Vitamin D status and longitudinal lung function decline in the Lung Health Study

Abstract

Low blood vitamin D levels have been postulated to be a risk factor for worse lung function, based largely on cross-sectional data. We sought to use longitudinal data to test the hypothesis that baseline plasma 25-hydroxyvitamin D (25(OH)D) is lower in subjects with more rapid lung function decline, compared to those with slow lung function decline. We conducted a nested, matched case-control study in the Lung Health Study 3 cohort. Cases and controls were continuous smokers with rapid and slow lung function decline, respectively, over ~6 yrs of follow-up. We compared baseline 25(OH)D levels between cases and controls, matching date of phlebotomy and clinical centre. Among 196 subjects, despite rapid and slow decliners experiencing strikingly and significantly different rates of decline of forced expiratory volume in 1 s (-152 versus -0.3 mL·yr⁻¹; p < 0.001), there was no significant difference in baseline 25(OH)D levels (25.0 versus 25.9 ng·mL⁻¹; p = 0.54). There was a high prevalence of vitamin D insufficiency (35%) and deficiency (31%); only 4% had a normal 25(OH)D level in the winter. Although vitamin D insufficiency and deficiency are common among continuous smokers with established mild-to-moderate chronic obstructive pulmonary disease, baseline 25(OH)D levels are not predictive of subsequent lung function decline.

Figure 1

Boxplots of 25(OH)D levels by season. Line=median, shaded box=interquartile range, whiskers=range, dots=outliers. Winter=January-March, Spring=April-June, Summer=July-September, Autumn=October-December. Results of statistical testing of means listed in Table 3 (one-way ANOVA with Bonferroni-corrected p-value) displayed at top with p-value and corresponding line to indicate the comparison tested. 25(OH)D = 25-hydroxyvitamin D.