Dietary Sodium Intake and Asthma: An Epidemiological and Clinical Review

T. D. Mickleborough; A. Fogarty


Int J Clin Pract. 2006;60(12):1616-1624. 

In This Article

Definitions and Prevalence of Asthma


Asthma is diagnosed clinically on the basis of symptoms of wheeze, dyspnoea and cough, and by objective evidence of variable airflow obstruction.[2] The causes of asthma are unknown, but the prevalence of wheeze has increased over the recent decades in developed countries,[3,4] and is consistently higher in countries that have adopted an affluent lifestyle, with 20-30% of children living in USA, UK and Australia reporting symptoms of asthma in the past year in the ISAAC study.[5] As well as significant morbidity, a diagnosis of asthma is associated with increased use of healthcare resources,[6] and premature mortality.[7,8]

Asthma is an inflammatory disease characterized by excess mucous production, bronchial wall oedema and reversible bronchiolar smooth muscle contraction. Typical triggers for airway obstruction in asthmatics include allergens (e.g. dust, mites, pollen, etc.), smoke, cold air, infectious agents, hyperventilation and exercise. Tests of airway reactivity as assessed by inhalation of controlled doses of methacholine or histamine are used to determine the airway responsiveness by both clinicians and researchers.[9] For methacholine, a post challenge fall in forced-expiratory volume in 1 s (FEV1) of at least 20% at a dose <16 mg/ml (PD20) inhaled methacholine is considered indicative of airway hyper-responsiveness.[9]

Exercise-Induced Bronchoconstriction

Exercise-induced bronchoconstriction is not an isolated disorder or specific disease, but rather part of the spectrum of asthmatic disease where exercise is one of many stimuli that may induce airflow limitation.[10] Exercise is a powerful trigger of asthma symptoms, and up to 90% of asthmatics experience EIB,[11,12,13] as defined by a >10% decrease in post exercise forced expiratory volume in 1 s (FEV1) compared with pre-exercise values.[14] In addition, 18-26% of Olympic winter sport athletes and 50% of non-atopic elite cross-country skiers and elite summer athletes have EIB,[15,16,17,18,19,20,21] compared with 3-24% of healthy individuals.[22,22]

While the factors driving the pathophysiology of EIB in non-atopic elite athletes and individuals with asthma are uncertain and may be different, both conditions result in active inflammation, remodelling and hyper-reactivity of the airways.[24,25,26]


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