Jones, Kerry S

Schoenmakers, Inez

Inez Schoenmakers

Kerry S. Jones

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The Journal of Clinical Endocrinology & Metabolism

Letter to the Editor: The Effect of Genetic Factors on the Response to Vitamin D Supplementation May Be Mediated by Vitamin D−Binding Protein Concentrations

Jones, Kerry S.

University of East Anglia digital repository

1  To the Editor: the effect of genetic factors on the response to vitamin D supplementation 1 may be mediated by vitamin D binding protein concentrations 2 Schoenmakers I1 and Jones KS2 3  4 1Inez Schoenmakers 5 Department of Medicine, Faculty of Medicine and Health Sciences, University of East Anglia, Norwich 6 NR4 7TJ, United Kingdom. 7 e-mail I.Schoenmakers@uea.ac.uk 8 2Kerry S. Jones 9 MRC Elsie Widdowson Laboratory, Fulbourn Road, Cambridge, CB1 7UR, United Kingdom. Email. 10 kerry.jones@mrc-ewl.cam.ac.uk 11  12  13  14 DISCLOSURE STATEMENT:  The authors have nothing to disclose 15  16  17  18  19   20 2  To the Editor: the effect of genetic factors on the response to vitamin D supplementation 1 may be mediated by vitamin D binding protein concentrations 2 We welcome the paper by Yao et al. (1), presenting the vitamin D binding (DBP) genotype 3 distribution and concentrations and their influence on the response to vitamin D 4 supplementation in a large cohort of Chinese adults. There are however several points the 5 reader should consider in the interpretation of these data.  6 Yao et al. report that supplementation with 2,000IU vitamin D per day failed to correct 7 vitamin D deficiency in 25% of Chinese participants. They used the Endocrine Society (ES) 8 thresholds for vitamin D deficiency for clinical populations (a plasma 25 hydroxy vitamin D 9 (25(OH)D) concentration <50nmol/L) (2). The ES however recommends that for the 10 correction of vitamin D deficiency an 8-week loading schedule of 50,000IU/week followed 11 by a maintenance dose of 1,500-2,000IU/d for adults should be used. However for a study 12 amongst healthy community dwelling adults, without conditions that may increase their 13 vitamin D requirements, the use of population guidelines (e.g. that of the Institute of 14 Medicine (3)) would have been more appropriate.  15 The authors appear to suggest that there are major racial differences in the increment of 16 25(OH)D in the response to vitamin D supplementation. However, the selected papers do 17 not represent the balance of available evidence, which shows a lack of influence of race on 18 the dose-response to vitamin D supplementation, albeit this was mostly based on black and 19 white populations (summarised by EFSA (4)). The authors suggest that the low increment in 20 25(OH)D in Chinese participants may be caused by the predominant vitamin D binding 21 protein (DBP) genotypes in this population and the associated differences in the binding 22 affinity for 25(OH)D. In support of this statement the authors quote the paper by Arnaud, 23 3  1993 (5). However, where Arnaud used vitamin D as a tracer and reported DBP genotype-1 dependent differences in the affinity for 25(OH)D by extrapolation, other studies using 2 [3H]25(OH)D  showed small, if any differences (6-8). The DBP genotype-dependent 3 differences in baseline 25(OH)D and the increment in its concentration after 4 supplementation reported by Yao, may be predominantly determined by the genotype-5 dependent differences in DBP concentrations. Through this mechanism, DBP genotype may 6 influence the fraction of 25(OH)D available for cellular uptake and hydroxylation (9).   7 Finally, the authors suggest that the response to vitamin D supplementation was greater for 8 total 25(OH)D than for 25(OH)DBio by comparing their respective changes, while ignoring 9 differences in their absolute values. A calculation of their proportional change shows that 10 these are similar (+105 and 107% for total and 25(OH)DBio, respectively), a finding that is to 11 be expected since 25(OH)DBio is derived from the concentrations of total 25(OH)D and its 12 binding proteins, DBP and albumin. The latter are known not to respond to vitamin D 13 supplementation (10).  14  15 Inez Schoenmakers, Ph.D. 16 Department of Medicine, Faculty of Medicine and Health Sciences, University of East Anglia, Norwich 17 NR4 7TJ, United Kingdom. e-mail I.Schoenmakers@uea.ac.uk 18 Kerry S. Jones, PhD 19 MRC Elsie Widdowson Laboratory, Fulbourn Road, Cambridge, CB1 7UR, United Kingdom. Email. 20 kerry.jones@mrc-ewl.cam.ac.uk 21 The authors report no potential conflict of interest relevant to this letter. 22  23 4  1. Yao P, Sun L, Lu L, Ding H, Chen X, Tang L, Xu X, Liu G, Hu Y, Ma Y, Wang F, Jin Q, Zheng H, 1 Yin H, Zeng R, Chen Y, Hu FB, Li H, Lin X. Effects of genetic and non-genetic factors on total 2 and bioavailable 25(OH)D responses to vitamin D supplementation. J Clin Endocrinol Metab. 3 2017;102:100-110. 4 2. Holick MF, Binkley NC, Bischoff-Ferrari HA, Gordon CM, Hanley DA, Heaney RP, Murad MH, 5 Weaver CM. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine 6 Society clinical practice guideline. J Clin Endocrinol Metab. 2011;96:1911-1930. 7 3. IOM 2011 Dietary reference intakes for calcium and vitamin D. Washington, DC: The 8 National Academies Press 9 4. EFSA Panel on Dietetic Products, Nutrition and Allergies. Dietary reference values for 10 vitamin D. EFSA Journal. 2016;14:e04547-n/a. 11 5. Arnaud J, Constans J. Affinity differences for vitamin D metabolites associated with the 12 genetic isoforms of the human serum carrier protein (DBP). Hum Genet. 1993;92:183-188. 13 6. Bouillon R, van Baelen H, de Moor P. Comparative study of the affinity of the serum vitamin 14 D-binding protein. J Steroid Biochem. 1980;13:1029-1034. 15 7. Boutin B, Galbraith RM, Arnaud P. Comparative affinity of the major genetic variants of 16 human group-specific component (vitamin D-binding protein) for 25-(OH) vitamin D. J 17 Steroid Biochem. 1989;32:59-63. 18 8. Kawakami M, Imawari M, Goodman DS. Quantitative studies of the interaction of 19 cholecalciferol ((vitamin D3) and its metabolites with different genetic variants of the serum 20 binding protein for these sterols. Biochem J. 1979;179:413-423. 21 9. Jones KS, Assar S, Harnpanich D, Bouillon R, Lambrechts D, Prentice A, Schoenmakers I. 22 25(OH)D2 half-life is shorter than 25(OH)D3 half-life and is influenced by DBP concentration 23 and genotype. J Clin Endocrinol Metab. 2014;99:3373-3381. 24 5  10. Alzaman NS, Dawson-Hughes B, Nelson J, D'Alessio D, Pittas AG. Vitamin D status of black 1 and white Americans and changes in vitamin D metabolites after varied doses of vitamin D 2 supplementation. Am J Clin Nutr. 2016;104:205-214. 3  4 

Letter to the Editor: The effect of genetic factors on the response to vitamin D supplementation may be mediated by vitamin D−binding protein concentrations

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Letter to the Editor: The effect of genetic factors on the response to vitamin D supplementation may be mediated by vitamin D−binding protein concentrations

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