In recognition of COPD Awareness month, we present study findings that look at the link between poor diet and lung function, and provide COPD resources.
A poor diet may be linked to worse lung function in patients with chronic obstructive pulmonary disease (COPD), according to research presented earlier this month at CHEST 2010, the 76th annual meeting of the American College of Chest Physicians (ACCP). The study finds that a low dietary intake of certain antioxidants increases the chance of decreased lung function in people with COPD, especially men.
"Our study, along with other research, suggests that strategies for dietary modification and supplementation should be considered in patients with COPD," said M. Salman Khan, DO, Summa Akron City Hospital, Akron, OH, in a statement. "Further studies are needed to clarify the role gender has on the loss of lung function in COPD and the impact of antioxidant nutrient intake."
In the study, Khan and colleagues analyzed data from 20 people with COPD (13 women and seven men) who completed a take-home food frequency questionnaire to assess typical intake of vitamins A, C, D, E, and selenium based on specific foods, portion size, and preparation methods. The researchers compared the nutrient data with nationally recognized dietary reference intakes (DRIs) and classified each person as deficient or not deficient in each nutrient. Each person’s lung function was assessed using FVC, the maximum volume of air exhaled with force.
Results of the analysis showed that a diet poor in antioxidants was common, with the following percentages of participants having deficiencies: 25% (selenium), 45% (vitamin C), 90% (vitamin E), 55% (vitamin A), and 70% (vitamin D). Decreased lung function was found in all subjects with a diet deficient in selenium. Of those who were deficient in vitamin C, vitamin A, and vitamin D, lung function was worse only in men, they found.
According to Khan, the difference in lung function between males and females could be attributed to the specific study population.
"The older male population studied may have been exposed to more lifestyle risks than our female population, including, but not limited to, primary or secondhand smoke," he said. "Recurrent lifestyle-related lung injury could deplete the lungs inherent antioxidant capacity, accentuating the role of dietary antioxidants."
The protective role of antioxidants may also extend to people with asthma. Although the pathophysiology of asthma is often different than COPD, there could be a chronic, recurrent, inhalational lung injury component to both diseases.
"We would guess that the role of antioxidant nutrients in a well-controlled asthma patient would be less than that seen in patients with COPD," said Khan. "However, in patients with severe asthma with poorly controlled symptoms and frequent, recurrent exacerbations, antioxidant nutrient intake may indeed play an important role in the preservation of lung function."
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