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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidemiological studies have implicated obstructive sleep apnea (OSA) as an independent comorbid factor in cardiovascular and cerebrovascular diseases. It is postulated that recurrent episodes of occlusion of upper airways during sleep result in pathophysiological changes that may predispose to vascular diseases. Insulin resistance is a known risk factor for atherosclerosis, and we postulate that OSA represents a stress that promotes insulin resistance, hence atherogenesis. This study investigated the relationship between sleep-disordered breathing and insulin resistance, indicated by fasting serum insulin level and insulin resistance index based on the homeostasis model assessment method (HOMA-IR). A total of 270 consecutive subjects (197 male) who were referred for polysomnography and who did not have known diabetes mellitus were included, and 185 were documented to have OSA defined as an apnea-hypopnea index (AHI) > or =5. OSA subjects were more insulin resistant, as indicated by higher levels of fasting serum insulin (p = 0.001) and HOMA-IR (p < 0.001); they were also older and more obese. Stepwise multiple linear regression analysis showed that obesity was the major determinant of insulin resistance but sleep-disordered breathing parameters (AHI and minimum oxygen saturation) were also independent determinants of insulin resistance (fasting insulin: AHI, p = 0.02, minimum O(2), p = 0.041; HOMA-IR: AHI, p = 0.044, minimum O(2), p = 0.022); this association between OSA and insulin resistance was seen in both obese and nonobese subjects. Each additional apnea or hypopnea per sleep hour increased the fasting insulin level and HOMA-IR by about 0.5%. Further analysis of the relationship of insulin resistance and hypertension confirmed that insulin resistance was a significant factor for hypertension in this cohort. Our findings suggest that OSA is independently associated with insulin resistance, and its role in the atherogenic potential of sleep disordered breathing is worthy of further exploration.
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PMID:Obstructive sleep apnea is independently associated with insulin resistance. 1187 3

Obesity is associated with a number of medical conditions that lead to increased morbidity and increased mortality. Both the National Institutes of Health and the World Health Organization define obesity as a body mass index (BMI) > or = 30 kg/m2 and overweight as a BMI 25-30. The most common conditions associated with obesity are insulin resistance, diabetes mellitus, hypertension, dyslipidemia, cardiovascular disease, gallstones and cholecystitis, sleep apnea and other respiratory dysfunction, and the increased incidence of certain cancers. These are discussed below.
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PMID:The medical risks of obesity. 1196 7

Despite years of investigation our fundamental and clinical knowledge of the major public health problem, obesity-hypertension, is relatively meager and certainly inadequate. We are at a loss to explain why the pathophysiological mechanisms of obesity and hypertension are so inextricably intertwined. Adding to this frustration is the inadequacy of the treatment for obesity. Hemodynamically, we recognize that the expanded plasma volume caused by obesity imparts a significant volume overload on the heart, thereby increasing cardiac output, while the hypertension compounds this ventricular stress by an associated pressure overload. Thus, the ventricle has an eccentric as well as a concentric adaptive hypertrophy. Associated with obesity is an increased burden of pressor (e.g., catecholamine, angiotensin II); peptide (e.g., endothelin, insulin, leptin, natriuretic); hormonal (e.g., growth, steroids, thyroid); and neural mechanisms. Further complicating these alterations are electrolytic, lipid, uric acid, and other metabolic factors. Both diseases (obesity and hypertension) are exacerbated by frequently encountered comorbid pathophysiological disorders including atherosclerosis, ventricular dysfunction, diabetes mellitus, hyperlipidemias, and sleep apnea. To add to these issues, therapy for obesity-hypertension is suboptimal. Behavioral modification (of overweight and obesity) is commonly characterized by recidivism, and pharmacotherapy of obesity is woefully inadequate; the present agents either raise arterial pressure or are fraught with adverse effects. Fortunately, there are no contraindications imparted by obesity that complicate the drug treatment of the associated hypertension. Each of the lifestyle modifications and seven classes of antihypertensive therapy that is discussed herein is done in light of the coexistent hypertension and comorbid diseases.
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PMID:Clinical management of the obese hypertensive patient. 1204 91

Sleep disordered breathing (SDB) is a complication of obesity estimated to occur in about 4-6% of overweight individuals. These respiratory disturbances during sleep incorporate a number of conditions including snoring, upper airway resistance syndrome and obstructive sleep apnoea syndrome (OSAS). It is thought that as well as having deleterious effects on sleep quality these conditions may also promote cardiovascular and hormonal changes leading to an elevated blood pressure and an increased incidence of cardiovascular morbidity. Evidence reviewed here points to an alteration in sympathovagal balance, baroreceptor sensitivity, insulin resistance and leptin, growth hormone and lipid levels. Whether these changes are a consequence of the associated obesity or the SDB itself remains to be proven.
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PMID:Sleep disordered breathing--a new component of syndrome x? 1211 97

Sleep and sleep disorders play a prominent role in hormone regulation. Given that sleep disordered breathing (SDB) and diabetes mellitus (DM) are thought to result from obesity, it has been assumed that when the two coexist, the diabetes was caused by the obesity. However, new data has shed light on the effects that SDB, sleep deprivation, and snoring have on glucose regulation. It now appears that in addition to causing daytime drowsiness, cardiovascular disease, mood and memory disturbances, impotence, and car wrecks, obstructive sleep apnea (OSA) also promotes insulin resistance. Though data is still sketchy on the optimum management of coexisting DM and OSA, large-scale studies will most likely prove that homeostatic glucose control in patients with sleep apnea will require aggressive treatment of their SDB.
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PMID:Sleep and the endocrine system: new associations to old diseases. 1239 57

Patients with sleep disordered breathing (SDB) are at increased risk for cardiovascular disease including hypertension, angina, myocardial infarction, and stroke. Neurohumoral and hemodynamic responses to untreated sleep apnea are likely mechanisms that produce functional and structural changes within the cardiovascular system. Obesity, higher blood pressure, and advancing age, which are common characteristics of patients with SDB, contribute to the overall risk for cardiovascular disease. Recent studies indicate that OSA is associated with or aggravates other risk markers for cardiovascular disease. These factors include leptin, C-reactive protein, homocysteine, and insulin resistance syndrome. Elevations in C-reactive protein and glucose intolerance may be correlated with the severity of SDB. The impact of alleviating SDB on these cardiovascular risk factors has not been fully elucidated. Regardless, assessment of overall cardiovascular risk in patients with sleep apnea is warranted to identify those individuals that are high-risk who require immediate attention and intervention or in those that should be treated more aggressively.
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PMID:Sleep disordered breathing and risk factors for cardiovascular disease. 1239 60

Possibly the most important outcomes of bariatric surgery involve changes in obesity-related illness, quality of life (QOL), and psychologic well-being. Dramatic improvement or resolution of serious medical comorbidity accompanies the weight loss following laparoscopic adjustable gastric banding with the LAP-BAND (INAMED Health, Santa Barbara, CA). There are major improvements in the conditions of the metabolic syndrome, which is characterized by impaired glucose tolerance, dyslipidemia, and hypertension. Improvement in insulin sensitivity and pancreatic beta-cell function associated with weight loss induces remission in the majority of type 2 diabetics and reduces the risk of others developing type 2 diabetes. Improvement in dyslipidemia is characterized by raised high-density lipoprotein cholesterol and lower triglyceride concentrations. Together with lower blood pressure, these changes provide a substantial reduction in cardiovascular risk. Other medical conditions caused or aggravated by obesity are also significantly improved, including sleep apnea, daytime sleepiness, asthma, and gastroesophageal reflux. Weight loss is associated with improved fertility and more favorable pregnancy outcomes. All aspects of QOL improve substantially, especially physical disability, and post-weight-loss QOL measures approximate those of the general population. There are also major improvements in body image and reduction in depressive illness. These changes provide perhaps the most compelling data regarding the value of LAP-BAND surgery and underlie the great satisfaction experienced by patients.
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PMID:Changes in comorbidities and improvements in quality of life after LAP-BAND placement. 1252 52

The obesity epidemic is driving metabolic (insulin resistance) syndrome-related health problems including an approximately threefold increased coronary heart disease risk. Sympathetic hyperfunction may participate in the pathogenesis and complications of the metabolic syndrome including higher blood pressure, a more active renin-angiotensin system, insulin resistance, faster heart rates, and excess cardiovascular disease including sudden death. Possible factors augmenting sympathetic activation in the metabolic syndrome include alterations of insulin, leptin, nonesterified fatty acids (NEFAs), cytokines, tri-iodothyronine, eicosanoids, sleep apnea, nitric oxide, endorphins, and neuropeptide Y. Of note, high plasma NEFAs are a risk factor for hypertension and sudden death. In short-term human studies, NEFAs can raise blood pressure, heart rate, and a(1)-adrenoceptor vasoreactivity, while reducing baroreflex sensitivity, endothelium-dependent vasodilatation, and vascular compliance. Efforts to further identify the mechanisms and consequences of sympathetic dysfunction in the metabolic syndrome may provide insights for therapeutic advances to ameliorate the excess cardiovascular risk and adverse outcomes.
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PMID:Insulin resistance and the sympathetic nervous system. 1272 58

We evaluated body weight loss and growth hormone secretion in patients with sleep-disordered breathing associated with chronic obstructive pulmonary disease. Of 11 patients hospitalized for pulmonary rehabilitation, five (WL group) had a history of body weight loss within two years before their interviews, while the other 6 patients (NWL group) had no changes in body weight. All patients underwent body index measurements, pulmonary function tests, blood gas analyses, assessments of nutritional status, and full night polysomnography for two consecutive days. Growth hormone levels were measured in the first 3-hour period following falling asleep. There were no significant inter-group differences between the results of pulmonary function tests, blood gas analyses, or nutritional status assessment. The WL group had a significantly higher percentage loss of body weight than the NWL group (mean +/- S.D. 11.5 +/- 4.7% in the WL group versus 2.7 +/- 1.8% in the NWL group, p < 0.01). The WL group had a significantly higher sleep apnea/hypopnea index than the NWL group (42.4 +/- 9.5/hr in the WL group versus 7.8 +/- 2.9/hr in the NWL group, p < 0.01). The WL group showed a higher rate of stage I + II sleep than the NWL group (84.9 +/- 7.0% versus 64.5 +/- 8.7%), with lower rates of slow wave sleep (2.2 +/- 2.1% versus 15.0 +/- 8.7%) and rapid eye movement sleep (12.9 +/- 6.3% versus 20.6 +/- 1.0%). The WL group showed a low level of growth hormone secretion with no peak in the sequential curve, but had a higher level of insulin growth factor-1 than the NWL group (148 +/- 36 ng/ml versus 90 +/- 22 ng/ml, p < 0.01). These results suggest that chronic obstructive pulmonary disease patients undergoing weight loss are likely to have an increase of growth hormone secretions in the daytime, possibly induced by underlying psychiatric disorders such as depression. Patients with chronic obstructive pulmonary disease may lose weight regardless of nutritional status because of a disturbance of growth hormone secretion resulting of sleep-disordered breathing.
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PMID:[Relationship between sleep disordered breathing and body weight loss in patients with chronic obstructive pulmonary disease]. 1279 81

Obstructive sleep apnoea (OSA) is a very prevalent disorder particularly amongst middle-aged, obese men, although its existence in women as well as in lean individuals is increasingly recognized. Despite the early recognition of the strong association between OSA and obesity, and OSA and cardiovascular problems, sleep apnoea has been treated as a 'local abnormality' of the respiratory track rather than as a 'systemic illness'. In 1997, we first reported that the pro-inflammatory cytokines interleukin (IL)-6 and tumour necrosis factor-alpha (TNF alpha) were elevated in patients with disorders of excessive daytime sleepiness (EDS) and proposed that these cytokines were mediators of daytime sleepiness. Also, we reported a positive correlation between IL-6 or TNF alpha plasma levels and the body mass index (BMI). In subsequent studies, we showed that IL-6, TNF alpha, leptin and insulin levels were elevated in sleep apnoea independently of obesity and that visceral fat, was the primary parameter linked with sleep apnoea. The association of OSA with insulin resistance and diabetes type 2 has been confirmed since then in several epidemiological and clinical studies. Furthermore, our findings that women with polycystic ovary syndrome (PCOS, a condition associated with hyperandrogenism and insulin resistance) were much more likely than controls to have sleep disordered breathing (SDB) and daytime sleepiness support the pathogenetic role of insulin resistance in OSA. Other findings that support the view that sleep apnoea and sleepiness may be manifestations of a serious metabolic disorder, namely the Metabolic or Visceral Obesity Syndrome, include: obesity without sleep apnoea is associated with daytime sleepiness; PCOS and diabetes type 2 are independently associated with EDS after controlling for SDB, obesity and age; and increased prevalence of sleep apnoea in postmenopausal women, with hormonal replacement therapy associated with a significantly reduced risk for OSA. In conclusion, accumulating evidence provides support to our model of the bi-directional, feedforward, pernicious association between sleep apnoea, sleepiness, inflammation and insulin resistance, all promoting atherosclerosis and cardiovascular disease.
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PMID:Metabolic disturbances in obesity versus sleep apnoea: the importance of visceral obesity and insulin resistance. 1282 41


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