In the context that one major purpose of a staging system is to establish prognosis, attention has focused on the value of including weight (ie, body mass index [BMI]), dyspnea, and exercise capacity (ie, the 6-minute walk distance), with FEV 1 in staging COPD. 19 Indeed, the resultant index, called BODE (for BMI, obstruction, dyspnea, and exercise capacity) has been shown to better predict survival in COPD than FEV 1 alone. BODE scores of 0 to 10 (most impaired) are stratified into 4 quartiles, which discriminate mortality risk better than FEV 1 alone. Other multifactorial prognostic systems (eg, ADO [for age, dyspnea, and obstruction] and DOSE [for dyspnea, obstruction, smoking, and exercise capacity]) have also been proposed. 20,21
Smoking cessation, immunization against influenza and pneumonia, and pulmonary rehabilitation have been shown to improve function and reduce subsequent COPD exacerbations. 6 , 7 , 30 Long-term oxygen therapy decreases the risk of hospitalization and shortens hospital stays in severely ill patients with COPD. 7 , 31 , 32 The indications for long-acting inhaled bronchodilators and inhaled corticosteroids to improve symptoms and reduce the risk of exacerbations in patients with stable COPD are reviewed elsewhere. 5 , 7 , 33 – 38
Genetics play a role in the development of COPD.  It is more common among relatives of those with COPD who smoke than unrelated smokers.  Currently, the only clearly inherited risk factor is alpha 1-antitrypsin deficiency (AAT).  This risk is particularly high if someone deficient in alpha 1-antitrypsin also smokes.  It is responsible for about 1–5% of cases   and the condition is present in about 3–4 in 10,000 people.  Other genetic factors are being investigated,  of which there are likely to be many.