The morbidity and mortality associated with asthma are rising, despite
increased usage of anti-asthma medications. This report attempts to p
rovide a plausible hypothesis for the ''asthma paradox.'' The hypothes
is involves the role of mast cell degranulation as an endogenous anti-
inflammatory mechanism to prevent antigens from entering the lower air
ways and to limit the extent of the subsequent repair process. By trea
ting symptoms of asthma with drugs such as beta2 agonists that inhibit
mast cell degranulation, increased inflammation is allowed to occur,
which may lead to the chronic appearance of excess repair tissue and t
he acceleration of the disease process.