Rennard and Vestbo have sounded a ringing call to arms (see page 643).1 Instead of trying to make minor improvements in the rate of decline of spirometry in patients with chronic obstructive pulmonary disease (COPD), they call for an all out effort to find a cure. Their arguments have attractions, but we believe that the evidence shows it would be easier to hatch out chickens from a plate of scrambled eggs than to cure COPD in adults.

COPD is defined for epidemiological and most clinical purposes by spirometry. When the underlying pathological changes cause spirometric measures to cross over a given threshold COPD is diagnosed. However, the crossing of this threshold depends on two factors, first the peak lung function attained as a young adult and secondly the deterioration with ageing accelerated by smoking and probably other environmental exposures.

First, some notes of caution. Spirometers are dangerous instruments in many contexts, not least public health. Extensive distal airway obstruction will not be detected by spirometry, and ‘a normal’ first second forced expired volume (FEV₁) is very far from being reassuring that all is well. By the time the potential patient with COPD has lost FEV₁, extensive and irreparable lung destruction will be present. Although well performed spirometry has a high reproducibility, extensive distal airway obstruction can occur before it is detected. Furthermore, the normal range of spirometry is very wide and so an individual who starts off with very good lung function can still be in the normal range, but for them it is a major loss of lung function.

Peak lung function is reached at 16–18 years in females and 20–25 years in males.2 3 The height of that plateau depends on two factors: the starting point for airway function immediately after birth, and the …