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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obstructive sleep apnea syndrome is caused by upper airway collapse during inspiration, causing intermittent hypoxemia, hypercapnia, acidosis, sympathetic nervous system activation, and arousal from sleep. Nighttime blood pressure is higher, but unexpectedly, daytime hypertension occurs. The prevalence of hypertension is very high and the incidence of hypertension increases as the number of apneic and hypopneic events per hour rises. Obesity is a major predisposing factor for the development of obstructive sleep apnea. Daytime sleepiness, snoring, and breathing pauses are important symptoms to elicit from the patient or sleep partner. Resistant hypertension is an important clue. Overnight polysomnography is required for diagnosis. Weight loss, avoidance of nocturnal sedatives, cessation of evening alcohol ingestion, and avoidance of the supine position during sleep are initial therapeutic actions in mild obstructive sleep apnea syndrome. Continuous positive airway pressure is the treatment of choice for patients unable to find relief from lifestyle changes. Blood pressure modestly improves with treatment.
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PMID:Obstructive sleep apnea syndrome. 1702 91

Obstructive sleep apnea (OSA) is characterized by repetitive partial and total collapse of the upper airway that induces stressful arousals throughout sleep to reestablish breathing. Although estimates vary, prevalence has been reported as high as 20% in the adult population. OSA is common in several chronic diseases, the most common of which is obesity. Evidence is strong that OSA increases the risk of hypertension and both fatal and nonfatal cardiovascular events. Several mechanisms linking OSA to hypertension have been proposed, with increased sympathetic activation implicated as the prime mediator. This review summarizes recent data on the influence of OSA on blood pressure, the effect of standard OSA therapy on improving blood pressure, and the potential of lifestyle modification for further decreasing hypertension risk. Challenges confronting the investigation of blood pressure outcomes in response to treatment in OSA patients are discussed.
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PMID:Hypertension research in sleep apnea. 1717 Jun 13

Hypoxia is an important topic both physiologically and clinically. Traditionally, physiology research has been focusing on the effect of acute and chronic sustained hypoxia and human adaptive response to high altitude. In the past 20 years, genetic studies by many have expanded our understanding of hypoxia to the molecular level. However, in contrast to our extensive knowledge about acute and chronic sustained hypoxia, we know relatively little about the effect of chronic intermittent hypoxia (CIH). In recent years, CIH has attracted more research attention because of the increasing prevalence of obesity and obstructive sleep apnea (OSA) in the western countries. Clinically, CIH is commonly seen in patients with sleep-disordered breathing including OSA, Cheyne-Stokes respiration and nocturnal hypoventilation. It was estimated that for OSA of at least mild severity prevalence estimates range from 3 to 28% in the general population. OSA is characterized by recurrent upper airway collapse during sleep leading to intermittent nocturnal hypoxia and sleep fragmentation. OSA is associated with significant mortality and morbidity including neurocognitive dysfunction, hypertension, many cardiovascular disorders and metabolic disorders such as diabetes and metabolic syndrome. The intermittent hypoxia in OSA closely mimics what is seen in the ischemia-reperfusion injury. Experimentally, there is no universally accepted definition for CIH. Laboratory protocols vary greatly in duration of hypoxia exposure, numbers of hypoxia episodes per day and the total number of days of exposure. Despite the lack of a uniform definition, recent data suggest that CIH may lead to multiple long-term pathophysiologic consequences similar to what we see in patients with OSA. Recent evidences also demonstrate that there are remarkable differences in the response of the physiologic systems to sustained hypoxia and intermittent hypoxia. This review is aimed to briefly discuss the clinical significance of sleep-disordered breathing and our current understanding of CIH.
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PMID:Obstructive sleep apnea and chronic intermittent hypoxia: a review. 1729 31

We report a patient with respiratory failure due to expiratory central airway collapse successfully treated with airway stents. A 74-year-old male with obesity and obstructive sleep apnea had recurrent episodes of acute respiratory failure. Noninvasive positive-pressure ventilation failed because of patient intolerance and lack of improvement, and soon after he stopped using the noninvasive ventilator he developed severe respiratory failure that required a tracheostomy. He was transferred to our institution one month later. Fiberoptic bronchoscopy revealed diffuse expiratory central airway collapse of both main bronchi and the lower two thirds of the trachea, caused by bulging of the posterior airway membrane. During rigid bronchoscopy we inserted studded silicone stents in the right and left mainstem bronchi and in the distal trachea. The patient was weaned from mechanical ventilation 72 hours later and discharged to a long-term care facility. Expiratory central airway collapse should be considered in the differential diagnosis of patients with respiratory failure, especially when weaning from mechanical ventilation is difficult.
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PMID:Respiratory failure due to expiratory central airway collapse. 1752 65

Obesity in Eastern Europe has been linked to privilege and status prior to the collapse of communism, and to exposure to free-market economics after it. Neither formulation is a complete explanation, and it is useful to examine the potential value of other models of population obesity for the understanding of this phenomenon. These include those of: thrifty genotypes; obesogenic behaviour; obesogenic environments; nutrition transition; obesogenic culture; and biocultural interactions of genetics, environment, behaviour and culture. At the broadest level, obesity emerges from the interaction of thrifty genotype with obesogenic environment. However, defining obesogenic environments remains problematic, especially in relation to sociocultural factors. Furthermore, since different identity groups may share different values concerning the obesogenicity of the environment, a priori assumptions about group homogeneity may lead to flawed interpretations of the importance of sociocultural factors in obesogenic environments. A new way to identify cultural coherence of groups and populations in relation to environments contributing to obesity is put forward here, that of cultural consensus modeling.
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PMID:Frameworks of population obesity and the use of cultural consensus modeling in the study of environments contributing to obesity. 1792 80

Obesity and its many complications potentially can collapse most medical plans, unless attempts at prevention and therapy become more effective and widespread. An important incentive for providing effective treatment is proper reimbursement. We present here an evaluation of the feasibility, constrains and requirements for comparative cost-effectiveness evaluation of weight loss intervention from the payer's and employer's points of view, and propose a general framework for this type of studies toward decision making.
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PMID:Cost-return prediction in morbidly obese employees following weight loss interventions: a study framework. 1800 19

Type 2, non-insulin-dependent diabetes has been increasing exponentially over the past decade and a half and it is estimated that within short it will comprise more than 350 million patients. The pathophysiology of type 2 diabetes is complex, but has two dominating factors, insulin resistance (which is mainly due to obesity and physical inactivity), and deficient insulin production. Indeed, although approximately 80% of type 2 diabetics are obese, 2/3 of overweight or obese persons show normal glucose metabolism. Data accumulated over the past few decades unequivocally indicate that diabetes can not develop in the absence of a major deficiency of insulin secretion. This deficiency is characterised by an early loss of first-phase insulin response to glucose, followed by gradual collapse of the later insulin response as well as of the maximal secretory capacity of the beta-cell. Interestingly, functional modifications in the beta-cell do not present a discontinuity; in fact, some of the characteristics of the diabetic beta-cell function can be found in a fraction of the healthy population. A major challenge has been to answer the question whether the population with decreased insulin secretory capacity represents the substratum from which future diabetics emerge. While many observations suggest that such may indeed be the case, conclusive evidence is still unavailable. The search for the beta-cell molecular mechanisms which prepare the ground for diabetes has been difficult and mainly limited to laboratory models of type 2 diabetes. Greater success has been achieved in elucidating the secondary beta-cell defects elicited once diabetes is established and the beta-cell exposed to chronically elevated glucose and fatty acid levels (so-called gluco-lipotoxicity). The latter reduces the responsiveness of insulin secretion to physiological stimuli, as it impairs the biosynthesis and processing of proinsulin. The leptin resistance of obesity certainly plays a role in this context, since leptin reduces, i.a., the lipid content of the islet. Similarly, the reduced adiponectin levels of obesity favour diminished beta-cell function. Nevertheless, it seems probable that the most important negative factor for the beta-cell in obesity is the inflammatory state. Indeed, several cytokines are deleterious for the beta-cell and may play a role in the pathogenesis of the islet dysfunction of diabetes, as demonstrated by the recent work of Donath and coworkers. We propose the working hypothesis that the "prediabetic" beta-cell in fact is a normal beta-cell whose functional capabilities (insulin secretion and biosynthesis, cell proliferation, resistance to stress...) is at the lower-end of the normal distribution. At times of "reasonable" metabolic requirements, i.e. reasonable energy balance, such a "prediabetic" beta-cell is fully adequate to cover the insulin needs of the organism. Insulin production by the "prediabetic" beta-cell becomes insufficient either when insulin needs become excessive, as is the case in over-nutrition (with or without insulin resistance), or when beta-cell function and adaptation are impaired by "external" factors such as the obesity-related inflammatory cytokines. Thus, deficient beta-cell function is seen as a relative factor against the metabolic background dictated by environmental factors. Type 2 diabetes is a hereditary disease, and many genes have been shown to be linked to diabetes. Our hypothesis is that such genes (or rather their polymorphism) define the range of the functional adaptability of the beta-cell to metabolic demand. This would be an excellent example of gene-environment interaction. Thus, we do not believe that sensu stricto diabetes genes exist. Against the above, optimal diabetes treatment would necessitate--reduction of the metabolic demand on the beta-cell,--support of its function and adaptive capabilities. Several new research avenues, discussed in the present meeting, may open new and improved therapeutic approaches for type 2 diabetes.
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PMID:[And what about diabetes?]. 1822 48

Obstructive sleep apnea is a chronic condition characterized by frequent episodes of upper airway collapse during sleep. Its effect on nocturnal sleep quality and ensuing daytime fatigue and sleepiness are widely acknowledged. Increasingly, obstructive sleep apnea is also being recognized as an independent risk factor for several clinical consequences, including systemic hypertension, cardiovascular disease, stroke, and abnormal glucose metabolism. Estimates of disease prevalence are in the range of 3% to 7%, with certain subgroups of the population bearing higher risk. Factors that increase vulnerability for the disorder include age, male sex, obesity, family history, menopause, craniofacial abnormalities, and certain health behaviors such as cigarette smoking and alcohol use. Despite the numerous advancements in our understanding of the pathogenesis and clinical consequences of the disorder, a majority of those affected remain undiagnosed. Simple queries of the patient or bed-partner for the symptoms and signs of the disorder, namely, loud snoring, observed apneas, and daytime sleepiness, would help identify those in need of further diagnostic evaluation. The primary objective of this article is to review some of the epidemiologic aspects of obstructive sleep apnea in adults.
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PMID:The epidemiology of adult obstructive sleep apnea. 1825 Feb 5

Obstructive sleep apnea (OSA) is a common disorder characterized by repetitive narrowing or collapse of the pharyngeal airway during sleep. The disorder is associated with major comorbidities including excessive daytime sleepiness and increased risk of cardiovascular disease. The underlying pathophysiology is multifactorial and may vary considerably between individuals. Important risk factors include obesity, male sex, and aging. However, the physiological mechanisms underlying these risk factors are not clearly understood. This brief review summarizes the current understanding of OSA pathophysiology in adults and highlights the potential mechanisms underlying the principal risk factors. In addition, some of the pathophysiological characteristics associated with OSA that may modulate disease severity are illustrated. Finally, the potential for novel treatment strategies, based on an improved understanding of the underlying pathophysiology, is also discussed with the ultimate aim of stimulating research ideas in areas where knowledge is lacking.
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PMID:Pathophysiology of adult obstructive sleep apnea. 1825 Feb 6

With the growing epidemic of obesity in an aging population, obstructive sleep apnea (OSA) is increasingly encountered in clinical practice. Given the acute cardiopulmonary stressors consequent to repetitive upper airway collapse, as well as evidence for cardiovascular homeostatic dysregulation in subjects with sleep apnea, there is ample biologic plausibility that OSA imparts increased cardiovascular risk, independent of comorbid disease. Indeed, observational studies have suggested strong associations with multiple disorders, such as systemic hypertension, heart failure, cardiac arrhythmias, and pulmonary hypertension. Further data in the form of longitudinal cohort studies and randomized controlled trials are accruing to add to the body of evidence. This review examines pathophysiologic mechanisms and explores current concepts regarding the impact of OSA and its treatment on selected clinical disease states.
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PMID:Obstructive sleep apnea, cardiovascular disease, and pulmonary hypertension. 1825 Feb 13


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