scholarly journals Neural reward processing in self-reported short sleepers: examination of gambling task brain activation in the Human Connectome Project database

SLEEP ◽  
2019 ◽  
Vol 42 (9) ◽  
Author(s):  
Brian J Curtis ◽  
Paula G Williams ◽  
Jeffrey S Anderson

Abstract Study Objectives Much of what we assume about the effects of short sleep duration on neural reward processing derives from total sleep deprivation studies. Although total sleep deprivation appears rare, habitual short sleep is common: 30% of working US adults report habitually sleeping ≤ 6 hours/night. It remains largely unknown whether habitual short sleepers exhibit similar reward processing brain activation patterns to those observed following total sleep deprivation in prior studies. Therefore, our aim was to test objectively reward processing brain activation patterns associated with self-reported habitual short sleep duration in a large sample. Methods Nine hundred and fifty-two adult participants from the Human Connectome Project database were grouped on reported habitual short (≤6 hours) vs. medium-length (7–9 hours) sleep duration using the Pittsburgh Sleep Quality Index (PSQI). Reward processing brain activation was examined using a gambling task during functional magnetic resonance imaging (fMRI). Subject-level covariates for age, sex, continuous sleep duration, daytime dysfunction, and PSQI total score are provided as supplemental analyses. Results Brain activation patterns revealed expected reward processing-related activation for age and sex. However, activation for sleep duration, dysfunction, and PSQI score did not correspond to those evident in previous total sleep deprivation studies. Conclusions Self-reported short sleep duration, perceived sleep-related dysfunction, and sleep quality via PSQI do not appear to be meaningfully associated with activation in well-described regions of the human neurobiological reward circuit. As these findings are counter to prior results using experimental sleep deprivation, future work focused on more direct comparisons between self-reported sleep variables and experimental sleep deprivation appears warranted.

Author(s):  
Ian M. Greenlund ◽  
Jason R. Carter

Short sleep duration and poor sleep quality are associated with cardiovascular risk, and sympathetic nervous system (SNS) dysfunction appears to be a key contributor. The present review will characterize sympathetic function across several sleep disorders and insufficiencies in humans, including sleep deprivation, insomnia, narcolepsy, and obstructive sleep apnea (OSA). We will focus on direct assessments of sympathetic activation (e.g., plasma norepinephrine and muscle sympathetic nerve activity), but include heart rate variability (HRV) when direct assessments are lacking. The review also emphasizes sex as a key biological variable. Experimental models of total sleep deprivation and sleep restriction are converging to support epidemiological studies reporting an association between short sleep duration and hypertension, especially in women. A systemic increase of SNS activity via plasma norepinephrine is present with insomnia, and has also been confirmed with direct, regionally-specific evidence from microneurographic studies. Narcolepsy is characterized by autonomic dysfunction via both HRV and microneurographic studies, but with opposing conclusions regarding SNS activation. Robust sympathoexcitation is well documented in OSA, and is related to baroreflex and chemoreflex dysfunction. Treatment of OSA with continuous positive airway pressure results in sympathoinhibition. In summary, sleep disorders and insufficiencies are often characterized by sympathoexcitation and/or sympathetic/baroreflex dysfunction, with several studies suggesting women may be at heightened risk.


Obesity Facts ◽  
2021 ◽  
Vol 14 (2) ◽  
pp. 214-221
Author(s):  
Maryam Mosavat ◽  
Mitra Mirsanjari ◽  
Diana Arabiat ◽  
Aisling Smyth ◽  
Lisa Whitehead

Emerging evidence has identified sleep as a significant, but modifiable, risk factor for metabolic syndrome, diabetes, and obesity. Leptin, an adipocyte-derived peptide and a regulator of food intake and energy expenditure, has been shown to be associated with a short sleep duration in the pathophysiology of obesity and consequently type 2 diabetes. This review focuses on the current evidence indicating the effects of a short sleep duration on the regulation of leptin concentration in association with obesity and diabetes mellitus. In summary, the evidence suggests that sleep deprivation, by affecting leptin regulation, may lead to obesity and consequently development of type 2 diabetes through increased appetite and food intake. However, findings on the role of leptin in diabetes due to sleep deprivation are contradictory, and further studies with larger sample sizes are needed to confirm previous findings.


2018 ◽  
Vol 3 (3) ◽  
pp. 556
Author(s):  
Mulyanti Roberto Muliantino ◽  
Tuti Herawati ◽  
Masfuri Masfuri

<p><em>Coronary Arterial Disease (CAD) is one of cardiovaskular disease that remain leading cause death and disability. Short sleep duration is the major symptoms in patients with CAD, during recovery period after cardiac events and during cardiac rehabilitation. Benson’s relaxation is one of relaxation as modalities therapy to increase sleep duration, </em><em>however few studies related to this</em><em> technique in planned</em><em> intervention</em><em>.</em><em> This study was to measured the effectiveness of Benson’s relaxation in short sleep duration of CAD patients during cardiac rehabilitation. It was a </em><em>quasi experimental pretest posttest control group design.</em><em> This study included 29 respondens in Dr.M.Djamil Hospital were assigned to intervention group which receiving Benson’s relaxation technique (n=15) and control group with routine care (n=14). </em><em>Benson’s relaxation </em><em>technique</em><em> was administered for 5 days 2 times a day, each 20 minutes to intervention group.</em><em> Short sleep duration was measured using </em><em>sleep diary (self report).</em><em> The result indicated significant increasing in mean of  sleep duration  before and after Benson’s relaxation in intervention group </em><em>(p value &lt; 0,001). </em><em>The study concluded that </em><em>Benson’s relaxation </em><em>technique is an effective non-pharmacological intervention to increase sleep duration in CAD patients.</em></p><p><em><br /></em></p><p>Penyakit jantung koroner menjadi masalah kardiovaskular yang mengakibatkan angka mortalitas yang tinggi. Durasi tidur pendek termasuk salah satu keluhan utama pasien penyakit jantung koroner pada masa recovery setelah serangan dan menjalani rehabilitasi fase 2. Relaksasi Benson merupakan teknik relaksasi sebagai terapi modalitas untuk mengurangi keluhan durasi tidur pendek, namum belum banyak penelitian terkait intervensi ini. Penelitian ini bertujuan untuk mengidentifikasi pengaruh relaksasi Benson terhadap durasi tidur pasien penyakit jantung koroner yang menjalani rehabilitasi fase 2. Penelitian ini menggunakan desain Quasi Eksperimen dengan pendekatan <em>control group pretest posttest design</em> pada 29 responden di RSUP. Dr.M.Djamil Padang yang dibagi dalam dua kelompok (kelompok intervensi dan kelompok kontrol). Hasil penelitian menunjukan ada perbedaan rerata durasi tidur yang signifikan antara sebelum dan setelah dilakukan intervensi relaksasi Benson pada kelompok intervensi (p value &lt; 0,001). Simpulan hasil penelitian ini dapat menjadi salah satu terapi modalitas bagi perawat untuk mengatasi masalah durasi tidur pendek pada pasien penyakit jantung koroner.</p><p><em><br /></em></p>


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A149-A149
Author(s):  
Andrew Kubala ◽  
Mara Egeler ◽  
Daniel Buysse ◽  
Martica Hall ◽  
Emma Barinas-Mitchell ◽  
...  

Abstract Introduction Cognitive behavioral therapy for insomnia (CBT-I) is efficacious, but there is mixed evidence as to whether improvement is blunted in adults with insomnia and short sleep duration. Exercise training can reduce physiologic hyperarousal and may increase homeostatic sleep drive, which could potentiate CBT-I treatment effects. This pilot study explored changes in self-reported outcomes from a CBT-I intervention augmented by exercise training in a sample of adults with insomnia and objective short sleep duration. Methods Eight adults (50% female, 62.5% white) with insomnia disorder and short sleep duration (mean actigraphic TST &lt;6.5 hr) completed a 12-week single-arm trial. Participants self-administered the online “Sleep Healthy Using the Internet” (SHUT-I) CBT-I program with additional staff guidance while completing a supervised exercise program (EX; 150 min/wk of moderate-intensity aerobic exercise and 2 days/wk of strength training). Participants completed assessments of self-reported sleep and daytime function pre- and post-intervention, including the Insomnia Severity Index (ISI), Flinders Fatigue Scale (FFS), Ford Insomnia Response to Stress Test (FIRST), Perceived Stress Scale (PSS), and Epworth Sleepiness Scale (ESS). Differences between timepoints were analyzed using paired t-tests and Cohen’s d effect size calculations. Results Insomnia severity significantly decreased after the intervention (ISI: p&lt;0.001, d=2.99), with 75% reporting post-intervention ISI ≤ 7. Likewise, fatigue significantly decreased after the intervention (FFS: p=0.032, d=0.95). Symptoms of stress-related sleep reactivity and stress were also reduced (FIRST: p=0.012, d=1.19; PSS: p=0.014, d=1.14). Though nonsignificant, large reductions in sleepiness were additionally observed (ESS: p=0.058, d=0.80). Conclusion In this pilot trial among patients with insomnia and short sleep duration, online CBT-I plus a supervised exercise program resulted in a significant reduction in insomnia severity. The intervention also produced large and meaningful reductions in fatigue and stress, which are common daytime impairments in patients with insomnia. Future research should attempt to disentangle the independent contributions of CBT-I and exercise on outcomes in this population. Support (if any) NIH: K23HL118318


Author(s):  
Sizhi Ai ◽  
Jihui Zhang ◽  
Guoan Zhao ◽  
Ningjian Wang ◽  
Guohua Li ◽  
...  

Abstract Aims Observational studies have suggested strong associations between sleep duration and many cardiovascular diseases (CVDs), but causal inferences have not been confirmed. We aimed to determine the causal associations between genetically predicted sleep duration and 12 CVDs using both linear and nonlinear Mendelian randomization (MR) designs. Methods and results Genetic variants associated with continuous, short (≤6 h) and long (≥9 h) sleep durations were used to examine the causal associations with 12 CVDs among 404 044 UK Biobank participants of White British ancestry. Linear MR analyses showed that genetically predicted sleep duration was negatively associated with arterial hypertension, atrial fibrillation, pulmonary embolism, and chronic ischaemic heart disease after correcting for multiple tests (P &lt; 0.001). Nonlinear MR analyses demonstrated nonlinearity (L-shaped associations) between genetically predicted sleep duration and four CVDs, including arterial hypertension, chronic ischaemic heart disease, coronary artery disease, and myocardial infarction. Complementary analyses provided confirmative evidence of the adverse effects of genetically predicted short sleep duration on the risks of 5 out of the 12 CVDs, including arterial hypertension, pulmonary embolism, coronary artery disease, myocardial infarction, and chronic ischaemic heart disease (P &lt; 0.001), and suggestive evidence for atrial fibrillation (P &lt; 0.05). However, genetically predicted long sleep duration was not associated with any CVD. Conclusion This study suggests that genetically predicted short sleep duration is a potential causal risk factor of several CVDs, while genetically predicted long sleep duration is unlikely to be a causal risk factor for most CVDs.


2015 ◽  
Vol 16 (12) ◽  
pp. 1482-1488 ◽  
Author(s):  
Kenneth Anujuo ◽  
Karien Stronks ◽  
Marieke B. Snijder ◽  
Girardin Jean-Louis ◽  
Femke Rutters ◽  
...  

2015 ◽  
Vol 212 (1) ◽  
pp. S141
Author(s):  
Francesca Facco ◽  
Kathryn Reid ◽  
William Grobman ◽  
Corette Parker ◽  
Robert Silver ◽  
...  

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