Jennifer J Koplin1, Noor H A Suaini2, Peter Vuillermin3, Justine A Ellis2, Mary Panjari4, Anne-Louise Ponsonby2, Rachel L Peters2, Melanie C Matheson1, David Martino2, Thanh Dang4, Nicholas J Osborne5, Pamela Martin4, Adrian Lowe1, Lyle C Gurrin1, Mimi L K Tang6, Melissa Wake7, Terry Dwyer4, John Hopper8, Shyamali C Dharmage1, Katrina J Allen9. 1. Murdoch Childrens Research Institute, Parkville, Australia; School of Population and Global Health, University of Melbourne, Parkville, Australia. 2. Murdoch Childrens Research Institute, Parkville, Australia; Department of Paediatrics, University of Melbourne, Parkville, Australia. 3. Murdoch Childrens Research Institute, Parkville, Australia; Child Health Research Unit, Barwon Health and Deakin University, Geelong, Australia. 4. Murdoch Childrens Research Institute, Parkville, Australia. 5. European Centre for Environment and Human Health, University of Exeter Medical School, Cornwall, United Kingdom. 6. Murdoch Childrens Research Institute, Parkville, Australia; Department of Paediatrics, University of Melbourne, Parkville, Australia; Department of Allergy and Immunology, Royal Children's Hospital, Parkville, Australia. 7. Murdoch Childrens Research Institute, Parkville, Australia; Department of Paediatrics, University of Melbourne, Parkville, Australia; Centre for Community Child Health, Royal Children's Hospital, Parkville, Australia. 8. School of Population and Global Health, University of Melbourne, Parkville, Australia. 9. Murdoch Childrens Research Institute, Parkville, Australia; Department of Paediatrics, University of Melbourne, Parkville, Australia; Department of Allergy and Immunology, Royal Children's Hospital, Parkville, Australia; School of Inflammation and Repair, University of Manchester, Manchester, United Kingdom. Electronic address: katie.allen@rch.org.au.
Abstract
BACKGROUND: There is evolving evidence that vitamin D insufficiency may contribute to food allergy, but findings vary between populations. Lower vitamin D-binding protein (DBP) levels increase the biological availability of serum vitamin D. Genetic polymorphisms explain almost 80% of the variation in binding protein levels. OBJECTIVE: We sought to investigate whether polymorphisms that lower the DBP could compensate for adverse effects of low serum vitamin D on food allergy risk. METHODS: From a population-based cohort study (n = 5276) we investigated the association between serum 25-hydroxyvitamin D3 (25[OH]D3) levels and food allergy at age 1 year (338 challenge-proven food-allergic and 269 control participants) and age 2 years (55 participants with persistent and 50 participants with resolved food allergy). 25(OH)D3 levels were measured using liquid chromatography-tandem mass spectrometry and adjusted for season of blood draw. Analyses were stratified by genotype at rs7041 as a proxy marker of DBP levels (low, the GT/TT genotype; high, the GG genotype). RESULTS: Low serum 25(OH)D3 level (≤50 nM/L) at age 1 years was associated with food allergy, particularly among infants with the GG genotype (odds ratio [OR], 6.0; 95% CI, 0.9-38.9) but not in those with GT/TT genotypes (OR, 0.7; 95% CI, 0.2-2.0; P interaction = .014). Maternal antenatal vitamin D supplementation was associated with less food allergy, particularly in infants with the GT/TT genotype (OR, 0.10; 95% CI, 0.03-0.41). Persistent vitamin D insufficiency increased the likelihood of persistent food allergy (OR, 12.6; 95% CI, 1.5-106.6), particularly in those with the GG genotype. CONCLUSIONS: Polymorphisms associated with lower DBP level attenuated the association between low serum 25(OH)D3 level and food allergy, consistent with greater vitamin D bioavailability in those with a lower DBP level. This increases the biological plausibility of a role for vitamin D in the development of food allergy.
BACKGROUND: There is evolving evidence that vitamin Dinsufficiency may contribute to food allergy, but findings vary between populations. Lower vitamin D-binding protein (DBP) levels increase the biological availability of serum vitamin D. Genetic polymorphisms explain almost 80% of the variation in binding protein levels. OBJECTIVE: We sought to investigate whether polymorphisms that lower the DBP could compensate for adverse effects of low serum vitamin D on food allergy risk. METHODS: From a population-based cohort study (n = 5276) we investigated the association between serum 25-hydroxyvitamin D3 (25[OH]D3) levels and food allergy at age 1 year (338 challenge-proven food-allergic and 269 control participants) and age 2 years (55 participants with persistent and 50 participants with resolved food allergy). 25(OH)D3 levels were measured using liquid chromatography-tandem mass spectrometry and adjusted for season of blood draw. Analyses were stratified by genotype at rs7041 as a proxy marker of DBP levels (low, the GT/TT genotype; high, the GG genotype). RESULTS: Low serum 25(OH)D3 level (≤50 nM/L) at age 1 years was associated with food allergy, particularly among infants with the GG genotype (odds ratio [OR], 6.0; 95% CI, 0.9-38.9) but not in those with GT/TT genotypes (OR, 0.7; 95% CI, 0.2-2.0; P interaction = .014). Maternal antenatal vitamin D supplementation was associated with less food allergy, particularly in infants with the GT/TT genotype (OR, 0.10; 95% CI, 0.03-0.41). Persistent vitamin Dinsufficiency increased the likelihood of persistent food allergy (OR, 12.6; 95% CI, 1.5-106.6), particularly in those with the GG genotype. CONCLUSIONS: Polymorphisms associated with lower DBP level attenuated the association between low serum 25(OH)D3 level and food allergy, consistent with greater vitamin D bioavailability in those with a lower DBP level. This increases the biological plausibility of a role for vitamin D in the development of food allergy.
Authors: Carina G Uasuf; Caterina Di Sano; Sebastiano Gangemi; Giuseppe Albeggiani; Diego Cigna; Paola Dino; Ignazio Brusca; Mark Gjomarkaj; Elisabetta Pace Journal: Inflamm Res Date: 2018-05-17 Impact factor: 4.575