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Introduction Several studies have shown that the insomnia with objective short sleep duration (ISSD) phenotype is associated with stage 2 hypertension and type 2 diabetes. We aimed to determine if there is an association between ISSD and metabolic syndrome (MetS). Methods We studied 1,741 adults from the Penn State Adult Cohort (age 20-88 years, 52.3% female, 12.4% racial/ethnic minority) who underwent a 1-night polysomnographic (PSG) evaluation, clinical history, and physical examination. Insomnia was defined as a complaint of insomnia with a duration ≥ 1 year, while poor sleep was defined as a complaint of difficulty falling asleep, staying asleep, nonrestorative sleep or early morning awakening. Objective short sleep duration was defined as < 6-hours. MetS was defined by the presence of 3 or more of: BMI≥30 kg/m2, elevated total cholesterol (≥200 mg/dL), triglycerides (≥150 mg/dL), fasting glucose (≥100 mg/dL), or treatment, and blood pressure (≥130/85 mm Hg) or treatment. Logistic regression models examined the odds of developing MetS, while simultaneously adjusting for sex, race, age, alcohol, smoking, sleep-disordered breathing, mental and physical problems, and sampling weight. Results Compared to normal sleepers with normal sleep duration, ISSD was associated with a significantly increased risk of MetS (OR=2.04, 95%CI=1.13-3.70), while insomnia with normal sleep duration (INSD) was not (OR=1.03, 95%CI=0.53-1.99). Neither normal sleepers with short sleep duration nor poor sleeper with normal or short sleep duration were associated with increased risk of MetS. Further analysis of the clustering of the cardiometabolic risk factors revealed that in the ISSD group who had MetS, 94% had elevated blood pressure, 78% had elevated cholesterol, 72% had insulin resistance, 53% had elevated triglycerides, and 53% had BMI≥30 kg/m2. Conclusion These data indicate that hypercholesterolemia, but not hypertriglyceridemia or obesity, contributes to the association of ISSD with MetS. These data suggest that in addition to the previously-identified elevated blood pressure and insulin resistance, treatment of hypercholesterolemia in patients with ISSD may prevent the development of cardiovascular and cerebrovascular disease. Support (if any)

Introduction Insomnia with objective short sleep duration (ISSD) has been associated with adverse cardiometabolic outcomes, including hypertension and diabetes. However, data on the association between ISSD and the development of cardiovascular and/or cerebrovascular disease (CBVD) are limited. We aimed to examine whether ISSD is associated with incident CBVD. Methods 1,211 men and women from the Penn State Adult Cohort (56.9% women, 51.82±12.85 years) without CBVD at baseline were followed up for 9.21±4.08 years. Based upon clinical history and physical examination, we defined the presence of CBVD as a history of diagnosis or treatment of heart disease and/or stroke. Insomnia was defined as a complaint of insomnia with a duration ≥ 1 year. Poor sleep was defined as a complaint of difficulty falling asleep, staying asleep, nonrestorative sleep or early morning awakening. Objective short sleep duration was defined as < 6-hours sleep based on a 1-night, 8-hours, in-lab polysomnography. Logistic regression models examined the odds of incident CBVD, while simultaneously adjusting for race, sex, age, BMI, smoking, alcohol use, physical and mental health problems, sleep-disordered breathing and follow-up duration. Results Compared to normal sleepers with normal sleep duration, the highest risk of incident CBVD was in the ISSD group (OR=2.68, 95%CI=1.17-6.14), and the second highest in normal sleepers with short sleep duration (OR=1.65, 95%CI=1.10-2.49). The risk for incident CBVD was not significantly increased, in poor sleepers or those with insomnia with normal sleep duration (INSD). Conclusion Our findings indicate that the combination of short sleep duration with the complaint of chronic insomnia (ISSD) is associated with an additive effect on incident heart disease and stroke. These data add to the cumulative evidence supporting the existence of two insomnia phenotypes and that ISSD is the more severe biological phenotype of the disorder associated with physiologic hyperarousal and cardiovascular morbidity. The diagnostic and treatment implications of insomnia phenotyping based on objective sleep duration will be discussed. Support (if any)

Introduction Insomnia with objective short sleep duration (ISSD) has been proposed as the most biologically severe phenotype of the disorder associated with cardiometabolic morbidity in population-based samples. Methods In this study, we investigated the association between ISSD and hypertension in a large clinical sample. We studied 348 patients diagnosed with chronic insomnia disorder (CID) based on International Classification of Sleep Disorders (ICSD-3) criteria and 150 normal sleepers. Objective short sleep duration was defined by the median total sleep time (TST) of the sample (< 7 hours) measured with 1-night polysomnography. Hypertension was defined based on blood pressure (BP) levels, antihypertensive medication use and/or a physician diagnosis. Results After adjusting for potential confounders, patients with CID who slept < 7 hours were associated with 2.8-fold increased odds of hypertension compared to normal sleepers who slept ≥7 hours (odds ratio [OR]=2.81, 95% confidence interval [95%CI]=1.068–7.411) or < 7 hours (OR=2.75, 95%CI=1.005-7.542), whereas patients with CID who slept ≥ 7 hours (OR=1.52, 95%CI=0.537-4.285) or normal sleepers who slept < 7 hours (OR=1.07, 95%CI=0.294-3.904) were not significantly associated with increased odds of hypertension compared to normal sleepers who slept ≥ 7 hours. Linear regression analyses showed that, for every hour decrease in TST, systolic and diastolic blood pressure increased by 1.014 mmHg (p=0.045) and 0.923 mmHg (p=0.015), respectively, in patients with CID but not in normal sleepers. Conclusion Our findings further support that ISSD is a risk factor for hypertension and objective short sleep duration may be a useful marker of the biological severity of CID in clinical practice. Support (if any) This study was supported by the National Natural Science Foundation of China (81970087), Guangdong Province Science and Technology Special Fund Project (200115165870512), and the 2020 Li Ka Shing Foundation Cross-Disciplinary Research Grant (2020LKSFG05B). The authors report no conflict of interest.

Study Objectives: Approximately 8-10% of the general population suffers from chronic insomnia, whereas another 20-30% of the population has insomnia symptoms at any given time (i.e., poor sleep). However, few longitudinal studies have examined risk factors of the natural history of poor sleep, and none have examined the role of polysomnographic (PSG) variables. Design: Representative longitudinal study. Setting: Sleep laboratory. Participants: From a random, general population sample of 1,741 individuals of the adult Penn State Cohort, 1,395 were followed up after 7.5 yr. Measurements: Full medical evaluation and 1-night PSG at baseline and telephone interview at follow-up. Results: The rate of incident poor sleep was 18.4%. Physical (e.g., obesity, sleep apnea, and ulcer) and mental (e.g., depression) health conditions and behavioral factors (e.g., smoking and alcohol consumption) increased the odds of incident poor sleep as compared to normal sleep. The rates of persistent, remitted, and poor sleepers who developed chronic insomnia were 39%, 44%, and 17%, respectively. Risk factors for persistent poor sleep were physical health conditions combined with psychologic distress. Shorter objective sleep duration and a family history of sleep problems were risk factors for poor sleep evolving into chronic insomnia. Conclusions: Poor sleep appears to be primarily a symptom of physical and mental health conditions, whereas the persistence of poor sleep is associated with psychologic distress. Importantly, sleep apnea appears to be associated with incident poor sleep but not with chronic insomnia. Finally, this study suggests that objective short sleep duration in poor sleepers is a biologic marker of genetic predisposition to chronic insomnia, This research was funded in part by the National Institutes of Health grants RO1 51931, RO1 40916 (to Dr. Bixler), and RO1 64415 (to Dr. Vgontzas).

Study Objectives: Because insomnia with objective short sleep duration is associated with increased morbidity, we examined the effects of this insomnia subtype on all-cause mortality.