To explore whether asthma and obesity share overlapping pathogenic features, we examined the impact of each alone, and in combination, on multiple aspects of lung function. We reasoned that if they influenced the lungs through similar mechanisms, the individual physiological manifestations in the comorbid state should interact in a complex fashion. If not, then the abnormalities should simply add. We measured specific conductance, spirometry, lung volumes, and airway responsiveness to adrenergic and cholinergic agonists in 52 normal, 53 asthmatic, 52 obese, and 53 asthmatic and obese patients using standard techniques. Six-minute walks were performed in subsets from each group. Asthma significantly lowered specific conductance and the spirometric variables while increasing airway reactivity and residual volume. Obesity also reduced the spirometric variables as well as total lung capacity and functional residual capacity. Residual volume, specific conductance, and airway responsivity were unaltered. With comorbidity, the disease-specific derangements added algebraically. Features that existed in isolation appeared unchanged in the combination, whereas shared ones either added or subtracted depending on the individual directional changes. Synergistic interactions were not observed. Body mass index weakly correlated with spirometry and lung volumes in asthma, but not with specific conductance or bronchial reactivity. Exercise performance did not aid in differentiation. Our findings indicate asthma and obesity appear to influence the respiratory system through different processes.
"Low ERV in obesity suggests occurrence of tidal breathing close to RV in distal high resistance airways, such as noncartilaginous small membranous terminal and respiratory bronchioles and alveolar duct, in obese populations (Figure 2). There is a pertinent linear direct relationship between FRC and airway resistance and inverse linear relation with airway conductance [72, 74, 98, 99]. Studies have shown that high respiratory resistance in obesity normalizes on correction with lung volumes [72, 74, 98, 99]. "
[Show abstract][Hide abstract] ABSTRACT: Obesity induces some pertinent physiological changes which are conducive to either development of asthma or cause of poorly controlled asthma state. Obesity related mechanical stress forces induced by abdominal and thoracic fat generate stiffening of the lungs and diaphragmatic movements to result in reduction of resting lung volumes such as functional residual capacity (FRC). Reduced FRC is primarily an outcome of decreased expiratory reserve volume, which pushes the tidal breathing more towards smaller high resistance airways, and consequentially results in expiratory flow limitation during normal breathing in obesity. Reduced FRC also induces plastic alteration in the small collapsible airways, which may generate smooth muscle contraction resulting in increased small airway resistance, which, however, is not picked up by spirometric lung volumes. There is also a possibility that chronically reduced FRC may generate permanent adaptation in the very small airways; therefore, the airway calibres may not change despite weight reduction. Obesity may also induce bronchodilator reversibility and diurnal lung functional variability. Obesity is also associated with airway hyperresponsiveness; however, the mechanism of this is not clear. Thus, obesity has effects on lung function that can generate respiratory distress similar to asthma and may also exaggerate the effects of preexisting asthma.
Journal of Allergy 07/2013; 2013:198068. DOI:10.1155/2013/198068
"Several genes have been associated with both obesity and asthma. Genes related to the β adrenergic receptor (locus 5q, gene ADRB2), insulin-like growth factor (locus 12q, gene IGF1), interleukin 1α (locus 12q, gene IL1A), leukotriene A4 hydroxylase (locus 12q, gene LTA4H), glucocorticoid receptor (locus 5q, gene NR3C1), signal transducer and activator of transcription gene (locus 12q), tumor necrosis factor (locus 6p, gene TNF), uncoupling protein (locus 11q13, gene UCP2 and 3) etc., have been postulated to be relevant to both obesity and asthma. "
[Show abstract][Hide abstract] ABSTRACT: Asthma is a chronic disorder affecting millions of people worldwide. The prevalence of asthma is around 300 million and is expected to increase another 100 million by 2025. Obesity, on the other hand, also affects a large number of individuals. Overweight in adults is defined when body mass index (BMI) is between 25 to 30 kg/m(2) and obesity when the BMI >30 kg/m(2). It has been a matter of interest for researchers to find a relation between these two conditions. This knowledge will provide a new insight into the management of both conditions. At present, obese asthma patients may be considered a special category and it is important to assess the impact of management of obesity on asthma symptoms.
Lung India 03/2013; 30(1):38-46. DOI:10.4103/0970-2113.106132
"The reduced EELV in obesity also means that the airways resistance is proportionately increased , in absolute terms , reflecting the reduced airway diameter compared with normal weight individuals. It is noteworthy that when the volume differences in health and obesity are accounted for as with measurements of specific airway resistance or specific conductance, this difference in airway resistance disappears   . In obesity, closing volume may occur at volumes above the lower EELV [37, 44–46]; thus, significant airway closure and gas trapping may occur in basal lung segments during the quiet tidal breathing cycle. "
[Show abstract][Hide abstract] ABSTRACT: In many parts of the world, the prevalence of obesity is increasing at an alarming rate. The association between obesity, multiple comorbidities, and increased mortality is now firmly established in many epidemiological studies. However, the link between obesity and exercise intolerance is less well studied and is the focus of this paper. Although exercise limitation is likely to be multifactorial in obesity, it is widely believed that the respiratory mechanical constraints and the attendant dyspnea are important contributors. In this paper, we examined the evidence that critical ventilatory constraint is a proximate source of exercise limitation in individuals with mild-to-moderate obesity. We first reviewed existing information on exercise performance, including ventilatory and perceptual response patterns, in obese individuals who are otherwise healthy. We then considered the impact of obesity in patients with preexisting respiratory mechanical abnormalities due to chronic obstructive pulmonary disease (COPD), with particular reference to the effect on dyspnea and exercise performance. Our main conclusion, based on the existing and rather sparse literature on the subject, is that abnormalities of dynamic respiratory mechanics are not likely to be the dominant source of dyspnea and exercise intolerance in otherwise healthy individuals or in patients with COPD with mild-to-moderate obesity.
Pulmonary Medicine 10/2012; 2012(11):818925. DOI:10.1155/2012/818925
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