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

One thousand and one men, aged 35-65 years, were identified from the age-sex register of one group general practice. Over four years 900 men were visited at home and asked questions about symptoms potentially related to sleep apnoea and snoring. Height, weight, neck circumference, resting arterial oxygen saturation (SaO2), and spirometric values were also determined. All night oximetry was then performed at home and the tracing analysed for the number of dips in SaO2 of more than 4%. Subjects with more than five dips of 4% SaO2 or more per hour were invited for sleep laboratory polysomnography. Seventeen per cent of the men admitted to snoring "often." Multiple linear regression techniques identified and ranked neck circumference (r2 = 7.2%), cigarette consumption (r2 = 3.4%), and nasal stuffiness (r2 = 2%) as the only significant independent predictors of snoring. Together these account for at least a sixfold variation in the likelihood of being an "often" snorer. Forty six subjects (5%) had greater than 4% SaO2 dip rates of over five an hour and 31 of these had full sleep studies. Three subjects had clinically obvious and severe symptomatic obstructive sleep apnoea, giving a prevalence of three per 1001 men (0.3%; 95% confidence interval 0.07-0.9%). Eighteen men had obstructive sleep apnoea only when supine and in 10 the cause of the SaO2 dipping on the original home tracing was not elucidated. The greater than 4% SaO2 dip rates correlated with the history of snoring. Multiple linear regression techniques identified and ranked neck circumference (r2 = 7.9%), alcohol consumption (r2 = 3.7%), age (r2 = 1%) and obesity (r2 = 1%) as the only significant independent predictors of the rate of overnight hypoxic dipping. This study shows that snoring in this randomly selected population correlates best with neck size, smoking, and nasal stuffiness. Obstructive sleep apnoea, defined by nocturnal hypoxaemia, correlates best with neck size and alcohol, and less so with age and general obesity.
Thorax 1991 Feb
PMID:Predictors and prevalence of obstructive sleep apnoea and snoring in 1001 middle aged men. 201 7

The morbidly obese are known to have impaired respiratory function. A prospective study of the changes in lung volumes, carbon monoxide transfer, and arterial blood gas tensions was undertaken in 29 morbidly obese patients before and after surgery to induce weight loss. Before surgery the predominant abnormality in respiratory function was a reduction in lung volumes. These increased towards normal predicted values after weight loss, with significant increases in functional residual capacity, residual volume, total lung capacity, and expiratory reserve volume. The increases ranged from 14% for total lung capacity to 54% for expiratory reserve volume. After weight loss had been induced the smokers showed mild hyperinflation and air trapping. Resting arterial blood gas tensions improved, with a rise in arterial oxygen tension from 10.63 to 13.02 kPa and a fall in arterial carbon dioxide tension from 5.20 to 4.64 kPa. There was no correlation between weight loss and the changes in blood gas tensions or lung volumes. Loss of weight in the morbidly obese is thus associated with improved lung function. The effects of smoking on lung function could be detected after weight loss, but were masked before treatment by the opposing effects of obesity on residual volume and functional residual capacity.
Thorax 1989 May
PMID:Respiratory function in the morbidly obese before and after weight loss. 250 5

Non-apnoeic oxygen desaturation related to rapid eye movement (REM) sleep in a patient with hypothyroidism, obesity, respiratory failure, and cardiac failure was improved by treatment with nasal continuous positive airway pressure of 10 cm H2O.
Thorax 1989 Jun
PMID:Non-apnoeic REM sleep induced nocturnal oxygen desaturation treated by nasal continuous positive airway pressure. 266 26

Obesity is the most common metabolic disease in the world and its prevalence has been increasing over several decades. The World Health Organization (WHO) predicts that, by 2015, around 700 million adults will be obese (at least 10% of the projected global population). This will be a huge health and economic burden with associated increases in diabetes, cardiovascular and musculoskeletal disease, and malignancy. While there has been little focus on the impact of obesity on respiratory disease, there are clear effects on pulmonary function and inflammation which will increase the prevalence and morbidity of lung disease. There is an inverse relationship between body mass index and forced expiratory volume in 1 s. Increases in body weight lead to worsening of pulmonary function. The reasons for this include the mechanical effects of truncal obesity and the metabolic effects of adipose tissue. Obesity is linked to a wide range of respiratory conditions including chronic obstructive pulmonary disease, asthma, obstructive sleep apnoea, pulmonary embolic disease and aspiration pneumonia. It is important for those providing care for people with respiratory disease to appreciate the impact of obesity and to provide appropriate advice for weight reduction. Healthcare planners should consider the impact of obesity for future resources in respiratory care.
Thorax 2008 Jul
PMID:Obesity and the lung: 1. Epidemiology. 1858 31

Epidemiological studies first demonstrated the association between obesity and asthma and they have begun to provide additional evidence to support causality: a dose-effect relationship, consistency across studies (especially among women) and the correct temporal order (ie, obesity before asthma). To date, relatively few studies have addressed reversibility, an important but less frequently demonstrated epidemiological criterion of causality. Reversibility suggests that if excessive weight is a risk factor for asthma, then reducing body weight should decrease the prevalence of asthma, or at least decrease asthma related symptoms or health care utilisation. We performed a systematic review on weight loss and asthma, based on searches between January 1966 and January 2007 of both PubMed and the Cochrane Clinical Trial Database. Of the 15 relevant studies, asthma was the primary outcome in only five. Only one study was conducted in children. Regardless of the type of intervention (surgical vs medical), all 15 studies noted an improvement in at least one asthma outcome after weight loss. The improvement was noted across studies that differed in sample age, gender or country of origin. The heterogeneity of the interventions and outcomes precluded quantitative synthesis. We briefly review the role of specific factors (eg, gastro-oesophageal reflux) in the weight loss-asthma association, and potential directions for future research.
Thorax 2008 Aug
PMID:Weight loss and asthma: a systematic review. 1866 68

As the prevalence of obesity increases in both the developed and the developing world, the respiratory consequences are often underappreciated. This review discusses the presentation, pathogenesis, diagnosis and management of the obstructive sleep apnoea, overlap and obesity hypoventilation syndromes. Patients with these conditions will commonly present to respiratory physicians, and recognition and effective treatment have important benefits in terms of patient quality of life and reduction in healthcare utilisation. Measures to curb the obesity epidemic are urgently required.
Thorax 2008 Aug
PMID:Obesity and the lung: 2. Obesity and sleep-disordered breathing. 1866 71

Obesity is a major problem from a public health perspective and a difficult practical matter for intensivists. The obesity pandemic has required treating clinicians to develop an appreciation of the substantial pathophysiological effects of obesity on the various organ systems. The important physiological concepts are illustrated by focusing on obstructive sleep apnoea, obesity hypoventilation syndrome, abdominal compartment syndrome and ventilatory management of the obese patient with acute respiratory distress syndrome.
Thorax 2008 Oct
PMID:Obesity and the lung: 3. Obesity, respiration and intensive care. 1882 Jan 19

Over the past 30 years there has been an epidemic of both obesity and asthma in the western world. A large body of robust epidemiological data has linked obesity with the development and severity of asthma in both children and adults and weight reduction with improvements in asthma severity and symptoms. However, it remains unsettled whether this relationship is causal or confounded by some other factor(s) as mechanistic and physiological studies have produced heterogeneous and at times conflicting findings. This review examines the clinical and epidemiological relationship between obesity and asthma and the purported mechanisms that may link these two processes together.
Thorax 2008 Nov
PMID:Obesity and the lung: 4. Obesity and asthma. 1898 17

Chronic obstructive pulmonary disease (COPD) and obesity are common and disabling chronic health conditions with increasing prevalence worldwide. A relationship between COPD and obesity is increasingly recognised, although the nature of this association remains unknown. This review focuses on the epidemiology of obesity in COPD and the impact of excessive fat mass on lung function, exercise capacity and prognosis. The evidence for altered adipose tissue functions in obesity--including reduced lipid storage capacity, altered expression and secretion of inflammatory factors, adipose tissue hypoxia and macrophage infiltration in adipose tissue--is also reviewed. The interrelationship between these factors and their contribution to the development of insulin resistance in obesity is considered. It is proposed that, in patients with COPD, reduced oxidative capacity and systemic hypoxia may amplify these disturbances, not only in obese patients but also in subjects with hidden loss of fat-free mass. The potential interaction between abnormal adipose tissue function, systemic inflammation and COPD may provide more insight into the pathogenesis and reversibility of systemic pathology in this disease.
Thorax 2008 Dec
PMID:Obesity and the lung: 5. Obesity and COPD. 1956 Dec 86

Obstructive sleep apnoea syndrome (OSAS) is a highly prevalent disease and is recognised as a major public health burden. Large-scale epidemiological studies have demonstrated an independent relationship between OSAS and various cardiovascular disorders. The pathogenesis of cardiovascular complications in OSAS is not completely understood but a multifactorial aetiology is likely. Inflammatory processes have emerged as critical in the pathogenesis of atherosclerosis at all stages of atheroma formation. Increased levels of various circulating markers of inflammation including tumour necrosis factor alpha (TNFalpha), interleukin 6 (IL6), IL-8 and C-reactive protein (CRP) have been reported as associated with future cardiovascular risk. There is increasing evidence of elevated inflammatory markers in OSAS with a significant fall after effective treatment with continuous positive airway pressure. This evidence is particularly strong for TNFalpha, whereas studies on IL6 and CRP have yielded conflicting results possibly due to the confounding effects of obesity. Cell culture and animal studies have significantly contributed to our understanding of the underlying mechanisms of the association between OSAS and inflammation. Intermittent hypoxia, the hallmark of OSAS, results in activation of pro-inflammatory transcription factors such as nuclear factor kappa B (NF-kappaB) and activator protein (AP)-1. These promote activation of various inflammatory cells, particularly lymphocytes and monocytes, with the downstream consequence of expression of pro-inflammatory mediators that may lead to endothelial dysfunction. This review provides a critical analysis of the current evidence for an association between OSAS, inflammation and cardiovascular disease, discusses basic mechanisms that may be responsible for this association and proposes future research possibilities.
Thorax 2009 Jul
PMID:Systemic inflammation: a key factor in the pathogenesis of cardiovascular complications in obstructive sleep apnoea syndrome? 1956 Dec 83


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