Dataset Information

Objective short sleep duration increases the risk of all-cause mortality associated with possible vascular cognitive impairment.

ABSTRACT:

Objectives

Cognitive impairment is a leading cause of disability worldwide, and cardiometabolic conditions are key contributors to its development. Short sleep is also a potential contributor to brain health; however, its role in predicting mortality remains poorly understood. We investigated whether objective short sleep duration increases the risk of all-cause mortality associated with coexisting cognitive impairment and cardiometabolic conditions, i.e., possible vascular cognitive impairment (VCI).

Design

This is a longitudinal study.

Setting

This is a population-based, in-lab study.

Participants

A total of 1,524 adults (aged 48.9±13.4 years, 53.4% women) from the Penn State Adult Cohort were included in the study.

Measurements

All-cause mortality was estimated after 19.1±5.1 years of follow-up. Neuropsychological testing was performed to ascertain cognitive impairment. Clinical history and physical examination were performed to ascertain stage 2 hypertension, type 2 diabetes, heart disease, and stroke. Possible VCI was defined as the presence of any of these cardiometabolic conditions and cognitive impairment. In-lab, 8-hour polysomnography (PSG) was performed to ascertain short sleep duration (i.e., <6 hours).

Results

Multivariable-adjusted Cox proportional-hazard models showed that the risk of all-cause mortality associated with cardiometabolic conditions (n=864) and possible VCI (n=122) was significantly increased in those who slept <6 hours at baseline (hazards ratio [HR] = 1.79, 95% confidence interval [CI] = 1.28-2.51 and HR = 4.01, 95% CI = 2.66-6.05, respectively), while it was negligible in those who slept ?6 hours (HR = 1.44, 95% CI = 0.99-2.09 and HR = 1.41, 95% CI = 0.70-2.83, respectively).

Conclusions

Objective short sleep duration predicts the mortality prognosis of adults with possible VCI. Sleep duration and cognition should be objectively evaluated in patients presenting with a cluster of cardiometabolic conditions and sleep and cognitive complaints. Short sleep is a useful risk factor in the prediction of adverse cardiometabolic and brain health outcomes.

SUBMITTER: Fernandez-Mendoza J

PROVIDER: S-EPMC6995415 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature

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Publications

Objective short sleep duration increases the risk of all-cause mortality associated with possible vascular cognitive impairment.

Fernandez-Mendoza Julio J He Fan F Calhoun Susan L SL Vgontzas Alexandros N AN Liao Duanping D Bixler Edward O EO

Sleep health 20191121 1

<h4>Objectives</h4>Cognitive impairment is a leading cause of disability worldwide, and cardiometabolic conditions are key contributors to its development. Short sleep is also a potential contributor to brain health; however, its role in predicting mortality remains poorly understood. We investigated whether objective short sleep duration increases the risk of all-cause mortality associated with coexisting cognitive impairment and cardiometabolic conditions, i.e., possible vascular cognitive imp ...[more]

PMID: 31759934

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Project description:Study objectivesThis study examined whether individuals with insomnia and objective short sleep duration <6 h, a subgroup with greater risks of adverse health outcomes, differ in their response to cognitive-behavioral therapy for insomnia (CBT-I) when compared to individuals with insomnia and normal sleep duration ?6 h.MethodsSecondary analyses of a randomized, clinical trial with 60 adult participants (n = 31 women) from a single academic medical center. Outpatient treatment lasted 8 weeks, with a final follow-up conducted at 6 months. Mixed-effects models controlling for age, sex, CBT-I treatment group assignment, and treatment provider examined sleep parameters gathered via actigraphy, sleep diaries, and an Insomnia Symptom Questionnaire (ISQ) across the treatment and follow-up period.ResultsSix months post-CBT-I treatment, individuals with insomnia and normal sleep duration ?6 h fared significantly better on clinical improvement milestones than did those with insomnia and short sleep duration <6 h. Specifically, individuals with insomnia and normal sleep duration had significantly higher insomnia remission (ISQ < 36.5; ?2[1, N = 60] = 44.72, p < .0001), more normative sleep efficiency (SE) on actigraphy (SE > 80%; ?2[1, N = 60] = 21, p < .0001), normal levels of middle of the night wake after sleep onset (MWASO) <31 minutes (?2[1, N = 60] = 37.85, p < .0001), and a >50% decline in MWASO (?2[1, N = 60] = 60, p < .0001) compared to individuals with insomnia and short sleep duration. Additionally, those with insomnia and normal sleep duration had more success decreasing their total wake time (TWT) at the 6-month follow-up compared to those with insomnia and short sleep duration (?2[2, N = 60] = 44.1, p < .0001). Receiver-operating characteristic curve analysis found that using a 6-h cutoff with actigraphy provided a 95.7% sensitivity and 91.9% specificity for determining insomnia remission, with the area under the curve = 0.986.ConclusionsFindings suggest that individuals with insomnia and objective short sleep duration <6 h are significantly less responsive to CBT-I than those with insomnia and normal sleep duration ?6 h. Using an actigraphy TST cutoff of 6 hours to classify sleep duration groups was highly accurate and provided good discriminant value for determining insomnia remission.

Project description:BackgroundStudies demonstrate an association between vitamin D (25(OH)D) deficiency and sleep disturbances, such as obstructive sleep apnea (OSA) and short sleep duration. However, to date, no studies have concurrently and objectively evaluated the effect of these factors on 25(OH)D.ObjectivesTo evaluate whether OSA and objective short sleep duration are independently associated with reduced 25(OH)D in an adult population sample.MethodsA cross-sectional study included 657 individuals from the city of Sao Paulo, Brazil, as part of the ERA project. Participants fulfilled questionnaires and underwent clinical evaluation, polysomnography and blood sample collection for 25(OH)D quantification. OSA was classified into three categories (mild, moderate and severe). The risk of 25(OH)D deficiency was considered as levels<30 ng/mL. Short sleep duration was defined as total sleep time<6 hours.ResultsThe risk of 25(OH)D deficiency was observed in 59.5% of the sample, affecting more individuals of the female gender, obese, with African American ethnicity, and those that were smokers, sedentary and presented hypertension and diabetes. In the final logistic model adjusted for age, gender, ethnicity, obesity, smoking, hypertension, diabetes, sedentary lifestyle, seasonality and creatinine serum levels, both OSA and short sleep duration showed significant independent associations with the risk of 25(OH)D deficiency (moderate OSA: OR for 25(OH)D<30 = 2.21, 95% CI: 1.35-3.64, p<0.01; severe OSA: OR for 25(OH)D<30 = 1.78, 95% CI: 1.06-3.00, p = 0.03; short sleep duration: OR for 25(OH)D<30 = 1.61, 95% CI: 1.15-2.26, p = 0.01). After a subgroup analysis, similar results were observed only in participants ≥50 years.ConclusionOSA and short sleep duration are independently associated with the risk of 25(OH)D deficiency in an adult population. Age-related changes in vitamin D metabolism and the frequency of sleep disorders may be involved in these associations. Future studies exploring whether 25(OH)D levels may modulate OSA and sleep curtailment-related outcomes are needed.

Dataset Information

Objective short sleep duration increases the risk of all-cause mortality associated with possible vascular cognitive impairment.

Objectives

Design

Setting

Participants

Measurements

Results

Conclusions

Publications

Objective short sleep duration increases the risk of all-cause mortality associated with possible vascular cognitive impairment.

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