling 34 , 35 and in individuals with obesity following weight loss 36 a state of partial leptin deficiency.
These physiological changes were predominantly mediated by falling leptin concentrations and could be reversed by concomitant leptin administration in previous studies.
However, intriguingly, we found that these parameters exceeded baseline values after 2 days of FF. The explanation for these findings is unclear.
Such changes could contribute to an exaggerated compensatory response to CR, for example, by overeating. Some participants were studied during a third day of FF as we hypothesized that their food intake would return to baseline levels. These findings warrant further investigation and, if replicated, may shed light on the physiological response to weight loss and the mechanisms that promote weight regain.
In this study, we did not observe a significant change in GH pulses with CR in contrast to some, but not all, previous studies.
Notably, we found that mean GH concentrations and integrated total AUC were significantly reduced during FF compared to baseline and CR.
The pulsatile secretion of GH is predominantly the product of stimulatory GH-releasing hormone GHRH -expressing neurons and inhibitory somatostatin-expressing neurons in the hypothalamus. Leptin treatment of rats food deprived for 48 h increases somatostatin messenger RNA levels, 38 which would result in suppression of pulsatile GH secretion as seen in this study.
It is recognized that pulsatile GH secretion is suppressed in obesity, but it is striking that we observed comparable levels of GH suppression after 2 days of FF when participants were consuming excess calories but had restored energy balance.
Variations in pulsatile release define the physiological actions of GH, which is a critical mediator of insulin action and glucose homeostasis. We postulate that the suppression of GH secretion as seen in this study may reflect the physiological response to maintain glucose homeostasis in light of excess caloric consumption.
This hypothesis requires further testing in experimental studies. These studies provide a mechanistic framework for investigating the well-recognized associations between obesity and sleep disorders and between sleep debt and obesity risk.
The authors thank the volunteers who took part in the study, as well as Dr. Keith Burling and Dr. Peter Barker who performed the biochemical assays NIHR Cambridge Biomedical Research Centre Core Biochemical Assay Laboratory. Google Scholar.
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Ablance was not an industry supported study. Energy balance and sleep quality work was supported Natural energy drinks the Wellcome Trust to Dr. van der Klaauw balancd Dr. Farooqibaance Energy balance and sleep quality Institute for Health Research Cambridge Biomedical Research Centre, the European Research Council, the Bernard Wolfe Health Neuroscience Fund all to Dr. Farooqithe Swiss National Science Foundation PBLAP, P3SMP, to Dr. Colletthe European Society of Endocrinology IESP grant, to Dr. Schmid and the German Research Foundation TR-SFBB01, to Dr. Thank Enerty for visiting nature. You are using ablance browser version Broccoli and cheddar dishes limited support for Balancf. To obtain the best Eneryg, we recommend you use a more up to date browser or turn off Belly fat burner motivation mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. It is unknown whether short sleep duration causatively contributes to weight gain. Studies investigating effects of partial sleep deprivation PSD on energy balance components report conflicting findings. Our objective was to conduct a systematic review and meta-analysis of human intervention studies assessing the effects of PSD on energy intake EI and energy expenditure EE.
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