Abstract
The morbidity and mortality associated with asthma are rising, despite increased usage of anti-asthma medications. This report attempts to provide a plausible hypothesis for the "asthma paradox." The hypothesis involves the role of mast cell degranulation as an endogenous anti-inflammatory mechanism to prevent antigens from entering the lower airways and to limit the extent of the subsequent repair process. By treating symptoms of asthma with drugs such as beta 2 agonists that inhibit mast cell degranulation, increased inflammation is allowed to occur, which may lead to the chronic appearance of excess repair tissue and the acceleration of the disease process.