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Quantity and quality of dietary carbohydrates, low-grade inflammation, and risk of chronic obstructive pulmonary
Fei Fang1, Ji-Mei Gu1, Yu-Wen Qian1
1The Fourth Affiliated Hospital of Soochow University, Department of Nutrition and Food Hygiene, School of Public Health, Suzhou Medical College of Soochow University, Suzhou, China.
Background:
The relationships between different dietary carbohydrates and risk of chronic obstructive pulmonary disease (COPD) have been rarely assessed. This study examined the relationships of different dietary carbohydrates with incident COPD and lung function, and the potential mediating role of chronic inflammation.
Methods:
A total of 205,752 UK Biobank participants were included. Dietary information was collected using up to five rounds of 24-h dietary recalls. Multivariable Cox regression models were used to assess different types of dietary carbohydrates (energy-adjusted) in association with incident COPD. In a subsample (n = 153,630), multivariate linear regression models were used to examine the cross-sectional relationships between dietary carbohydrates and lung function.
Results:
Over an average follow-up period of 12.2 years, 4591 participants developed COPD. After multivariable adjustment, higher dietary fiber and non-free sugar intakes both were associated with a lower risk of COPD, whereas a higher intake of free sugar was associated with a higher risk of COPD. Dietary fiber and non-free sugar were associated with better lung function reflected by higher levels of forced vital capacity (FVC), forced expiratory volume in 1-s (FEV1), and FEV1/FVC ratio. Conversely, dietary free sugar intake was associated lower levels of these measures. The mediation analysis revealed that low-grade chronic inflammation explained 9.22 %-25.17 % of the observed relationships of different dietary carbohydrates with incident COPD and lung function measures.
Conclusions:
Dietary fiber and non-free sugar intakes were associated with a lower risk of COPD and improved lung function, whereas free sugar intake showed opposite associations, partially through the regulation of chronic inflammation.
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