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

Obesity has epidemic proportions in Western societies and, because of its significant association with morbidity and mortality, is a major public health issue. Excessive daytime sleepiness (EDS) and fatigue (tiredness without increased sleep propensity)--which have been associated with obesity--have a significant impact on individual well-being and public safety. In this article, we review data that challenge the belief that sleep apnea and sleep disruption per se are the primary determinants of obesity-related daytime sleepiness and fatigue. Specifically, it appears that obesity per se is associated with objective and subjective daytime sleepiness compared to normal-weight controls regardless of sleep apnea and sleep loss. Indeed, obese patients without sleep apnea are sleepier compared to nonobese controls whereas within the morbidly obese, those who have high sleep efficiency at night are sleepier than those who have low sleep efficiency. In addition, in recent studies based on large random samples of the general population, the primary determinants of subjective EDS were depression and metabolic disturbances, that is, obesity/diabetes, and not sleep apnea or objective sleep disruption. Furthermore, sleepiness and fatigue are very prevalent in conditions associated with insulin resistance, for instance, the polycystic ovary syndrome (PCOS), independently of sleep apnea or obesity, or in conditions of insufficient physical activity. On the basis of these data, we propose that obesity-related objective daytime sleepiness and fatigue are associated primarily with metabolic and psychological factors and less with sleep apnea and sleep disruption per se. Furthermore, we suggest that objective sleepiness is primarily related to metabolic factors, whereas fatigue appears to be related to psychological distress. Finally, based on data from studies in normal controls and patients with sleep disorders, we propose that the interaction of the hypothalamic-pituitary-adrenal (HPA) axis and proinflammatory cytokines determines the level of sleep/arousal within the 24-h cycle, that is, "hypercortisolemia" plus hypercytokinemia is associated with low sleep efficiency and fatigue, whereas "eucortisolemia" or "hypocortisolemia" plus hypercytokinemia is associated with high sleep efficiency and objective sleepiness.
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PMID:Obesity-related sleepiness and fatigue: the role of the stress system and cytokines. 1714 48

Raised plasma levels of insulin, glucose and glucagon are found in patients affected by 'hyperinsulinism'. Obesity, hypertension, mammary plus ovary cysts and rheumatic symptoms are frequently observed in these patients. Sleep disorders and depression are also present in most subjects affected by this polysymptomatic disorder. The simultaneous increases of glucose, insulin and glucagon plasma levels seen in these patients indicate that the normal crosstalk between A cells, B cells and D cells is disrupted. With respect to this, it is well known that glucose excites B cells (which secrete insulin) and inhibits A cells (which secrete glucagon), which in turn excites D cells (which secrete somatostatin). Gastrointestinal hormones (incretins) modulate this crosstalk both directly and indirectly throughout pancreatic and hepatobiliary mechanisms. The above factors depend on autonomic nervous system mediation. For instance, acetylcholine released from parasympathetic nerves excites both B and A cells. Noradrenaline released from sympathetic nerves and adrenaline secreted from the adrenal glands inhibit B cells and excite A cells, which are crowded with beta(2)- and alpha(2)-receptors, respectively. Noradrenaline released from sympathetic nerves also excites A cells by acting at alpha(1)-receptors located at this level. According to this, the excessive release of noradrenaline from these nerves should provoke an enhancement of glucagon secretion which will result in overexcitation of insulin secretion from B cells. That is the disorder seen in the so-called 'hyperinsulinism', in which raised plasma levels of glucose, insulin and glucagon coexist. Taking into account that neural sympathetic activity is positively correlated to the A5 noradrenergic nucleus and median raphe serotonergic neurons, and negatively correlated to the A6 noradrenergic, the dorsal raphe serotonergic and the C1 adrenergic neurons, we postulate that this unbalanced central nervous system circuitry is responsible for the hyperinsulinism syndrome.
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PMID:Central nervous system circuitry involved in the hyperinsulinism syndrome. 1716 39

Patients with obesity hypoventilation syndrome (OHS) have a lower quality of life, more healthcare expenses, a greater risk of pulmonary hypertension, and a higher mortality compared to eucapnic patients with obstructive sleep apnea (OSA). Despite significant morbidity and mortality associated with OHS, it is often unrecognized and treatment is frequently delayed. The objective of this observational study was to determine the prevalence of OHS in patients with OSA seen at the sleep disorders clinic of a large public urban hospital serving predominantly minority population and to identify clinical--not mechanistic--predictors that should prompt clinicians to measure arterial blood gases. In the first stage, we randomly selected 180 patients referred to our sleep disorders clinic between 2000 and 2004 for suspicion of OSA. From this retrospective random sample we calculated the prevalence of OHS in patients with OSA and identified independent clinical predictors using logistic regression. In the second stage, we prospectively validated these predictors in a sample of 410 consecutive patients referred to the sleep disorders clinic for suspicion of OSA between 2005 and 2006. The prevalence of OHS in patients with OSA was 30% in the retrospective random sample and 20% in the prospective sample. Three variables independently predicted OHS in both samples: serum bicarbonate level (p < 0.001), apnea-hypopnea index (p = 0.006), and lowest oxygen saturation during sleep (p < 0.001). Due to the serious morbidity associated with OHS, we selected a highly sensitive threshold of serum bicarbonate level. A threshold of 27 mEq/l had a sensitivity of 92% and a specificity of 50%. Only 3% of patients with a serum bicarbonate level <27 mEq/l had hypercapnia compared to 50% with a serum bicarbonate > or =27 mEq/l. In conclusion, OHS is common in severe OSA. A normal serum bicarbonate level excludes hypercapnia and an elevated serum bicarbonate level should prompt clinicians to measure arterial blood gases.
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PMID:Obesity hypoventilation syndrome: prevalence and predictors in patients with obstructive sleep apnea. 1765 82

Obstructive sleep apnea (OSA) affects approximately 5% of women and 15% of men in the middle-aged adults, and associated with adverse health outcomes. Cardiovascular disturbances are the most serious complications of OSA. These complications include heart failure, left/right ventricular dysfunction, acute myocardial infarction, arrhythmias, stroke, systemic and pulmonary hypertension. All these cardiovascular complications increase morbidity and mortality of OSA. Several epidemiologic studies have demonstrated that sleep related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic activity, and altered baroreflex control during sleep. Arterial hypertension, obesity, diabetes mellitus and coronary artery disease (CAD) which are independent predictors of left ventricular dysfunction, often have co-existence with OSA. Especially severe OSA patients having diastolic dysfunction might have an increased risk of heart failure, since diastolic dysfunction might be combined with systolic dysfunction. Early recognition and appropriate therapy of ventricular dysfunction is advisable to prevent further progression to heart failure and death. Patients with acute myocardial infarction, especially if they had apneas and hypoxemia without evident heart failure should be evaluated for sleep disorders. So, patients with CAD should be evaluated for OSA and vice versa. Early recognition and treatment of OSA may improve cardiovascular functions. Continuous positive airway pressure (CPAP) applied by nasal mask, is still the gold standard method for treatment of the disease and prevention of complications.
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PMID:Cardiovascular diseases in obstructive sleep apnea. 1720 27

Recent studies suggest a significant association between obesity and attention-deficit/hyperactivity disorder (ADHD). The factors underlying this newly described comorbidity are still unclear and unexplored. In the present article, we propose that excessive daytime sleepiness (EDS) contributes to explaining the association between ADHD and obesity. The background for this hypothesis comes from studies on the association between ADHD and EDS, as well as from investigations on EDS in obese individuals. Available studies suggest that ADHD behaviours are significantly associated with EDS. Moreover, increasing evidence indicates that obesity is significantly associated with EDS independently of sleep-disordered breathing (SDB) or any other sleep disorders. Given the relationship between EDS and ADHD behaviors, we hypothesize that the higher than expected rates of EDS in obese individuals contribute to explaining the association between obesity and ADHD behaviors. We further speculate on the role of the brain derived neurotrophic factor (BDNF) and other molecules such as the proinflammatory cytokines IL-6 and TNF-alpha. Our hypothesis generates potentially relevant clinical and therapeutic implications. From a clinical standpoint, it may suggest to systematically look for ADHD symptoms (including hyperactivity and impulsivity) in obese patients described as sleepy. With regard to the therapeutic implications, we suggest that wake-promoting agents with anorexigenic effect, such as mazindol, might be particularly indicated for the treatment of ADHD symptoms in obese patients, since they might address both ADHD symptoms and weight reduction. In conclusion, considering the burden that ADHD adds to obesity, we believe that further studies on the comorbidity between obesity and ADHD are necessary. Research on the role of EDS might allow advancements in this field, suggesting a more effective management and, ultimately, a better quality of life of patients with both obesity and ADHD.
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PMID:Does excessive daytime sleepiness contribute to explaining the association between obesity and ADHD symptoms? 1758 9

Vagus nerve stimulation (VNS) is an established treatment for selected patients with medically refractory seizures. Recent studies suggest that VNS could be potentially useful in the treatment of resistant depressive disorder. Although a surgical procedure is required in order to implant the VNS device, the possibility of a long-term benefit largely free of severe side effects could give VNS a privileged place in the management of resistant depression. In addition, VNS appears to affect pain perception in depressed adults; a possible role of VNS in the treatment of severe refractory headache, intractable chronic migraine and cluster headache has also been suggested. VNS is currently investigated in clinical studies, as a potential treatment for essential tremor, cognitive deficits in Alzheimer's disease, anxiety disorders, and bulimia. Finally, other studies explore the potential use of VNS in the treatment of resistant obesity, addictions, sleep disorders, narcolepsy, coma and memory and learning deficits.
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PMID:Vagus nerve stimulation: indications and limitations. 1769 14

Sleep disordered breathing is a term which includes simple snoring, upper airway resistance syndrome, and obstructive sleep apnea (OSA). Simple snoring is a common complaint affecting 45% of adults occasionally and 25% of adults habitually and is a sign of upper airway obstruction. Snoring has also been identified as a possible risk factor for hypertension, ischemic heart disease, and stroke. The role of dentistry in sleep disorders is becoming more significant, especially in co-managing patients with simple snoring and mild to moderate OSA. The practicing dental professional has the opportunity to assist patients at a variety of levels, starting with the recognition of a sleep-related disorder, referring patients to a physician for evaluation, and assisting in the management of sleep disorders. Obesity is the main predisposing factor for OSA. In nonobese patients, craniofacial anomalies like micrognathia and retrognathia may also predispose to OSA. Diagnosis of OSA is made on the basis of the history and physical examination and investigations such as polysomnography, limited channel testing, split-night testing, and oximetry. Nocturnal attended polysomnography, which requires an overnight stay in a sleep facility, is the standard diagnostic modality in determining if a patient has OSA. As far as treatment is concerned, the less invasive procedures are to be preferred to the more invasive options. The first and simplest option would be behavior modification, followed by insertion of oral devices suited to the patient, especially in those with mild to moderate OSA. Continuous positive airway pressure (CPAP) and surgical options are chosen for patients with moderate to severe OSA. The American Academy of Sleep Medicine (AAOSM) has recommended oral appliances for use in patients with primary snoring and mild to moderate OSA. It can also be used in patients with a lesser degree of oxygen saturation, relatively less day time sleepiness, lower frequency of apnea, those who are intolerant to CPAP, or those who refuse surgery. Oral appliances improve the blood oxygen saturation levels as they relieve apnea in 20-75% of patients. They reduce the apnea-hypopnea index (AHI) by 50% or to < 10 events per h. Oral appliances also reduce the AHI to normal in 50-60% patients.
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PMID:Management of obstructive sleep apnea: A dental perspective. 1793 99

Obesity has emerged as one of the most serious public health concerns in the 21st century. Obese children tend to become obese adults. The dramatic rise in pediatric obesity closely parallels the rapid increase in the prevalence of adult obesity. As overweight children become adults they face the multitude of health problems associated with obesity at younger ages. The morbidity and mortality associated with obesity continue to increase. Obesity is one of the leading causes of preventable death. Complications of obesity include cardiovascular risks, hypertension, dyslipidemia, endothelial dysfunction, type 2 diabetes mellitus and impaired glucose tolerance, acanthosis nigricans, hepatic steatosis, premature puberty, hypogonadism and polycystic ovary syndrome, obstructive sleep disorder, orthopedic complications, cholelithiasis and pseudotumor cerebri. Genetic and molecular and environmental factors play an important role in the assessment and management of obesity.
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PMID:Obesity: genetic, molecular, and environmental aspects. 1800 Sep 69

Obesity reflects an imbalance between energy uptake and expenditure that is mediated by behavior. Obesity is a growing epidemic and a major risk factor for neurobiological diseases like stroke, dementia, intracranial hypertension and sleep disorders. Conversely, obesity can also be induced by neurobiological disorders and drugs. The etiology of obesity is complex and includes biology, behavior and environment. Physicians are faced with the need to manage obesity while strategies for prevention and sustained weight reduction are limited. Present treatment options comprise lifestyle modification, diet, pharmacotherapy and bariatric surgery. Considerable headway has been made into elucidating the neurobiological underpinnings of obesogenic behavior. There is now a growing understanding of the metabolic, hormonal and behavioral circuitries that contribute to the complex and redundant system for energy balance. Changing the net balance of this system to prevent or reduce obesity requires multimodal and long-term interventions.
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PMID:Obesity in neurobiology. 1800 38

Several basic research studies have recently demonstrated the impact of sleep disorders in the occurrence or development of increasing diseases such as obesity, diabetes or hypertension. More recently epidemiological surveys seem to confirm this link. These studies have observed that a total sleep time under 6 hours was associated with an increased BMI, and a higher occurrence of diabetes and hypertension. However theses studies are often prospective cohorts non mainly focussed on sleep. The sleep estimates are subjective and there are many possible biases. More studies are necessary to enlighten the implication of sleep in the development of metabolic disorders.
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PMID:[Metabolic and cardiovascular comorbidities and sleep disorders]. 1801 54


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