Energy balance and sleep quality -
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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Journal Article. Tinh-Hai Collet, MD , Tinh-Hai Collet, MD. Oxford Academic. Individuals were required to have stable self-reported sleep habits for the past 6 months. They were recruited from the community and completed an initial online survey followed by a face-to-face interview.
Race and ethnicity data were self-reported at this time and included the following race and ethnicity categories: Asian, Black or African American, Hispanic, and White. Those who met the inclusion criteria underwent laboratory screening polysomnography, oral glucose tolerance test, and blood tests to determine eligibility.
Habitual sleep duration was confirmed by a 1-week screening wrist actigraphy at home. Detailed eligibility criteria are provided in the eMethods in Supplement 2.
After a 2-week habitual sleep period at baseline, participants were randomized to either 2-week sleep extension sleep extension group or 2-week continued habitual sleep control group Figure 1.
Participants continued their daily routine activities at home without any prescribed diet or physical activity. This approach allowed us to capture habitual sleep-wake patterns without influencing participants' usual behavior or creating selection bias with only participants interested in improving sleep habits.
After study completion, all participants were provided with information about the health benefits of optimal sleep duration. Block randomization, stratified by sex, was performed using computer-generated random numbers.
Before the trial, randomization assignments were prepared by a biostatistician K. using opaque, sealed, and numbered envelopes and were given to the research coordinator E.
Sleep-wake patterns were continuously monitored at home by wrist actigraphy throughout the 4-week study. Participants were asked to wear an accelerometer motion -based monitor Actiwatch Spectrum Plus; Philips and to press a built-in event marker button when they went to bed to sleep each night and when they got out of bed each morning.
Sleep was automatically scored Actiware, version 6. During the 2-week baseline, all participants were instructed to continue their habitual sleep patterns at home.
On the morning of day 15, participants met with study investigators E. and E. in the research center. Those who were randomized to the sleep extension group received individualized sleep hygiene counseling through a structured interview E. eMethods in Supplement 2. On day 22, participants returned for a brief follow-up visit.
Actigraphy data from the first intervention week were reviewed, and further sleep counseling was provided as needed.
To minimize any imbalance in contact with the investigators between the 2 groups, we asked participants in the control group to meet with the study investigators on days 15 and Actigraphy data of these participants were downloaded, but the participants did not receive any specific sleep recommendations and were instructed to continue their daily routine and habitual sleep behaviors until the end of the study.
For each 2-week period, the energy intake was calculated from the sum of total energy expenditure and change in body energy stores using the principle of energy balance.
Participants were provided a cellular-enabled weight scale BodyTrace; BodyTrace Inc and instructed to take their nude weights twice every morning after awakening before eating or drinking. Weight values were hidden from the participants to minimize potential influence on behavior.
Changes in body composition were converted to changes in energy stores using 9. Thermic effect of the meal was calculated, which was previously described elsewhere.
The primary outcome was change in energy intake from baseline. Categorical data are presented as counts and percentages. Continuous data are presented as means and SDs.
Linear mixed-effects models were fit to determine the treatment differences between the groups. To confirm the robustness of primary findings, we fit additional models using the analysis of covariance approach with the period 2 value as the dependent variable, treatment group as the independent variable, and period 1 value as covariates.
In secondary analyses, mixed models that adjusted for sex or menstrual cycle were also fit; these covariates were chosen because of the known influence of menstrual cycle on short-term changes in weight. A Pearson correlation coefficient was calculated to assess the relationships between the changes from baseline in sleep duration and the changes from baseline in energy intake.
No adjustments were made to P values or CIs for multiple comparisons. Baseline characteristics of participants with complete data were compared with those of participants with incomplete data using unpaired, 2-tailed t tests and Fisher exact tests.
No imputation for missing values was performed. Of the adults who provided consent and were assessed for eligibility, 81 were randomized 41 to the control group and 40 to the sleep extension group initially Figure 1.
One participant in the control group revealed adhering to a weight loss regimen and thus did not meet the study inclusion criteria and was deemed ineligible after randomization.
Baseline characteristics of participants were similar between randomization groups Table 1. None of the participants were using any antihypertensive or lipid-lowering agents or any prescription medication that can affect sleep or metabolism. Figure 2 illustrates the mean nightly sleep duration by actigraphy in each group throughout the 4-week study.
Participants in the sleep extension group had a significant increase from baseline in mean sleep duration by actigraphy compared with those in the control group 1.
The findings were similar with regard to change in sleep duration when only participants' workdays 1. No difference was found in change in sleep efficiency percentage of time spent asleep during time in bed between the 2 groups —0.
Figure 3 A through D illustrates the changes from baseline in energy intake and the changes from baseline in sleep duration in individual participants. There was a significant increase in energy intake from baseline in the control group No statistically significant treatment effect was found in total energy expenditure or other measures of energy expenditure Table 2.
There was weight gain from baseline in the control group 0. The findings on energy intake, energy expenditure, and weight were similar after adjustment for the effects of sex or menstrual cycle. No statistically significant differences in baseline characteristics were found between the 75 participants The proportion of participants with complete data on energy intake was not significantly different between the sleep extension and control groups When all reported outcomes were considered, no significant differences except for depressive symptoms in baseline characteristics were found between participants with complete data and participants with incomplete or missing data eTable 3 in Supplement 2.
The proportion of participants with complete data on all reported outcomes was similar between the sleep extension and control groups In this RCT of adults with overweight who habitually curtailed their sleep duration, sleep extension reduced energy intake and resulted in a negative energy balance ie, energy intake that is less than energy expenditure in real-life settings.
To our knowledge, this study provides the first evidence of the beneficial effects of extending sleep to a healthy duration on objectively assessed energy intake and body weight in participants who continued to live in their home environment.
Modest lifestyle changes in energy intake or expenditure are increasingly promoted as viable interventions to reverse obesity. Nevertheless, these modeling predictions on weight change suggest that continued adequate sleep duration and beneficial effect on energy intake could translate into clinically meaningful weight loss and help reverse or prevent obesity.
Thus, the findings of this study may have important public health implications for weight management and policy recommendations. The findings of decreased energy intake, negative energy balance, and weight reduction resulting from sleep extension are in agreement with the findings of short-term laboratory sleep-restriction studies showing increased energy intake and weight gain 17 as well as the findings of prospective epidemiologic studies linking sleep restriction to obesity risk.
A few observations suggest that sleeping 7 to 8 hours per night is associated with greater success in weight loss interventions. In this RCT, we found an overall increase in objective sleep duration of approximately 1.
The change in sleep duration from baseline varied between participants and from night to night in the real-life setting. Overall, the sleep extension group compared with the control group had significantly higher subjective scores in obtaining sufficient sleep, with more daytime energy and alertness and better mood eTable 4 in Supplement 2.
Similar to a previous study of sleep extension, 22 the present RCT used an individualized counseling approach. Another study used bedtime extension in habitual short sleepers in real-life conditions but obtained variable benefits on sleep, likely because of a lack of an individualized approach or appropriate blinding.
Future similarly rigorous intervention studies of longer duration and using objective assessments of energy balance under real-life conditions are warranted to elucidate the underlying mechanisms and to investigate whether sleep extension could be an effective, scalable strategy for reversing obesity in diverse populations.
Along with a healthy diet and regular physical activity, healthy sleep habits should be integrated into public messages to help reduce the risk of obesity and related comorbidities. This study has several strengths. The major strengths are the randomized design and the objective tracking of energy intake and sleep in real-life settings.
Most epidemiologic studies linking short sleep duration to body weight relied on self-reported dietary intake. We used a validated method to objectively track energy intake by the doubly labeled water method and change in energy stores.
Participant blinding and use of actigraphy allowed us to capture true habitual sleep patterns at baseline. This study also has several limitations.
We enrolled adults with overweight and used selective eligibility criteria, which may limit generalizability to more diverse populations. The increase in energy intake and weight from baseline that we observed in the control group may have contributed to the significant treatment effects.
However, in RCTs, performing a between-group comparison, rather than separate tests against baseline within the groups, is strongly recommended. We did not assess the underlying biological mechanisms of food frequency and the circadian timing of food intake.
Multiple interrelated factors could contribute to the finding of decreased energy intake after sleep extension. This RCT found that short-term sleep extension reduced objectively measured energy intake and resulted in a negative energy balance in real-life settings in adults with overweight who habitually curtailed their sleep duration.
The findings highlighted the importance of improving and maintaining adequate sleep duration as a public health target for obesity prevention and increasing awareness about the benefits of adequate sleep duration for healthy weight maintenance.
Published Online: February 7, Open Access: This is an open access article distributed under the terms of the CC-BY License. JAMA Internal Medicine.
Corresponding Author: Esra Tasali, MD, Department of Medicine, The University of Chicago, S Maryland Ave, Chicago, IL etasali uchicago. Author Contributions: Author Dr Tasali and Ms Wroblewski had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.
Critical revision of the manuscript for important intellectual content: All authors. Administrative, technical, or material support: Tasali, Kahn, Kilkus, Schoeller.
Conflict of Interest Disclosures: None reported. Data Sharing Statement : See Supplement 3. Additional Contributions: Timothy Shriver, MS, University of Wisconsin—Madison, assisted with doubly labeled water measurements.
Maureen Costello, MS, The University of Chicago, assisted with dual-energy x-ray absorptiometry scans. Becky Tucker, BA, Harry Whitmore, RPSGT, and Kristin Hoddy, PhD, RD, The University of Chicago, assisted with data collection. We thank the nurses, dieticians, and technicians at the Clinical Research Center at The University of Chicago for their expert assistance in data collection.
We also thank the staff of the Sleep Research Center at The University of Chicago for their support. These individuals received no additional compensation, outside of their usual salary, for their contributions.
We thank the volunteers for participating in this study. full text icon Full Text. Download PDF Comment. Top of Article Key Points Abstract Introduction Methods Results Discussion Conclusions Article Information References.
Visual Abstract. Effect of sleep extension on objectively assessed energy intake in adults with overweight in real-life settings. View Large Download. Figure 1. CONSORT Flow Diagram. Figure 2.
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Clin Trials London, England — Download references. We are indebted to the participants in the NHS for their continuing outstanding support and colleagues working in this study for their valuable help.
This work is supported by National Institute of Health NIH grants UM1CA, NCI U54CA and NIDDK T32 DK All authors critically revised the manuscript for important intellectual content and approved the final version.
EMC had full access to all the data, analysed the data, wrote and revised the manuscript, and is responsible for the integrity of the work as a whole.
EMC, FBH, BR and SR conceived and designed the study question. SNB and YL assisted in analysing and interpreting the data. Department of Nutrition, Harvard T. Chan School of Public Health, Boston, MA, USA. Elizabeth M. Cespedes, Shilpa N. Department of Epidemiology, Harvard T. Division of Research, Kaiser Permanente Northern California, Broadway, 5th Floor, Oakland, CA, , USA.
Channing Division of Network Medicine, Harvard Medical School, Boston, MA, USA. Department of Biostatistics, Harvard T.
You can also search for this author in PubMed Google Scholar. Correspondence to Elizabeth M. Reprints and permissions.
Participants continued Thermogenic supplements for cutting live in their home environment quaoity any prescribed diet or abd activity during qualityy 28 consecutive days of the study. Error bars are Holistic wellness coaching halance the mean. The vertical dashed line separates the two 2-week sleep periods. A-D, Data are in ascending order of change in sleep duration for the control group and sleep extension group. E, Data were from 74 participants. All available data were used. The line represents the line of best fit from the linear regression model. Baseline sleep duration Insulin sensitivity and insulin signaling a U-shaped relationship with type Holistic wellness coaching diabetes, but Enerrgy research examines slepe Fat loss aid changes. We qualkty long-term changes in sleep duration Holistic wellness coaching concomitant changes in diet, physical activity, weight and subsequent diabetes. The cohort includes 59, women aged 55—83 years in the Nurses' Health Study without diabetes in Change in sleep duration is the difference between self-reported 24 h sleep duration in and Diet, physical activity and covariates were updated every 2—4 years. Self-reported diabetes was confirmed via validated questionnaires.
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