A possible association between fructose consumption and pulmonary emphysema

Abstract

Chronic Obstructive Pulmonary Disease (COPD) is a syndrome that comprises several distinct and overlapping phenotypes. In addition to persistent airflow limitation and respiratory symptoms, COPD is also characterized by chronic systemic inflammation. Epidemiological studies have shown that dietary fibers, fruits and vegetables intake protects against the COPD development, while fructose-loading is associated with increased risk of asthma and chronic bronchitis. Since dietary factors might affect susceptibility to COPD by modulating oxidative stress and inflammatory responses, we evaluated how fructose feeding might affect the smoking-induced emphysema in mice. We found that chronic fructose intake induced destruction and remodeling of lung parenchyma and impairment of respiratory mechanics, which are associated with distinctive cytokine profiles in bronchoalveolar lavage fluid, blood plasma and skeletal muscle. The combined effects of chronic fructose intake and cigarette smoking on destruction of lung parenchyma are more pronounced than the effects of either alone. Excessive intake of fructose might directly cause pulmonary emphysema in mice rather than just altering its natural history by facilitating the installation of a low-grade systemic inflammatory milieu.

Negative Effects of Chronic High Intake of Fructose on Lung Diseases

“…Nutrition-related NCDs include chronic obstructive pulmonary disease (COPD) and asthma. Current studies have found associations between SSBs intake and pulmonary diseases [ 19 , 20 , 21 ]. COPD and asthma are common chronic airway diseases that substantially contribute to morbidity and mortality [ 22 ].…”

“…Current studies have shown that fructose intake from SSBs is associated with alterations in lung function [ 20 , 21 , 28 , 29 , 30 , 31 ]. A cohort of 1068 healthy mother–infant pairs consuming a mean of 32.5 g/day and 27.8 g/day, respectively, of fructose from SSBs for three months, showed that low intake of fructose from SSBs during pregnancy was associated with increased odds of current asthma in middle childhood (odds ratio [OR], 1.70; 95% confidence intervals [CI]: 1.08–2.67) [ 20 ], and in early childhood, low SSB intake for one month was also associated with current asthma in middle childhood, in models adjusted for maternal SSBs (OR, 1.79; 95% CI: 1.07–2.97) [ 20 ].…”

“…Studies in animal models have demonstrated lung injury by high intake of fructose. An experimental mouse model showed that an intake of 20% weight/volume ( w / v ) fructose in drinking water for 12 weeks altered respiratory mechanics, increasing airway resistance and decreasing lung tissue elastance [ 21 ]. Also, the fructose promoted the destruction and remodeling of the lung parenchyma, by increasing the number of mononuclear cells, and decreasing the content of elastic fibers, as well as increasing the production of interleukin (IL)-10, IL-6, and IL-1β, and decreasing the concentration of IL-1Ra in plasma, resulting in the development of pulmonary emphysema [ 21 ].…”

“…An experimental mouse model showed that an intake of 20% weight/volume ( w / v ) fructose in drinking water for 12 weeks altered respiratory mechanics, increasing airway resistance and decreasing lung tissue elastance [ 21 ]. Also, the fructose promoted the destruction and remodeling of the lung parenchyma, by increasing the number of mononuclear cells, and decreasing the content of elastic fibers, as well as increasing the production of interleukin (IL)-10, IL-6, and IL-1β, and decreasing the concentration of IL-1Ra in plasma, resulting in the development of pulmonary emphysema [ 21 ]. Another study showed that an intake of 10% ( w / v ) fructose for 16 weeks increased neutrophil infiltration in the lung and pulmonary fibrosis, due to the presence of connective tissue in the bronchial tree, while the stroma increased the production of collagen fibers [ 34 ].…”