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A cross-sectional study found a strong relationship between serum concentrations of 25-hydroxy vitamin D and FVC-Forced Vital Capacity (the amount of air which can be forcibly exhaled from the lungs after taking the deepest breath possible) and FEV1-Forced Expiratory Volume in One Second (the amount of air which can be forcibly exhaled from the lungs in the first second of a forced exhalation):
RESULTS: After adjustment for age, gender, height, body mass index, ethnicity, and smoking history, the mean FEV1 was 126 mL (SE, 22 mL), and the mean FVC was 172 mL (SE, 26 mL) greater for the highest quintile of serum 25-hydroxy vitamin D level (> or = 85.7 nmol/L) compared with the lowest quintile (< or = 40.4 nmol/L; p < 0.0001). With further adjustment for physical activity, the intake of vitamin D supplements, milk intake, and the level of serum antioxidants, the mean difference between the highest and lowest quintiles of 25-hydroxy vitamin D was 106 mL (SE, 24 mL) for FEV1, and 142 mL (SE, 29 mL) for FVC (p < 0.0001).
CONCLUSIONS: There is a strong relationship between serum concentrations of 25-hydroxy vitamin D, FEV1, and FVC. Further studies are necessary to determine whether supplementation with vitamin D is of any benefit in patients with respiratory disease1.
Vitamin D deficiency occurs frequently in COPD and correlates with severity of COPD as in a study of (ex)-smokers in the Netherlands. “In patients with COPD, 25-OHD levels correlated significantly with forced expiratory volume in 1 s (FEV(1)) (r=0.28, p<0.0001). Compared with 31% of the smokers with normal lung function, as many as 60% and 77% of patients with GOLD (Global Initiative for Obstructive Lung Disease) stage 3 and 4 exhibited deficient 25-OHD levels <20 ng/ml (p<0.0001)”2. In addition, those with the rs7041 T vitamin D-binding gene allele had about double the risk of those without this allele. Vitamin D binding protein (DBP) is the major carrier of vitamin D and its metabolites [Sinotte, 2009].
On the other hand, a study in Japan found baseline 25(OH)D levels are not predictive of subsequent lung function decline3 suggesting that lower serum 25(OH)D are not causally linked to risk of COPD. However, since smoking is perhaps the most important risk factor for COPD and smoking is associated with lower serum 25(OH)D levels4 5 and lower parathyroid hormone levels5, an interaction may still be plausible.
Page last edited: 06 May 2011
- Black, P. N. Scragg, R. Relationship between serum 25-hydroxyvitamin d and pulmonary function in the third national health and nutrition examination survey. Chest. 2005 Dec; 128 (6): 3792-8.
- Janssens, W. Bouillon, R. Claes, B. Carremans, C. Lehouck, A. Buysschaert, I. Coolen, J. Mathieu, C. Decramer, M. Lambrechts, D. Vitamin D deficiency is highly prevalent in COPD and correlates with variants in the vitamin D-binding gene. Thorax. 2010 Mar; 65 (3): 215-20.
- Kunisaki, K. M. Niewoehner, D. E. Singh, R. J. Connett, J. E. “Vitamin D Status and Longitudinal Lung Function Decline in the Lung Health Study”. Eur Respir J. 2010 Jul 1;
- Brot, C. Jorgensen, N. R. Sorensen, O. H. The influence of smoking on vitamin D status and calcium metabolism. Eur J Clin Nutr. 1999 Dec; 53 (12): 920-6.
- Jorde, R. Saleh, F. Figenschau, Y. Kamycheva, E. Haug, E. Sundsfjord, J. Serum parathyroid hormone (PTH) levels in smokers and non-smokers. The fifth Tromsø study. Eur J Endocrinol. 2005 Jan.; 52 (1): 39-45.