326 Comparison of Psychological and Physiological Features Between Insomnia Patients with Short and Normal Objective Sleep Duration

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A130-A131
Author(s):  
Yun-Kai Lin ◽  
Chien-Ming Yang ◽  
Hsin-Chien Lee ◽  
Ya-Chuan Huang ◽  
Chia-Yu Lin ◽  
...  
Keyword(s):  
Sleep Duration ◽  
Rating Scales ◽  
Psychological Profile ◽  
Short Sleep Duration ◽  
Coping With Stress ◽  
Short Sleep ◽  
Cognitive Subscale ◽  
Normal Sleep ◽  
Physiological Hyperarousal ◽  
The Impact

Abstract Introduction Objective sleep duration has been suggested to be a novel biomarker in the phenotyping of insomnia (Vgontzas & Fernandez-Mendoza, 2013). It was hypothesized that insomnia phenotype with PSG-defined short sleep duration (< 6 hours) is associated with physiological hyperarousal, while the phenotype with normal sleep duration (≥ 6 hours), is associated with anxious-ruminative psychological profile and poor resources for coping with stress. The aim of this study was to assess whether these two insomnia phenotypes differ in terms of self-reported psychological and physiological features. Methods A total 45 (mean age=36.6, female=76%) insomnia patients underwent a polysomnographic evaluation, completed several self-rating scales (include ISI, BAI, BDI, FIRST, DBAS, and PSAS), and were split into two groups base on their objective sleep duration (cut-off 6 hours). Results When compared to the short sleep group using independent sample t-test, the normal sleep group showed a significant higher mean score on FIRST (t= -2.13; p< .05). The short sleep group showed non-significant trends to have higher mean scores on BDI and BAI. The scores on the other scales showed no significant differences between the two groups. The FIRST score correlated positively with the score of DBAS (r= 0.32; p< .05) and the total (r= 0.36; p< .05) and cognitive-subscale scores (r= 0.41; p< .01) on PSAS. The BAI score correlated positively with the score of the total (r= 0.53; p< .001) and somatic subscale (r= 0.59; p< .001) on PSAS. Conclusion These results support the hypotheses that the normal sleep phenotype tends to be more vulnerable to the impact of stress, especially on sleep, due to pre-sleep cognitive hyperarousal. Since the BAI scale contains more items regarding physiological symptoms of anxiety disorders, the tendency of higher BAI score in short sleep group may indicate that the short sleep phenotype has higher physiological arousal, which supports the phenotyping model proposed by Vgontzas and Fernandez-Mandoza. Support (if any):

Abstract P545: Insufficient Sleep and Nitric Oxide-Mediated Endothelium-Dependent Vasodilation in Adults With Elevated Blood Pressure

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Kelly A Stockelman ◽  
Anthony R Bain ◽  
Dana M Withrow ◽  
Tracey A Larson ◽  
Elizabeth M Boland ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Blood Pressure ◽  
Sleep Duration ◽  
Elevated Blood Pressure ◽  
Elevated Blood ◽  
Short Sleep Duration ◽  
Insufficient Sleep ◽  
Short Sleep ◽  
Normal Sleep

Elevated blood pressure (BP ≥130/80 mmHg) is associated with increased risk for myocardial infarction, heart failure, stroke and vascular disease. Insufficient nightly sleep (<7 h/night) has been linked not only to the etiology of elevated blood pressure but is a prevalent, often ignored, comorbidity. Indeed, short sleep duration is now considered to be a plausible risk factor for elevated blood pressure and a harbinger of increased cardiovascular risk. A high prevalence of insufficient nightly sleep has been reported in adults with elevated blood pressure. The influence of insufficient sleep on endothelial vasodilator function in adults with elevated blood pressure is unknown. We tested the hypotheses that chronic insufficient sleep is associated with diminished nitric oxide (NO)-mediated endothelium-dependent vasodilation in adults with elevated blood pressure. Moreover, the insufficient sleep-related reduction in endothelial vasodilator function is due, at least in part to increased oxidative stress. Thirty-five middle-aged and older adults with elevated blood pressure were studied: 15 with normal nightly sleep duration (11M/4F; age: 58±2 yr; BP: 136/82±1/2 mmHg; sleep: 7.6±0.2 h/night) and 20 with short nightly sleep duration (14M/6F; 58±1 yr; BP: 138/84±1/1 mmHg; sleep: 6.0±0.1 h/night). Forearm blood flow (FBF) responses to intra-arterial infusion of acetylcholine (ACh), in the absence and presence of the endothelial NO synthase inhibitor N G -monomethyl-L-arginine (L-NMMA) and the antioxidant vitamin C were determined by venous occlusion plethysmography. The FBF response to ACh was significantly lower (~20%) in the short sleep (from 3.8±0.2 to 11.0±0.6 ml/100 ml tissue/min) compared with the normal sleep duration group (from 4.2±0.2 to 13.6±0.6 ml/100 ml tissue/min). L-NMMA significantly reduced (~25%) the FBF response to ACh in the normal sleep but not the short sleep group. Vitamin C markedly increased (~35%; P<0.05) the vasodilator response to ACh in short sleepers only. In summary, habitual short sleep duration worsens NO-mediated endothelium-dependent vasodilation in adults with elevated blood pressure. Furthermore, the sleep-related diminishment in endothelial vasodilator function is due, in part, to increased oxidative stress.

Insomnia and sleep state misperception: Clinical features, diagnosis, management and implications

2017 ◽  
Vol 41 (S1) ◽  
pp. s853-s853
Author(s):  
J. Isaac ◽  
C. Santos ◽  
A. Matos Pires
Keyword(s):  
Sleep Duration ◽  
Clinical Features ◽  
Mental Disease ◽  
Sleep Time ◽  
Sleep State ◽  
Short Sleep Duration ◽  
Short Sleep ◽  
Psychological Therapies ◽  
Normal Sleep ◽  
Competing Interest

BackgroundInsomnia is a highly prevalent complaint, largely associated with mental disease. Clinical evidence classifies insomnia in 2 subtypes: with sleep misperception (WSM) and without sleep misperception (wSM). That presents distinctive pathophysiologic pathways and different public health implications.ObjectivesDescribe the main differences between primary insomnia WSM and wSM regarding:– clinical features;– diagnosis;– management;– implications.MethodsWe conducted a systematic review. PubMed, Embase and PsycInfo were searched from 2000–2016. The reference lists of systematic reviews, narrative synthesis and some important articles were included. Following the inclusion criteria, we selected 25 studies from 59 articles.ResultsThe prevalence of sleep-state misperception in primary insomniacs (total sleep time > 6.5 h and sleep efficiency > 85%) is around 26%. Insomniacs with normal sleep duration showed a profile of high depression and anxiety and low ego strength, whereas insomniacs with short sleep duration showed a profile of a medical disorder.Cortical hyperarousal is higher in insomniacs and could be related to an alteration in sleep protection mechanisms. The sleep architecture was relatively normal for the WSM comparing with the group wSM. Risk of cardiometabolic, neurocognitive morbidity and mortality, and responses to treatment are different between these two insomnia phenotypes. Patients with short sleep duration may respond better to biological treatments, whereas insomnia with normal sleep duration may respond primarily to psychological therapies.ConclusionsThe clinical characteristics of patients with sleep-state misperception differed from those without this condition. Available research related to these conditions is expanding rapidly, but many questions remain unanswered.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Abstract 2455: Short Sleep Duration is an Independent Predictor of Cardiovascular Events in Hypertensive Patients

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Kazuo Eguchi ◽  
Thomas G Pickering ◽  
Joseph E Schwartz ◽  
Satoshi Hoshide ◽  
Joji Ishikawa ◽  
...  
Keyword(s):  
Sleep Duration ◽  
Short Duration ◽  
Cardiovascular Events ◽  
Sleep Time ◽  
Cvd Risk ◽  
Short Sleep Duration ◽  
Hypertensive Patients ◽  
Short Sleep ◽  
Multivariable Analyses ◽  
Normal Sleep

We aimed this study to test the hypothesis that short duration of sleep is independently associated with incident cardiovascular diseases (CVD) in hypertensive patients. We performed ambulatory BP monitoring (ABPM) in 1255 subjects with hypertension (mean age: 70.4 ± 9.9 years) and they were followed for an average of 50 ± 23 months. Short sleep duration was defined as <7.5 hrs (20 th percentile). Multivariable Cox hazard models predicting CVD events were used to estimate the adjusted hazard ratio (HR) and 95% CI for short sleep duration. A riser pattern was defined when average nighttime SBP exceeded daytime SBP. The end point was cardiovascular events: stroke, fatal or non-fatal myocardial infarction (MI), and sudden cardiac death. In multivariable analyses, short duration of sleep (<7.5 hrs) was associated with incident CVD (HR=1.68; 1.06 –2.66, P=.03). A synergistic interaction was observed between short sleep duration and the riser pattern (P=.089). When subjects were categorized on the basis of their sleep time and riser/non-riser patterns, the shorter sleep+riser group had a highest incidence of CVD among the 4 groups ( Figure ), and substantially and significantly higher incidence of CVD than the predominant normal sleep+non-riser group (HR=4.43; 2.09 –9.39, P<0.001), independent of covariates. Short duration of sleep is associated with incident CVD risk, and the combination of riser pattern and short duration of sleep that is most strongly predictive of future CVD, independent of ambulatory BP levels. Physicians should inquire about sleep duration in the risk assessment of hypertensive patients.

Abstract P183: Influence of Insufficient Sleep on Endothelial Fibrinolytic Capacity in Adults With Elevated Blood Pressure

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Anthony R Bain ◽  
Caitlin A Dow ◽  
Kyle J Diehl ◽  
Tyler D Bammert ◽  
Jared J Greiner ◽  
...  
Keyword(s):  
Sleep Duration ◽  
Tissue Type ◽  
Short Sleep Duration ◽  
Insufficient Sleep ◽  
Short Sleep ◽  
Type Plasminogen Activator ◽  
Increased Risk ◽  
Normal Sleep ◽  
Middle Aged Adults

The capacity of the endothelium to release tissue-type plasminogen activator (t-PA) is impaired in adults with elevated BP, leading to an increased risk of thrombotic events. Insufficient sleep is independently associated with elevated BP and impaired t-PA release. However, the compounded influence of insufficient sleep on t-PA release in adults with elevated BP is unknown. We tested the hypothesis that impairments in the capacity of the endothelium to release t-PA in adults with elevated BP is worse in those who sleep <7 h/night (short sleep duration) compared with those who sleep 7 to 9 h/night (normal sleep duration). We studied 38 sedentary, middle-aged adults: 10 with normal BP and normal nightly sleep duration (6M/4F; age: 55±2 yr; BP: 114/94±2/3 mmHg, sleep duration: 7.4±0.2 h); 14 with elevated BP and normal nightly sleep duration (8M/6F; 60±2 yr; 141/87±2/2 mmHg; 7.8±0.1 h); and 14 with elevated BP and short nightly sleep duration (10M/4F; 57±2 yr; 139/85±2/2 mmHg; 6.1±0.2 h). All subjects were free of overt metabolic and coronary disease. Net endothelial release of t-PA was determined, in vivo, in response to intra-brachial infusions of bradykinin (BK: 125-500 ng/min) and sodium nitroprusside (SNP: 2.0-8.0 μg/min). In the normal sleep groups, as expected, endothelial t-PA release in response to BK was significantly blunted (~30%) in the adults with elevated BP (from -1.2±0.8 to 50.2±4.8 ng/100mL tissue/min) compared with normal BP (from 0.9±3.4 to 73.0±8.0 ng/100mL tissue/min); and total t-PA release (area under the BK curve) was ~25% lower (p<0.05) in the adults with elevated (307±33 ng/100mL tissue) vs. normal (396±27 ng/100mL tissue) BP. Importantly, net endothelial release rate (from -1.5±1.0 to 40.6±4.3 ng/100mL tissue/min) and total amount of t-PA released (222±28 ng/100mL tissue) in response to BK were markedly lower (~25% and 30%, respectively, P<0.05) in the elevated BP and short sleep duration group compared with the elevated BP and normal sleep duration group. In the elevated BP population, sleep duration was positively correlated with total t-PA release (r=0.46, P<0.05). There was no effect of SNP on t-PA release in any group. In summary, insufficient sleep is associated with exacerbated impairments in t-PA release in adults with elevated BP.

Abstract 28: Regular Aerobic Exercise Counteracts Endothelial Vasomotor Dysfunction Associated With Insufficient Sleep

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Kelly A Stockelman ◽  
Anthony R Bain ◽  
Caitlin A Dow ◽  
Jared J Greiner ◽  
Brian L Stauffer ◽  
...  
Keyword(s):  
Exercise Training ◽  
Aerobic Exercise ◽  
Sleep Duration ◽  
Middle Aged ◽  
Short Sleep Duration ◽  
Insufficient Sleep ◽  
Short Sleep ◽  
Vasomotor Regulation ◽  
Normal Sleep ◽  
Middle Aged Adults

Insufficient sleep, defined as chronic short sleep duration (<7 h/night), is an independent risk factor for cardiovascular disease (CVD). We have previously demonstrated that insufficient sleep is associated with reduced endothelium-dependent vasodilation and enhanced endothelin (ET)-1-mediated vasoconstrictor tone. Impaired endothelial vasomotor regulation is thought to contribute mechanistically to the increased risk of atherosclerotic vascular disease incurred with chronic insufficient sleep. Regular aerobic exercise is an effective lifestyle strategy for improving endothelial function and, in turn reducing cardiovascular risk. It is currently unknown if regular aerobic exercise can counteract the negative impact of insufficient sleep on endothelial vasomotor regulation. We tested the hypotheses that regular aerobic exercise would: 1) improve endothelial vasodilation; and 2) decrease ET-1-mediated vasoconstrictor tone in middle-aged adults who chronically sleep less than 7 h/night. We studied 36 healthy, middle-aged adults: 16 with normal sleep duration (10M/6F; age: 57±2 yr; sleep duration: 7.4±0.1 h/night) and 20 with short sleep duration (11M/9F; 56±1 yr; sleep duration: 6.2±0.1 h/night). The 20 short sleepers completed a 3-month aerobic exercise training intervention. Forearm blood flow (FBF; plethysmography) was determined in response to intra-arterial doses of acetylcholine (ACh), sodium nitroprusside (SNP), BQ-123 (ET A receptor antagonist) and ACh + BQ-123 in both groups and after the exercise intervention in the short sleepers. As expected, forearm vasodilator responses to ACh were lower (20%; P<0.05) in the short (from 4.2±0.2 to 10.5±0.6 mL/100 mL tissue/min) vs normal (4.2±0.2 to 12.7±0.6 mL/100 mL tissue/min) sleepers. FBF responses to SNP were comparable between the groups. In response to BQ-123, short sleep group had a greater increase in resting FBF than normal sleep group (~25% vs ~8%; P< 0.05). ACh+BQ-123 resulted in an ~25% increase in the ACh-vasodilation in the short sleep group only. After exercise training, although nightly sleep duration was not affected (6.4±0.1 h/night), ACh-mediated vasodilation was ~20% higher (P<0.05), ET-1-mediated vasoconstriction was ~90% lower (P<0.05) and vasodilator response to ACh was not significantly increased with ET A receptor blockade. These results indicate that regular aerobic exercise can reverse the negative influence of insufficient sleep on endothelial vasomotor function, independent of changes in nightly sleep duration.

Abstract MP085: Cognitive Impairment Mediates the Impact of Short Sleep Duration on Mortality in Individuals with Cardiovascular or Cerebrovascular Disease

Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Julio Fernandez-Mendoza ◽  
Fan He ◽  
Alexandros N Vgontzas ◽  
Duanping Liao ◽  
Edward O Bixler
Keyword(s):  
Cognitive Impairment ◽  
Sleep Duration ◽  
Processing Speed ◽  
Short Term Memory ◽  
Executive Attention ◽  
Short Term ◽  
Short Sleep Duration ◽  
Short Sleep ◽  
History Of ◽  
The Impact

Background: Cardiovascular disease (CVD) and cerebrovascular disease (CBV) have been associated with short sleep duration and mortality. Furthermore, short sleep duration has been associated with impaired cognition. Most studies have been limited by using self-report measures and treating sleep duration as a sole, independent predictor, thus, its role in predicting mortality is still not well-established. Hypothesis: We hypothesized that 1) short sleep duration increases the impact of CVD and CBV on mortality and 2) cognitive impairment mediates the association of short sleep duration with mortality in those with CVD or CBV. Methods: We addressed this question in the Penn State Adult Cohort, a random, general population sample of 1,741 men and women (48.7 ± 13.5 years) who were studied in the sleep laboratory and followed-up for 16.7 ± 4.6 years. CVD was defined by a history of heart disease, including hypertension or diabetes, and CBV by a history of stroke. Polysomnographic (PSG) total sleep time was classified as normal (≥ 6 hours) and short (< 6 hours) sleep duration based on the median of the cohort. All individuals underwent a comprehensive neuropsychological evaluation, including Symbol Digit Modalities Test, Trail Making Test, Benton Visual Retention Test, Thurstone Word Fluency Test, and Mini-Mental State Examination. We tested the interaction between CVD, CBV and PSG sleep duration on mortality using Cox proportional hazard models controlling for multiple potential confounders. Results: The hazard ratios (95%CI) of mortality associated with CVD and CBV were 0.9 (0.6-1.3) and 1.3 (0.5-3.1) for individuals with normal sleep duration and 1.8 (1.3-2.5) and 2.4 (1.3-4.4) for individuals with short sleep duration (P-interaction < .05). In individuals with CVD or CBV, short sleep duration was associated with impaired processing speed, executive attention, and short-term memory (all Ps < .05). Cognitive impairment significantly mediated the impact of short sleep duration on mortality in those with CVD or CBV [proportion of mediation effects were 6.5% (1.4%-18.6%), 4.5% (0.4%-14.2%), and 6.2% (1.0%-18.4%) for processing speed, executive attention and short-term memory, respectively]. Conclusions: The risk of mortality associated with CVD and CBV is significantly increased in those with short sleep duration. Although cognitive impairment significantly mediated this association, its modest effect suggests that future studies should examine other underlying mechanisms linking short sleep duration with mortality in individuals with CVD or CBV.

scholarly journals Insomnia with objective short sleep duration is associated with longer duration of insomnia in the Freiburg Insomnia Cohort compared to insomnia with normal sleep duration, but not with hypertension

PLoS ONE ◽  
2017 ◽  
Vol 12 (7) ◽  
pp. e0180339 ◽  
Author(s):  
Anna F. Johann ◽  
Elisabeth Hertenstein ◽  
Simon D. Kyle ◽  
Chiara Baglioni ◽  
Bernd Feige ◽  
...  
Keyword(s):  
Sleep Duration ◽  
Short Sleep Duration ◽  
Short Sleep ◽  
Normal Sleep

scholarly journals 1055 THE IMPACT OF SHORT SLEEP DURATION ON INSTRUMENTAL ACTIVITIES OF DAILY LIVING (IADL) AMONG STROKE SURVIVORS

SLEEP ◽  
2017 ◽  
Vol 40 (suppl_1) ◽  
pp. A392-A392
Author(s):  
D Chung ◽  
A Seixas ◽  
SL Richards ◽  
G Casimir ◽  
E Auguste ◽  
...  
Keyword(s):  
Activities Of Daily Living ◽  
Sleep Duration ◽  
Daily Living ◽  
Stroke Survivors ◽  
Short Sleep Duration ◽  
Short Sleep ◽  
Instrumental Activities ◽  
The Impact

scholarly journals Associations between fecal short-chain fatty acids and sleep continuity in older adults with insomnia symptoms

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Faiga Magzal ◽  
Carmel Even ◽  
Iris Haimov ◽  
Maayan Agmon ◽  
Kfir Asraf ◽  
...  
Keyword(s):  
Older Adults ◽  
Fatty Acids ◽  
Sleep Duration ◽  
Sleep Onset ◽  
Short Chain Fatty Acids ◽  
Short Sleep Duration ◽  
Short Sleep ◽  
Sleep Continuity ◽  
Normal Sleep ◽  
Insomnia Symptoms

AbstractInsomnia is a disorder characterized by difficulty falling asleep and poor sleep continuity and is associated with increased risks for physical and cognitive decline. Insomnia with short sleep duration is considered the most biologically severe phenotype of the disorder. Evidence suggests that short-chain fatty acids (SCFAs), the main byproducts of fiber fermentation in the gut, may affect sleep via gut–brain communications. This study explores associations between SCFAs and sleep continuity and compares SCFA concentrations in short vs. normal sleep insomnia phenotypes in older adults. Fifty-nine participants with insomnia symptoms (≥ 65 years), completed 2 weeks of objective sleep monitoring (actigraphy), and were divided into short and normal sleep duration phenotypes via cluster analysis. Sleep measures included total sleep time (TST), sleep onset latency (SOL), sleep efficiency (SE), and wake after sleep onset (WASO). Stool samples were collected and fecal SCFA concentrations were determined by gas-chromatography-mass-spectrometry (GCMS). Higher concentrations of acetate, butyrate, and propionate, and total SCFAs, were associated with lower SE and longer SOL after controlling for Body Mass Index (BMI). Concentrations were higher in the short sleep duration phenotype. Age, BMI, TST, and SOL explained 40.7% of the variance in total SCFAs. Findings contribute to understanding pathways along the gut–brain axis and may lead to the use of SCFAs as biomarkers of insomnia phenotypes.

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