Chronic Obstructive Pulmonary Disease (COPD) is an umbrella term used to describe progressive lung diseases including emphysema, chronic bronchitis, refractory (non-reversible) asthma, and some forms of bronchiectasis (1,2). This disease is characterized by increasing breathlessness. (1,2)

People with emphysema are referred to as “pink puffers” and experience shortness of breath due to a loss of elasticity, and eventual damage to the air sac walls (3,4,5).  This leads to impaired exhalation and a buildup of gas in the lungs. “Pink puffers” are typically thin, often exhibiting significant weight loss due to the increased energy requirements associated with labored breathing. In contrast, people with chronic bronchitis are referred to as “blue bloaters” (3,4,5).  They are typically normal weight or overweight, frequently barrel chested, and experience persistent cough, increased mucous production, and shortness of breath due to inflammation, scarring, and eventual narrowing of the airways (3,4,5).

About 85 to 90 percent of all COPD cases are caused by cigarette smoking (1,2).  Long-term exposure to air pollution, secondhand smoke, dust, fumes, and chemicals (which are often work-related) can cause COPD (1,2).  A small number of people have a rare form of COPD called alpha-1 deficiency-related emphysema, caused by a genetic condition (1,2). COPD is recognized as a systemic inflammatory disorder associated with increased production of inflammatory cytokines such as interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α, and chemokines (3,4).

COPD promotes inactivity, which promotes further loss of exercise capacity (deconditioning) through the loss of muscle mass, creating a “vicious” cycle. Indeed, COPD has substantial manifestations beyond the lungs, such as unintentional weight loss and skeletal muscle dysfunction (3).  Undernutrition leads to lung and chest wall mechanical changes, such as distorted structure of diaphragm and intercostals, reduction of surfactant and decrease in elastic fiber content of pulmonary tissue (6).   The diaphragm, as a main inspiratory muscle, suffers from muscle protein degradation and loss of contractile protein with poor nutrition (6).  Inspiratory muscle weakness and maximum inspiratory pressure generation was an independent determinant of survival in severe COPD (6).

In COPD patients, resting energy expenditure (REE) has been reported to be 15–20% above predicted values due to the increased energy required for breathing (6).  Energy expenditure changes due to impaired mechanical efficiency may be partially reversed by reducing hyperinflation with medication, breathing techniques, or surgical lung volume reduction (6). This could reduce oxygen cost for breathing.  This in turn can increase oxygen availability, allowing improved carbohydrate metabolism and allowing improvement in body composition, decreasing body fat and increased muscle mass (6).   Studies indicate that chronic obstructive lung disease may induce insulin resistance and changes glucose metabolism.

The question on how much we should give nutritional repletion still remains.  In study, it was described that total daily energy intake of REE x 1.3 was preferable than REE x 1.7 in mild stable COPD patients. They found that administration of nutritional supplements, high in proteins, with predominance of carbohydrates over fat, and enriched in antioxidants to achieve total daily defined energy intake in patients in group REE x 1.3 was followed by a significant improvement of body weight, handgrip strength, decrease airflow limitation and increase quality of life (6). Total calories being administered as 20% proteins seemed to be the optimal in nutritional supplements for stable malnourished COPD patients. Small portion of carbohydrate and protein-rich supplementation seemed to have an impact on weight gain after 8 weeks when compared to normal size supplements of similar macronutrient composition, probably because many patients still usually took ordinary meals outside the supplementation (6). Goal is to avoid large volumes at meals and supplements due to potential compromise of diaphragm movement and postprandial dyspnea because it will prevent the diaphragm to move easily due to gastric filling (6).


  1. COPD Foundation:
  2. American Lung Association:
  3. Corhay, J. et al. “Pulmonary Rehabilitation and COPD: Providing Patients a Good Environment for Optimizing Therapy.” International Journal of Chronic Obstructive Pulmonary Disease 9 (2014): 27–39. Accessed 11/7/17.
  4. Florian, I. Nutrition and COPD – Dietary Considerations for Better Breathing. Today’s Dietitian.  Vol. 11. 2(2009): 54.
  5. Hallin, R. et al. Nutritional status, dietary energy intake and the risk of exacerbations in patients with chronic obstructive pulmonary disease (COPD). Respiratory Medicine. Vol 100: 3, (2006): 561-567.
  6. Aniwidyaningsih, Wahju et al. “Impact of Nutritional Status on Body Functioning in Chronic Obstructive Pulmonary Disease and How to Intervene.” Current Opinion in Clinical Nutrition and Metabolic Care 11.4 (2008): 435–442. Accessed 11/7/17.