Diet, Obesity, and Asthma

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Abstract

Obesity has reached epidemic proportions in many developed countries as Western dietary patterns have been widely adopted. These diets are characterized by excess energy intake as well as regular consumption of processed or “fast” foods and limited consumption of fruit, vegetables, and whole grains. The result is a high intake of saturated fat, refined carbohydrates, and sodium; and a low intake of fiber, vitamins, and other phytochemicals. This type of poor-quality diet has been associated with increased risk of chronic inflammatory diseases, including asthma. Of particular note, high intake of saturated fat stimulates proinflammatory pathways via activation of pattern recognition receptors, endoplasmic reticulum stress, and fatty acid-binding protein activity. Conversely, with a low intake of soluble fiber, beneficial antiinflammatory mechanisms, such as free fatty acid receptor activation and histone deacetylase inhibition, are suppressed. Similarly, with a low intake of antioxidants such as vitamin C, vitamin E, and carotenoids, nuclear factor κ-light-chain-enhancer of activated B cells activity is enhanced, creating a proinflammatory environment. There is evidence derived from human and experimental models of asthma suggesting that these mechanisms contribute to the development of airway inflammation, loss of asthma control, and/or worse lung function. Obese individuals have increased asthma morbidity and reduced quality of life, so strategies for better management of these patients are urgently needed. Evidence suggests that, in addition to reducing the quantity of food consumed, interventions should also target the quality of food consumed to improve both asthma management and the overall health and well being of these patients.

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