Background: Higher serum total 25-hydroxyvitamin D (25(OH)D) concentrations have been associated with better lung function and lower risk of allergic disease. 25(OH)D3 constitutes the majority of total 25(OH)D and has been suggested to be more potent than 25(OH)D2. We studied the prospective associations of 25(OH)D2 and 25(OH)D3 with asthma, wheezing, flexural dermatitis, and lung function in children who participated in the Avon Longitudinal Study of Parents and Children—a population-based contemporary birth cohort of children born in 1991–1992 from South West England.
Methods: Serum 25(OH)D2 and 25(OH)D3 concentrations, measured at a mean age of 9.8 years, were related to incident cases of wheezing (study sample: n = 3,323, 141 cases; 4%), asthma (n = 3,323, 464 cases; 14%), and flexural dermatitis (n = 3,748, 300 cases; 8%), as well as lung function (forced expiratory volume in 1 second [FEV1], forced vital capacity [FVC], and mid-forced expiratory flow assessed at a mean age of 15.5 years: n = 2,259).
Results: 25(OH)D2 was inversely associated with flexural dermatitis (adjusted odds ratio per doubling of exposure = 0.83 [95% confidence interval = 0.72–0.94]) and wheezing (0.83 [0.68–1.00]), and 25(OH)D3 was positively associated with flexural dermatitis (1.09 [1.00–1.18]) and wheezing (1.14 [1.03–1.28]). 25(OH)D2 was weakly positively associated with FEV1, and FVC. 25(OH)D3 was not associated with lung function.
Conclusions: These results suggest that higher 25(OH)D3 concentrations are associated with increased risk of wheezing and flexural dermatitis. Despite being one of the few prospective studies and being able to adjust for confounders, these findings need replication. Our results do not provide strong evidence that lower concentrations of vitamin D are detrimental to respiratory and allergic health in children.
From the aMRC Centre for Causal Analyses in Translational Epidemiology, School of Social and Community Medicine, University of Bristol, Bristol, UK; bSchool of Social and Community Medicine, University of Bristol, Bristol, UK; and cNorwich Medical School, Faculty of Medicine and Health Sciences, University of East Anglia, Norwich, UK.
Submitted 16 February 2012; accepted 30 November 2012.
Supported by an UK Medical Research Council (MRC) (grant G0701603), which also pays A.M.T.’s salary. Salary support for A.S. is provided by Wellcome Trust (grant 079960). The UK MRC, the Wellcome Trust, and the University of Bristol provide core funding support for ALSPAC. The MRC (grant G0600705) and the University of Bristol provide core funding for the MRC Centre of Causal Analyses in Translational Epidemiology.
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Correspondence: Anna-Maija Tolppanen, MRC Centre for Causal Analysis in Translational Epidemiology, School of Social and Community Medicine, University of Bristol, Oakfield House, 15-23 Oakfield Grove, Clifton, Bristol BS8 2BN, UK. E-mail: firstname.lastname@example.org.