Overview and Risk Factors
Chronic obstructive pulmonary disease (COPD) is a progressive and irreversible airway disorder usually caused by smoking. It is characterized by diminished inspiratory and expiratory lung capacity, airflow obstruction, and impaired gas exchange. COPD is the fourth most common cause of death in the United States and the sixth most common cause of death worldwide. Its incidence and mortality rate are on the rise, due to increasing worldwide cigarette use and air pollution.
COPD pathophysiology involves chronic bronchitis and emphysema. Chronic bronchitis is characterized by airway inflammation and defined by the presence of a productive cough that lasts at least 3 months and occurs in more than 2 successive years. Emphysema entails enlargement of air spaces and destruction of the lung parenchyma, resulting in closure of small airways and loss of lung elasticity.
Smoking. Cigarette smoking is the most important risk factor for COPD, and it accounts for more than 90% of cases. Secondhand smoke also contributes to COPD.
Occupation. A number of occupational pollutants, especially aerosol sprays and fine airborne particulates, have been linked to an increased incidence of COPD.
Air pollution. The role of pollutants in the pathogenesis of COPD is unclear. However, the incidence of COPD and the frequency of acute exacerbations are significantly increased in heavily polluted areas.
Genetics. There is a clear genetic predisposition toward the development of COPD, although specific genes have yet to be identified.
a1-antitrypsin deficiency. a1-antitrypsin is an inhibitor of the elastase enzyme. This disorder predisposes a person to emphysema due to the uncontrolled action of elastase, which destroys the lung parenchyma.
Diagnosis and Treatment
Pulmonary function testing showing an obstructive pattern is the most reliable indicator for diagnosis. This would be a ratio of forced expiratory volume in 1 second to the forced vital capacity of less than 70% (FEV1/FVC ratio <70%).
Chest x-rays may reveal hyperinflation of the lungs, indicated by flattening of the diaphragm and radiolucency of the lung fields. However, x-rays may appear normal until the emphysema component is quite advanced.
Hematocrit levels may be elevated due to chronic hypoxia.
Arterial blood gas concentration may reveal hypoxia and hypercarbia.
Quitting smoking is essential at any stage of the disease. Although lung damage will not be reversed (especially in advanced cases), smoking cessation will lead to improvements in pulmonary function.
Physical exercise, as part of a pulmonary rehabilitation program, can improve functional status in COPD. Exercise programs do not necessarily increase lung function, but they should increase patients' ability to perform activities of daily living. Inspiratory muscle training in particular is associated with significant improvements in pulmonary capacity, endurance, exercise capacity, and dyspnea.1 As with other forms of exercise, benefits are lost if patients do not maintain their efforts.2
Respiratory therapy and pulmonary rehabilitation improve quality of life and exercise capacity.
Continuous or nighttime supplemental oxygen provides symptomatic relief and improves mortality in patients with chronic hypoxemia.
Bronchodilators, including β2-adrenergic agents (eg, albuterol) and anticholinergics (eg, ipratropium bromide) may alleviate symptoms by reducing bronchial tone. However, some COPD patients will be unresponsive to bronchodilator therapy.
Methylxanthines (eg, theophylline) are a controversial treatment. They may be beneficial by augmenting the action of the diaphragm during exhalation, improving gas exchange, and increasing airway caliber.
The role of corticosteroids is still under investigation. Inhaled steroids, although often prescribed, have not been beneficial in most patients. Systemic steroids may help hospitalized patients with acute exacerbations.
Antibiotics are useful in exacerbations, but should not be used prophylactically.
Surgical intervention may be helpful in a minority of advanced cases. Lung-volume-reduction surgery may benefit selected end-stage patients by increasing elastic recoil, improving expiratory airflow, and improving the function of the diaphragm and intercostal muscles. Lung transplantation may also be considered.
Acute exacerbations of COPD must be treated emergently. It is important to identify and treat the cause of the exacerbation (eg, infection, excessive sedation), administer bronchodilator therapy (eg, beta agonists) and supplemental oxygen, ensure clearance of pulmonary secretions, and closely monitor for signs of respiratory failure.
If respiratory failure occurs, intubation may be necessary. Noninvasive positive pressure ventilation (BiPAP) is often used in deteriorating patients, as it may preclude the need for intubation.
While the mechanism by which cigarette smoke causes COPD in some persons is unclear, a growing body of evidence supports the hypothesis that COPD is influenced by oxidative stress, inflammation, and an imbalance between protease and antiprotease activity.3 Antioxidants and fatty acids influence these processes and thus have theoretical roles in the prevention and treatment of COPD. However, most studies of specific nutrients and foods relate to COPD prevention, rather than treatment, and further research is necessary to establish their value. Of course, nutritional interventions, if shown to be clinically useful, must be used along with avoidance of smoking or other causative agents and with appropriate treatment.
The following dietary factors are under investigation for their possible roles in preventing COPD or affecting its course:
Fruits and Vegetables
Although cause and effect cannot be established from existing evidence, a number of studies have associated higher intakes of fruits and vegetables with a lower risk for COPD. In a population of smokers, eating at least 4 ounces of fruit and 3 ounces of vegetables daily was associated with a 50% lower COPD risk, compared with individuals who ate the least amounts of these foods.4 Similarly, a slower rate of decline in FEV1 was found in a general population with higher average intake of foods containing vitamin C.5
However, benefits of higher fruit and vegetable intakes on COPD risk were not apparent in a study of both smokers and nonsmokers.6 A British study found no association between average fruit intake and lung function (FEV1), but did find a decline in FEV1 in individuals whose fruit intakes decreased over time.7
The putative protective effects of these foods may be partly related to the antioxidant effects of carotenoids8 and flavonoids,9 and to replacement of the vitamin C that COPD patients lose as a result of a systemic oxidant/antioxidant balance imbalance.10 However, these mechanisms and effects are speculative only, and the effect of diets high in fruits or vegetables on the incidence or progression of COPD remains to be assessed in clinical trials.
Omega-3 Fatty Acids
In human subjects with COPD, supplementation with an omega-3-containing calorie supplement (400 cals/day) for 2 years significantly improved dyspnea and reduced the rate of decline in arterial oxygen saturation, compared with a group given an isocaloric supplement containing omega-6 fatty acids.11 Other evidence indicates benefits of omega-3 fatty acid supplements on exercise capacity in patients with COPD, in comparison with those on placebo.12 Additional controlled clinical trials are needed to determine if omega-3 fats reduce the incidence or rate of progression of COPD.
If omega-3 fatty acids influence COPD, the mechanism may relate to their antiinflammatory effects. Through competition for the lipoxygenase pathway, omega-3 fatty acids interfere with production of omega-6 fat-derived leukotrienes (eg, LTB4), which have proinflammatory, bronchoconstrictive effects.13
Some observational studies have found protective effects of dietary (not supplementary) vitamin E intake on lung function.6 However, in the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study involving over 29,000 subjects, neither alpha-tocopherol (50 mg/d) or beta carotene (20 mg/d) supplements lessened COPD symptoms, although high baseline blood levels of vitamin E were associated with a lower risk for COPD and dyspnea in smokers, compared with individuals who had the lowest levels.8 Clinical trials have not yet assessed the value of diets high in vitamin E for reducing COPD risk or decreasing its rate of progression.
The association between certain antioxidants and COPD derives some theoretical support from the fact that a deficiency of alpha-1 protease inhibitor leads to lung tissue breakdown and pulmonary emphysema. Blood vitamin E concentrations correlate positively with serum alpha-1 protease inhibitor levels in smokers.14
Maintenance of Adequate Body Weight
In several studies, lower than ideal bodyweight was associated with a greater risk for death from COPD,15 and a loss of fat-free mass appears to be an independent predictor of mortality in these patients.16 However, clinical trials have not yet established whether the associations between low body weight or lean body mass and COPD mortality are causal or incidental. Protein-calorie supplements do not appear to benefit most COPD patients. By some estimates, almost one in four patients with COPD is malnourished.17 Although nutritional supplements are commonly used to correct this condition, a review of existing evidence concluded that supplementation has no significant effect on anthropometric measures, lung function, or exercise capacity in COPD patients.18
Nutritional supplements, if indicated and per recommendation of registered dietitian.
What to Tell the Family
COPD is preventable in most cases by not smoking or by quitting smoking early. As disease severity progresses, patients will need varying amounts of medications to reduce lung inflammation, dilate the bronchi, and reduce airway obstruction. Eventually, supplemental oxygen becomes necessary. The role of diet in preventing the progression of COPD is unclear.
4. Watson L, Margetts B, Howart P, Dorward M, Thompson R, Little P. The association between diet and chronic obstructive pulmonary disease in subjects selected from general practice. Eur Respir J.2002;20:313-318.
9. Tabak C, Arts ICW, Smit HA, Heederik D, Kromhout D. Chronic obstructive pulmonary disease and intake of catechins, flavonols, and flavones. Am J Respir Crit Care Med. 2001;164:61-64.
10. Calikoglu M, Unlu A, Tamer L, Ercan B, Bugdayci R, Atik U. The levels of serum vitamin C, malonyldialdehyde, and erythrocyte reduced glutathione in chronic obstructive pulmonary disease and in healthy smokers. Clin Chem Lab Med. 2002;40:1028-1031.
13. Kostikas K, Gaga M, Papatheodorou G, Karamanis T, Orphanidou D, Loukides S. Leukotriene B4 in exhaled breath condensate and sputum supernatant in patients with COPD and asthma. Chest. 2005;127:1553-1559.
17. Cochrane WJ, Afolabi OA. Investigation into the nutritional status, dietary intake, and smoking habits of patients with chronic obstructive pulmonary disease. J Hum Nutr Diet. 2004;17:3-11, quiz 13-15.