Insomnia with objective short sleep duration appears to be a biologically more severe phenotype of the disorder. No longitudinal study to date has examined the association of this type of insomnia with incident hypertension using polysomnography. From a random, general population sample of 1741 adults of the Penn State Cohort, 1395 were followed-up after 7.5 years and 786 did not have hypertension at baseline. Hypertension was determined by a self-report of receiving treatment for high blood pressure. Chronic insomnia was defined as a complaint of insomnia lasting ≥ 1 year, while poor sleep was defined as moderate-to-severe sleep difficulties. All subjects underwent 8-hour polysomnography. Sleep disordered breathing (SDB) was defined as an obstructive apnea/hypopnea index ≥ 5. We used the median polysomnographic percent of sleep time to define short sleep duration (i.e., < 6 hours). We controlled for gender, race, age, caffeine, cigarettes, alcohol consumption, depression, SDB, diabetes, obesity, and blood pressure in our analyses. Compared to normal sleepers who slept ≥ 6 hours, the highest risk for incident hypertension was in chronic insomniacs with short sleep duration (OR= 3.8, 95% CI=1.6–9.0). The risk for incident hypertension in poor sleepers with short sleep duration was significantly increased but became marginally significant after controlling for obesity (OR= 1.6, 95% CI=0.9–2.8). Chronic insomnia with short sleep duration is associated with an increased risk for incident hypertension in a degree comparable to SDB. Objective short sleep duration in insomnia may serve as a useful predictor of the biological severity of the disorder.

Insomnia with objective short sleep duration in men is associated with increased mortality, a risk that has been underestimated.

Objective-Sleep misperception is considered by some investigators a common characteristic of chronic insomnia, whereas others propose it as a separate diagnosis. The frequency and the determinants of sleep misperception in general population samples are unknown. In this study we examined the role of objective sleep duration, a novel marker in phenotyping insomnia, and psychological profiles on sleep misperception in a large, general population sample.Methods-142 insomniacs and 724 controls selected from a general random sample of 1,741 individuals (age ≥ 20 years) underwent a polysomnographic evaluation, completed the Minnesota Multiphasic Personality Inventory-2, and were split into two groups based on their objective sleep duration: "normal sleep duration" (≥ 6 hours) and "short sleep duration" (< 6 hours).Results-The discrepancy between subjective and objective sleep duration was determined by two independent factors. Short sleepers reported more sleep than they objectively had and insomniacs reported less sleep than controls with similar objective sleep duration. The additive effect of these two factors resulted in underestimation only in insomniacs with normal sleep duration. Insomniacs with normal sleep duration showed a MMPI-2 profile of high depression and anxiety, and low ego strength, whereas insomniacs with short sleep duration showed a profile of a medical disorder.Conclusions-Underestimation of sleep duration is prevalent among insomniacs with objective normal sleep duration. Anxious-ruminative traits and poor resources for coping with stress appear to mediate the underestimation of sleep duration. These data further support the validity and clinical utility of objective sleep measures in phenotyping insomnia.

SynopsisIn insomnia, which is a very common sleep disorder, objective sleep measures, EEG activity, physiologic findings, HPA axis activity and inflammation markers suggest that it is not a state of sleep loss, but a disorder of hyperarousal present both during the night and the daytime. Several psychological and physiological factors contribute to the onset and perpetuation of insomnia, such as anxious-ruminative personality traits, stressful events, age-related sleep homeostasis weakening mechanisms, menopause and biologic - genetic diathesis of CNS hyperarousal. The therapeutic approach in insomnia should be multidimensional reducing the overall emotional and physiologic hyperarousal and its underlying factors present throughout the 24-h sleep/wake period.

Nonpsychologically distressed, normally sleeping, obese men had low cortisol secretion. The cortisol secretion was slightly activated by SA and returned to low by CPAP use. The low cortisol secretion in obesity through its inferred hyposecretion of hypothalamic CRH might predispose the obese to sleep apnea.

Our results suggest that sleep breathing disorders, predominantly obstructive, seem to be common in PD and those events correlate with the severity of the disease.

Sleep loss has been associated with increased sleepiness, decreased performance, elevations in inflammatory cytokines, and insulin resistance. Daytime napping has been promoted as a countermeasure to sleep loss. To assess the effects of a 2-h midafternoon nap following a night of sleep loss on postnap sleepiness, performance, cortisol, and IL-6, 41 young healthy individuals (20 men, 21 women) participated in a 7-day sleep deprivation experiment (4 consecutive nights followed by a night of sleep loss and 2 recovery nights). One-half of the subjects were randomly assigned to take a midafternoon nap (1400-1600) the day following the night of total sleep loss. Serial 24-h blood sampling, multiple sleep latency test (MSLT), subjective levels of sleepiness, and psychomotor vigilance task (PVT) were completed on the fourth (predeprivation) and sixth days (postdeprivation). During the nap, subjects had a significant drop in cortisol and IL-6 levels (P < 0.05). After the nap they experienced significantly less sleepiness (MSLT and subjective, P < 0.05) and a smaller improvement on the PVT (P < 0.1). At that time, they had a significant transient increase in their cortisol levels (P < 0.05). In contrast, the levels of IL-6 tended to remain decreased for approximately 8 h (P = 0.1). We conclude that a 2-h midafternoon nap improves alertness, and to a lesser degree performance, and reverses the effects of one night of sleep loss on cortisol and IL-6. The redistribution of cortisol secretion and the prolonged suppression of IL-6 secretion are beneficial, as they improve alertness and performance.

Background Visceral adiposity and obstructive sleep apnoea (OSA) may be independently associated with daytime sleepiness/low performance, insulin resistance, hypercytokinaemia, and/or hypertension. The objectives of this study are to simultaneously test these associations at baseline and after 3 months of continuous positive airway pressure (CPAP) therapy. Materials and methods Sixteen obese men with OSA; 13 non-apnoeic, obese controls, and 15 non-obese controls were monitored in the sleep laboratory for four consecutive nights. Objective measures of daytime sleepiness and performance, serial 24 h plasma measures of interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α), TNF receptor 1 (TNF-r1) and adiponectin, fasting blood glucose and insulin, visceral adiposity and blood pressure were obtained. Sleep apnoeics were re-assessed using the same protocol after 3 months of CPAP. Results At baseline, IL-6, TNF-r1, and insulin resistance were highest in OSA patients, intermediate in obese controls, and lowest in non-obese controls (P < 0·05). Visceral fat was significantly greater in sleep apnoeics than obese controls and predicted insulin resistance and IL-6 levels, whereas OSA predicted TNF-r1 levels (P < 0·05). CPAP decreased daytime sleepiness and blood pressure (P < 0·05), but did not affect fasting glucose or insulin or around the clock adiponectin, IL-6, TNF-α, or TNF-r1 levels. Conclusions In obese sleep apnoeics, visceral fat is strongly associated with insulin resistance and inflammation. CPAP decreases sleepiness and moderates hypertension but does not affect visceral adiposity, insulin resistance, hypoadiponectinaemia or hypercytokinaemia, all of which are independent risk factors for cardiovascular disease and diabetes.