Maria Basta

Insomnia With Objective Short Sleep Duration and Incident Hypertension The Penn State Cohort

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, whereas poor sleep was defined as moderate-to-severe sleep difficulties. All of the subjects underwent 8-hour polysomnography. Sleep-disordered breathing (SDB) was defined as an obstructive apnea/hypopnea index ≥5. We used the median polysomnographic percentage of sleep time to define short sleep duration (ie, <6 hours). We controlled for sex, race, age, caffeine, cigarettes and alcohol consumption, depression, sleep-disordered breathing, diabetes mellitus, obesity, and blood pressure in our analyses. Compared with normal sleepers who slept ≥6 hours, the highest risk for incident hypertension was in chronic insomniacs with short sleep duration (odds ratio, 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 (odds ratio, 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 sleep-disordered breathing. Objective short sleep duration in insomnia may serve as a useful predictor of the biological severity of the disorder.

Sleep misperception and chronic insomnia in the general population: role of objective sleep duration and psychological profiles.

Objective: To examine the role of objective sleep duration, a novel marker in phenotyping insomnia, and psychological profiles on sleep misperception in a large, general population sample. 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. Methods: A total of 142 insomniacs and 724 controls selected from a general random sample of 1,741 individuals (aged ≥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 Minnesota Multiphasic Personality Inventory-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 seem to mediate the underestimation of sleep duration. These data further support the validity and clinical utility of objective sleep measures in phenotyping insomnia. BMI = body mass index; DSM-IV = Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition; MANCOVA = multivariate analysis of covariance; MMPI-2 = Minnesota Multiphasic Personality Inventory-2; PLMS = periodic limb movements; SDB = sleep disordered breathing.

Selective effects of CPAP on sleep apnoea-associated manifestations

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.

Leptin and Hunger Levels in Young Healthy Adults After One Night of Sleep Loss

Short‐term sleep curtailment associated with activation of the stress system in healthy, young adults has been shown to be associated with decreased leptin levels, impaired insulin sensitivity, and increased hunger and appetite. To assess the effects of one night of sleep loss in a less stressful environment on hunger, leptin, adiponectin, cortisol and blood pressure/heart rate, and whether a 2‐h mid‐afternoon nap reverses the changes associated with sleep loss, 21 young healthy individuals (10 men, 11 women) participated in a 7‐day sleep deprivation experiment (four consecutive nights followed by one night of sleep loss and two recovery nights). Half of the subjects were randomly assigned to take a mid‐afternoon nap (14:00–16:00 hours) the day following the night of total sleep loss. Serial 24‐h blood sampling and hunger scales were completed on the fourth (predeprivation) and sixth day (postdeprivation). Leptin levels were significantly increased after one night of total sleep loss, whereas adiponectin, cortisol levels, blood pressure/heart rate, and hunger were not affected. Daytime napping did not influence the effects of sleep loss on leptin, adiponectin, or hunger. Acute sleep loss, in a less stressful environment, influences leptin levels in an opposite manner from that of short‐term sleep curtailment associated with activation of the stress system. It appears that sleep loss associated with activation of the stress system but not sleep loss per se may lead to increased hunger and appetite and hormonal changes, which ultimately may lead to increased consumption of ‘comfort’ food and obesity.

Unveiling the longitudinal association between short sleep duration and the incidence of obesity: the Penn State Cohort.

Objective:Several epidemiologic, longitudinal studies have reported that short sleep duration is a risk factor for the incidence of obesity. However, the vast majority of these studies used self-reported measures of sleep duration and did not examine the role of objective short sleep duration, subjective sleep disturbances and emotional stress.Design:Longitudinal, population-based study.Subjects:We studied a random sample of 815 non-obese adults from the Penn State Cohort in the sleep laboratory for one night using polysomnography (PSG) and followed them up for a mean of 7.5 years. Subjective and objective measures of sleep as well as emotional stress were obtained at baseline. Obesity was defined as a body mass index (BMI) ⩾30 kg/ m-2.Results:The incidence of obesity was 15% and it was significantly higher in women and in individuals who reported sleep disturbances, shorter sleep duration and higher emotional stress. Significant mediating effects showed that individuals with subjective sleep disturbances who developed obesity reported the shortest sleep duration and the highest emotional stress, and that subjective sleep disturbances and emotional stress were independent predictors of incident obesity. Further analyses revealed that the association between short sleep duration, subjective sleep disturbances and emotional stress with incident obesity was stronger in young and middle-age adults. Objective short sleep duration was not associated with a significantly increased risk of incident obesity.Conclusion:Self-reported short sleep duration in non-obese individuals at risk of developing obesity is a surrogate marker of emotional stress and subjective sleep disturbances. Objective short sleep duration is not associated with a significant increased risk of incident obesity. The detection and treatment of sleep disturbances and emotional stress should become a target of our preventive strategies against obesity.

Effects of recovery sleep after one work week of mild sleep restriction on interleukin-6 and cortisol secretion and daytime sleepiness and performance

One workweek of mild sleep restriction adversely impacts sleepiness, performance, and proinflammatory cytokines. Many individuals try to overcome these adverse effects by extending their sleep on weekends. To assess whether extended recovery sleep reverses the effects of mild sleep restriction on sleepiness/alertness, inflammation, and stress hormones, 30 healthy young men and women (mean age ± SD, 24.7 ± 3.5 yr; mean body mass index ± SD, 23.6 ± 2.4 kg/m(2)) participated in a sleep laboratory experiment of 13 nights [4 baseline nights (8 h/night), followed by 6 sleep restriction nights (6 h/night) and 3 recovery nights (10 h/night)]. Twenty-four-hour profiles of circulating IL-6 and cortisol, objective and subjective daytime sleepiness (Multiple Sleep Latency Test and Stanford Sleepiness Scale), and performance (Psychomotor Vigilance Task) were assessed on days 4 (baseline), 10 (after 1 wk of sleep restriction), and 13 (after 2 nights of recovery sleep). Serial 24-h IL-6 plasma levels increased significantly during sleep restriction and returned to baseline after recovery sleep. Serial 24-h cortisol levels during restriction did not change compared with baseline, but after recovery they were significantly lower. Subjective and objective sleepiness increased significantly after restriction and returned to baseline after recovery. In contrast, performance deteriorated significantly after restriction and did not improve after recovery. Extended recovery sleep over the weekend reverses the impact of one work week of mild sleep restriction on daytime sleepiness, fatigue, and IL-6 levels, reduces cortisol levels, but does not correct performance deficits. The long-term effects of a repeated sleep restriction/sleep recovery weekly cycle in humans remain unknown.

Persistent Insomnia: the Role of Objective Short Sleep Duration and Mental Health

STUDY OBJECTIVES Few population-based, longitudinal studies have examined risk factors for persistent insomnia, and the results are inconsistent. Furthermore, none of these studies have examined the role of polysomnographic (PSG) variables such as sleep duration or sleep apnea on the persistence of insomnia. DESIGN Representative longitudinal study. SETTING Sleep laboratory. PARTICIPANTS From a random, general population sample of 1741 individuals of the adult Penn State Cohort, 1395 were followed-up after 7.5 years. MEASUREMENTS Individuals underwent one-night PSG and full medical evaluation at baseline and a telephone interview at follow-up. PSG sleep duration was analyzed as a continuous variable and as a categorical variable: < 6 h sleep (short sleep duration) and ≥ 6 h sleep (longer sleep duration). RESULTS The rates of insomnia persistence, partial remission, and full remission were 44.0%, 30.0%, and 26.0%, respectively. Objective short sleep duration significantly increased the odds of persistent insomnia as compared to normal sleep (OR = 3.19) and to fully remitted insomnia (OR = 4.92). Mental health problems at baseline were strongly associated with persistent insomnia as compared to normal sleep (OR = 9.67) and to a lesser degree compared to fully remitted insomnia (OR = 3.68). Smoking, caffeine, and alcohol consumption and sleep apnea did not predict persistent insomnia. CONCLUSIONS Objective short sleep duration and mental health problems are the strongest predictors of persistent insomnia. These data further support the validity and clinical utility of objective short sleep duration as a novel marker of the biological severity of insomnia.

Sleep apnoea, sleepiness, inflammation and insulin resistance in middle-aged males and females

In obese males obstructive sleep apnoea (OSA) is associated with inflammation and insulin resistance; however, findings are confounded by adipose tissue, a hormone- and cytokine-secreting organ. Our goal was to examine whether in a relatively nonobese population, OSA is associated with sleepiness and inflammation/insulin resistance, and to assess the effects of a 2-month placebo-controlled continuous positive airway pressure (CPAP) use. 77 subjects, 38 middle-aged males and post-menopausal females with OSA and 39 male and female controls, were studied in the sleep laboratory for 4 nights. Measures of sleepiness (objective and subjective), performance, serial 24-h blood samples for interleukin (IL)-6, tumour necrosis factor receptor (TNFR)-1, leptin and adiponectin, and single samples for high-sensitivity C-reactive protein (hsCRP), fasting glucose and insulin levels were obtained. Apnoeic males were significantly sleepier and had significantly higher hsCRP, IL-6, leptin and insulin resistance than controls. Apnoeic females had significantly higher hsCRP; however, objective sleepiness, IL-6, TNFR-1, insulin resistance (Homeostatic Model Assessment index), leptin and adiponectin were similar to controls. CPAP improved subjective sleepiness, but no changes were observed in any of the biomarkers. In conclusion, OSA is associated with sleepiness, inflammation and insulin resistance, even in nonobese males, and this association is stronger in males than in females. Short-term CPAP does not improve the inflammatory/metabolic aberrations in OSA. OSA is associated with sleepiness and inflammation/insulin resistance in nonobese males and females http://ow.ly/qesMA

Sleep apnoea and visceral adiposity in middle-aged male and female subjects

In obese male subjects, visceral adiposity has been associated with obstructive sleep apnoea (OSA), while studies in overweight males and females are limited. Our goal was to examine the association between OSA and visceral fat in a relatively nonobese population and assess the effects of 2 months placebo-controlled continuous positive airway pressure (CPAP) use on abdominal fat. 81 subjects, 22 middle-aged males and 20 post-menopausal females with OSA, and 19 male and 20 female controls were studied in the sleep laboratory for four nights. Abdominal (visceral (VAT) and subcutaneous (SAT) adipose tissue) and liver fat were assessed with computed tomography. OSA patients were re-assessed post-CPAP and post sham-CPAP. Apnoeic males had significantly higher VAT than controls, while apnoeic females had higher SAT than controls. In both sexes, OSA was associated with increased liver fat. In males, apnoea was associated with VAT whereas in females it was associated with subcutaneous, visceral and total fat. CPAP did not affect abdominal and liver fat. In overweight males, visceral adiposity is associated with OSA whereas in females it is associated with global adiposity. In overweight males, our therapeutic goal should be the reduction of visceral adiposity and its metabolic correlates, whereas, in females, weight loss may be sufficient. Short-term CPAP treatment does not affect general, abdominal or intra-hepatic adiposity.

Sleep apnoea and the hypothalamic-pituitary-adrenal axis in men and women: effects of continuous positive airway pressure.

Previous findings on the association of obstructive sleep apnoea (OSA) and the hypothalamic–pituitary–adrenal (HPA) axis are inconsistent, partly due to the confounding effect of obesity and infrequent sampling. Our goal was to examine whether in a relatively nonobese population, OSA is associated with elevated cortisol levels and to assess the effects of a 2-month placebo-controlled continuous positive airway pressure (sham-CPAP) use. 72 subjects (35 middle-aged males and post-menopausal females with OSA, and 37 male and female controls) were studied in the sleep laboratory for four nights. 24-h blood sampling was performed every hour on the fourth day and night in the sleep laboratory at baseline, after sham-CPAP and after CPAP treatment. In both apnoeic men and women, OSA was associated with significantly higher 24-h cortisol levels compared with controls, whereas CPAP lowered cortisol levels significantly, close to those of controls. These results suggest that OSA in nonobese men and slightly obese women is associated with HPA axis activation, similar albeit stronger compared with obese individuals with sleep apnoea. Short-term CPAP use decreased cortisol levels significantly compared with baseline, indicating that CPAP may have a protective effect against comorbidities frequently associated with chronic activation of the HPA axis, e.g. hypertension. OSA in nonobese men/slightly obese women is associated with HPA axis activation and CPAP lowers HPA axis activity http://ow.ly/Stn94