Deficits in daytime performance due to sleep loss are experienced universally and associated with a significant social, financial, and human cost. Microsleeps, sleep attacks, and lapses in cognition increase with sleep loss as a function of state instability. Sleep deprivation studies repeatedly show a variable (negative) impact on mood, cognitive performance, and motor function due to an increasing sleep propensity and destabilization of the wake state. Specific neurocognitive domains including executive attention, working memory, and divergent higher cognitive functions are particularly vulnerable to sleep loss. In humans, functional metabolic and neurophysiological studies demonstrate that neural systems involved in executive function (i.e., prefrontal cortex) are more susceptible to sleep deprivation in some individuals than others. Recent chronic partial sleep deprivation experiments, which more closely replicate sleep loss in society, demonstrate that profound neurocognitive deficits accumulate over time in the face of subjective adaptation to the sensation of sleepiness. Sleep deprivation associated with disease-related sleep fragmentation (i.e., sleep apnea and restless legs syndrome) also results in neurocognitive performance decrements similar to those seen in sleep restriction studies. Performance deficits associated with sleep disorders are often viewed as a simple function of disease severity; however, recent experiments suggest that individual vulnerability to sleep loss may play a more critical role than previously thought.

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Neurocognitive Consequences of Sleep Deprivation

Sleep-disordered breathing is a prevalent condition associated with impairment of daytime function and may predispose individuals to metabolic abnormalities independent of obesity. The primary objective of this study was to determine the metabolic consequences and community prevalence of sleep-disordered breathing in mildly obese, but otherwise healthy, individuals. One hundred and fifty healthy men, without diabetes or cardiopulmonary disease, were recruited from the community. Measurements included polysomnography, a multiple sleep latency test, an oral glucose tolerance test, determination of body fat by hydrodensitometry, and fasting insulin and lipids. The prevalence of sleep-disordered breathing, depending on the apnea-hypopnea index (AHI) cutoff, ranged from 40 to 60%. After adjusting for body mass index (BMI) and percent body fat, an AHI gt-or-equal, slanted 5 events/h was associated with an increased risk of having impaired or diabetic glucose tolerance (odds ratio, 2.15; 95% CI, 1.05-4.38). The impairment in glucose tolerance was related to the severity of oxygen desaturation (DeltaSa(O(2))) associated with sleep-disordered breathing. For a 4% decrease in oxygen saturation, the associated odds ratio for worsening glucose tolerance was 1.99 (95% CI, 1.11 to 3.56) after adjusting for percent body fat, BMI, and AHI. Multivariable linear regression analyses revealed that increasing AHI was associated with worsening insulin resistance independent of obesity. Thus, sleep-disordered breathing is a prevalent condition in mildly obese men and is independently associated with glucose intolerance and insulin resistance.

Sleep-disordered Breathing and Insulin Resistance in Middle-aged and Overweight Men

Background: Clinical observations have linked sleepdisordered breathing, a condition of repeated apneas and hypopneas during sleep, with hypertension but evidence for an independent association has been lacking. Understanding this relationship is important because the prevalence of sleep-disordered breathing is high in adults. Objective: To test the hypothesis that sleep-disordered breathing is related to elevated blood pressure independent of confounding factors. Methods: The sample included 1060 employed women and men aged 30 through 60 years who had completed an overnight protocol as part of the Wisconsin Sleep Cohort Study. In-laboratory polysomnography was used to determine sleep-disordered breathing status, quantified as the number of apneas and hypopneas per hour of sleep (apnea-hypopnea index). Blood pressure was measured on the night polysomnography was performed. Results: Blood pressure increased linearly with increasing apnea-hypopnea index (P=.003 for systolic,P=.01 for diastolic, adjusted for confounding factors). The magnitude of the linear association increased with decreasing obesity. At a body mass index (weight in kilograms divided by the square of the height in meters) of 30 kg/m2, an apnea-hypopnea index of 15 (vs 0) was associated with blood pressure increases of 3.6 mm Hg for systolic (95% confidence interval, 1.3-6.0) and 1.8 mm Hg for diastolic (95% confidence interval, 0.3-3.3). The odds ratio for hypertension associated with an apneahypopnea index of 15 (vs 0) was 1.8 (95% confidence interval, 1.3-2.4). Conclusions: There is a dose-response relationship between sleep-disordered breathing and blood pressure, independent of known confounding factors. If causal, the high prevalence of sleep-disordered breathing could account for hypertension in a substantial number of adults in the United States. Arch Intern Med. 1997;157:1746-1752

https://jamanetwork.com/HttpHandlers/ArticlePdfHandler.ashx?journal=INTEMED&articleId=623690&pdfFileName=archinte_157_15_019.pdf

Population-Based Study of Sleep-Disordered Breathing as a Risk Factor for Hypertension

Background: Continuous positive airway pressure (CPAP) in patients with obstructive sleep apnea syndrome (OSAS) might lower blood pressure, but evidence from clinical studies is inconsistent, perhaps as a result of small sample size or heterogeneity in study design. This study aimed to assess whether CPAP reduces ambulatory blood pressure in patients with OSAS, to quantify the effect size with precision, and to identify trial characteristics associated with the greatest blood pressure reductions.

https://jamanetwork.com/journals/jamainternalmedicine/articlepdf/412333/ira60024_757_765.pdf

The impact of continuous positive airway pressure on blood pressure in patients with obstructive sleep apnea syndrome: evidence from a meta-analysis of placebo-controlled randomized trials.

ContextSleep-disordered breathing (SDB) is both prevalent and associated with
serious chronic illness. The incidence of SDB and the effect of risk factors
on this incidence are unknown.ObjectiveTo determine the 5-year incidence of SDB overall and as influenced by
risk factors.Design, Setting, and ParticipantsOf the 1149 participants in the Cleveland Family Study, those aged 18
years or older, from either case or control families, who had 2 in-home sleep
studies 5 years apart. The first had to have been performed before June 30,
1997, and had to have normal results (apnea hypopnea index [AHI] <5). Data
included questionnaire information on medical and family history, SDB symptoms;
measurement of height, weight, blood pressure, waist and hip circumference,
and serum cholesterol concentration; and overnight sleep monitoring.Main Outcome MeasureApnea hypopnea index, defined as number of apneas and hypopneas per
hour of sleep. Sleep-disordered breathing was defined by an AHI of at least
10 (mild to moderate) or of at least 15 (moderate).ResultsForty-seven (16%) of 286 eligible participants, (95% confidence interval
[CI], 13%-21%) had a second-study AHI of at least 10 and 29 (10%) participants
(95% CI, 7%-14%) had a second-study AHI result of at least 15. For the AHI
results of at least 15, we estimate that about 2.5% may represent test variability.
By ordinal logistic regression analysis, AHI was significantly associated
with age (odds ratio [OR] per 10-year increase, 1.79; 95% CI, 1.41-2.27),
body mass index (BMI; OR per 1-unit increase, 1.14; 95% CI, 1.10-1.19), sex
(OR for men vs women, 4.12; 95% CI, 2.29-7.43), waist-hip ratio (OR per 0.1
unit increase, 1.61; 95% CI, 1.04-2.28), and serum cholesterol concentration
(OR per 10-mg/dL [0.25-mmol/L] increase, 1.11; 95% CI, 1.03-1.19). Interactions
were noted between age and both sex (P = .003) and
BMI (P = .05). The OR for increased AHI per 10-year
age increase was 2.41 in women (95% CI, 1.78-3.26) and 1.15 in men (95% CI,
0.78-1.68), with the male vs female OR decreasing from 5.04 (95% CI, 2.19-11.6)
at age 30 years to 0.54 (95% CI, 0.15-1.99) at age 60 years. The OR for increased
AHI per 1-unit increase in BMI decreased from 1.21 (95% CI, 1.11-1.31) at
age 20 years to 1.05 (95% CI, 0.96-1.15) at age 60 years.ConclusionsThe 5-year incidence is about 7.5% for moderately severe SDB and 16%
(or less) for mild to moderately severe SDB. Incidence of SDB is influenced
independently by age, sex, BMI, waist-hip ratio, and serum cholesterol concentration.
Predominance in men diminishes with increasing age, and by age 50 years, incidence
rates among men and women are similar. The effect of BMI also decreases with
age and may be negligible at age 60 years.

https://jamanetwork.com/journals/jama/articlepdf/196491/JOC22269.pdf

Incidence of Sleep-Disordered Breathing in an Urban Adult Population: The Relative Importance of Risk Factors in the Development of Sleep-Disordered Breathing

Sleep-disturbed breathing, which includes apneas, hypopneas, and oxygen desaturations, occurs in asymptomatic individuals and increases with age. Obstructive apnea is the most frequent type of respiratory disturbance documented by polysomonography, the gold standard test for assessing sleep-disturbed breathing. Many of the prevalence studies done to date have had one or more methodological weaknesses, including selection biases, varying definitions of obstructive sleep apnea, failure to distinguish types of apneas, failure to control for confounding variables, and small sample size. Although there is consensus on the definitions of sleep-disturbed breathing, the appropriate number of apneas and hypopneas for diagnosing clinically significant obstructive sleep apnea is uncertain. While the cutoff of five or more apneas and hypopneas per hour is historically considered abnormal, the origins of this number are vague, and the longevity of those who have this value on polysomnography is not necessarily reduced. This is particularly true among those without symptoms of obstructive sleep apnea syndrome, which include excessive daytime sleepiness, snoring, nocturnal awakenings, and morning headaches. Investigators should be careful to distinguish symptomatic study subjects from asymptomatic subjects, and to exclude central apneas in calculating their estimates. In addition, various studies have used different definitions of sleep apnea syndrome, making comparisons of point estimates difficult. It would be more appropriate for researchers to estimate morbidity and mortality indices with confidence intervals, using several different cutoff points. Subject selection in all studies should follow a two-stage sampling procedure. All subjects with symptoms compatible with obstructive sleep apnea syndrome and a subsample of asymptomatic individuals should be studied with all-night polysomnography. If portable monitoring is used, the validity and reproducibility of this diagnostic method should be assessed. Subjects with significant comorbidity should be excluded from prevalence studies. Factors that clearly increase the risk of sleep-disturbed breathing and obstructive sleep apnea and its related symptoms include age, structural abnormalities of the upper airway, sedatives and alcohol, and probably family history. Although endocrine changes such as growth hormone, thyroid hormone, and progesterone deficiency also have been suggested as risk factors for exacerbating obstructive sleep apnea syndrome, there is minimal epidemiologic evidence to support this. Case-control studies are recommended to assess the relation of endocrine factors to obstructive sleep apnea syndrome in a rigorous fashion. A limited number of mortality studies have suggested decreased survival in persons with the obstructive sleep apnea syndrome, possibly primarily due to vascular-related disease.(ABSTRACT TRUNCATED AT 400 WORDS)

Rochelle Goldberg

Papers

Epidemiology of Obstructive Sleep Apnea