Oxidant–Antioxidant Imbalance and Diet Quality in COPD

Oxidative stress and associated inflammation in the lung and in the circulation in response to exposure to air pollution, tobacco smoke, infection, or potentially obesity are leading pathogenic processes in COPD. Compared to healthy controls, patients with COPD tend to have increased systemic and airway oxidative damage markers (relative to DNA, lipid, and proteins) [34], coupled to altered antioxidant defense, as evidenced by marked reduction in both plasma antioxidant capacity and soluble and enzymatic antioxidants levels [34–36]. Moreover, oxidative stress persists long after smoking cessation as a result of continuous production of pro-oxidants [37]. Low serum antioxidant vitamin levels appeared to increase the risk of obstructive airways diseases associated to smoking exposure [38]. In accordance, higher levels of oxidative markers in COPD were correlated with decreased lung function [39–41], while higher serum levels of antioxidant enzymes (catalase, superoxide dismutase, glutathione peroxidase) [40,41], as well as of soluble antioxidants (vitamins, carotenoids, etc.) [35,42,43], were positively associated with lung function. Therefore, it can be hypothesized that targeting oxidative stress with antioxidants or boosting endogenous levels of antioxidants might be beneficial in COPD.
Diet may contribute to antioxidant/oxidant and inflammatory status in COPD. Compared to
healthy controls, COPD subjects have diets with lower fruit and vegetable intake [44] and with poorer antioxidant content, which was correlated with impaired lung function and risk of having COPD [35,36]. Moreover, lower energy intake (accompanied by elevated resting energy expenditure), unbalanced intake of macronutrients (e.g., low proteins), and defective intake of several micronutrients (minerals and vitamins, e.g., iron, calcium, potassium, zinc, folate, vitamin B6, retinol, niacin) have been documented in COPD patients compared to healthy controls [45], mostly in the presence of obesity [46], suggesting an increased risk of malnutrition and related adverse consequences in COPD. The poor diet quality and the nutrient deficiencies in COPD, which are related to disease-specific factors such as symptoms (e.g., dyspnea, fatigue, anxiety, depression, anorexia, periodontal disease, loss of taste, poor dentition, dysphagia, poor chewing and swallowing ability) or social problems (e.g., living or eating alone, or poverty) [47], require improvement through dietary intervention to satisfy nutritional requirements and even to supplement further protective factors able to counteract disease pathogenesis. The inflammatory/oxidative status in COPD and the associated procatabolic state contributing to weight loss and muscle wasting in severe COPD represent further possible targets
for nutritional intervention.