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. 1. Introduction The obesity prevalence has alarmingly and unprecedentedly increased by more than 3-fold in last three decades, irrespective of socioeconomic status, gender, or age, worldwide [1]. Globally, there are more than 1 billion overweight adults which constitute 300 million clinically obese individuals [1]. Obesity is the prime risk factor for various morbidities related to cardiovascular system, metabolic system, and endocrine system. However, in the last 50 years there is a consistent accumulation of evidence to suggest that obesity can significantly impair respiratory well being as well. There is substantial evidence to suggest that obesity enhances the risk of having asthma [2–30] antedate development of asthma [3, 4, 6, 20] and induces asthma worsening amongst preexisting asthmatics [30–33]. The mechanism of this link is however not fully understood and elucidated. The current mechanistic understanding of asthma and obesity is a complexity of dietetic factors deficient in antioxidants [34–39], attributes of reduced physical exercise [40, 41], gastroesophageal reflux disease (GERD) [42–44], components of systemic inflammation released from adipose tissue, and
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