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Mechanisms for differences in the efficacy of vitamin D2 and vitamin D3: assessment of post-supplementation decline in vitamin D status in the D2-D3 Study

Published online by Cambridge University Press:  24 November 2016

L.R. Wilson ,
L. Tripkovic ,
K. Hart ,
C.P. Smith ,
G. Bucca ,
R. Elliott ,
S. Penson ,
G. Chope ,
E. Hyppönen  and
J. Berry
...Show all authors
L.R. Wilson
Affiliation:
Department of Nutritional Sciences, University of Surrey, GU2 7XH
L. Tripkovic
Affiliation:
Department of Nutritional Sciences, University of Surrey, GU2 7XH
K. Hart
Affiliation:
Department of Nutritional Sciences, University of Surrey, GU2 7XH
C.P. Smith
Affiliation:
School of Pharmacy & Biomolecular Sciences, University of Brighton, BN2 4GJ
G. Bucca
Affiliation:
School of Pharmacy & Biomolecular Sciences, University of Brighton, BN2 4GJ
R. Elliott
Affiliation:
Department of Nutritional Sciences, University of Surrey, GU2 7XH
S. Penson
Affiliation:
Campden BRI, Chipping Campden, Gloucestershire GL55 6LD
G. Chope
Affiliation:
Campden BRI, Chipping Campden, Gloucestershire GL55 6LD
E. Hyppönen
Affiliation:
University of South Australia, Adelaide, Australia
J. Berry
Affiliation:
Institute of Human Development, University of Manchester, M13 9PT
S. Lanham-New
Affiliation:
Department of Nutritional Sciences, University of Surrey, GU2 7XH
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Abstract

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Vitamin D is available in two forms; vitamin D2 (plant source) and vitamin D3 (animal source), and there has been controversy within the field as to whether both forms are equally effective in raising vitamin D status (as assessed by 25OHD levels)(Reference Tripkovic, Lambert and Hart1). However, in the largest randomized-controlled trial to date (The D2-D3 Study: n335) vitamin D3 was shown to be conclusively superior to vitamin D2 in raising total 25OHD levels(Reference Tripkovic, Wilson and Hart2–Reference Wilson, Hart and Elliott3). There is now a need to determine the mechanisms for this difference. We therefore aimed to assess the rate of metabolism or clearance of total 25OHD and the relevant metabolites; 25OHD2 and 25OHD3, after supplementation with vitamin D2 vs. vitamin D3 had ceased.

In the D2-D3 Study, participants were randomized to receive either placebo, 600IU/d vitamin D2 or 600IU/d vitamin D3 for 12-weeks, delivered via fortified foods. A sub-set of 38 participants completed an additional study visit at week 16 (wk16), four weeks after supplementation stopped at week 12 (wk12). Blood samples were collected at baseline (wk0), wk12 and wk16 to measure total 25OHD, 25OHD2 and 25OHD3 levels.

Total 25OHD, 25OHD2 and 25OHD3 levels are shown in Table 1. In the four weeks after supplementation had ended (from wk12 to wk16), total 25OHD levels significantly decreased in both the vitamin D2 (−15·4 ± 9·9 nmol/L, P < 0·002) and vitamin D3 group (−16·0 ±10·9 nmol/L, P < 0·001), and this total change did not differ between the two groups (P > 0·99). Between wk12 and wk16, there was also a significant decrease in 25OHD2 in the vitamin D2 group (−22·7 ±9·9 nmol/L P < 0·001), and in 25OHD3 in the vitamin D3 group (−17·0 ±10·9 nmol/L P < 0·001). Although we observed a slightly greater decrease in the D2 group, these were not significantly different from one another (P = 0·134). Interestingly, at wk16 total 25OHD levels only remained significantly higher than at wk0 (prior to any vitamin D supplementation) in the vitamin D3 group (D2: P > 0·99; D3: P = 0·008).

Table 1.

Serum total 25OHD, 25OHD2 and 25OHD3 levels at baseline (wk0), after the 12-week D2-D3 intervention (wk12), and four weeks after the intervention ended (wk16) within each treatment group

This study shows that vitamin D3 is not only superior to vitamin D2 in its ability to increase 25OHD levels, but it is also able to prolong the maintenance of total 25OHD levels to a greater extent than vitamin D2. These results suggest that this may be due to the initial greater rise in total 25OHD levels during supplementation with vitamin D3, as opposed to differences in the metabolism or clearance of 25OHD2 and 25OHD3. However, greater study numbers are required to confirm these findings, particularly in light of the recognised shorter half-life of 25OHD2(Reference Jones, Assar and Harnpanich4).

References

1.Tripkovic, L, Lambert, H, Hart, K et al. (2012) Am J Clin Nutr 95(6);1357–136410.3945/ajcn.111.031070Google Scholar
2.Tripkovic, L, Wilson, LR, Hart, K, et al. (2015) Proc Nutr Soc 74, OCE1, E16Google Scholar
3.Wilson, LR, Hart, K, Elliott, R et al. (2015) Proc Nutr Soc 74, OCE1, E11610.1017/S0029665115001317Google Scholar
4.Jones, KS, Assar, S, Harnpanich, D et al. (2014) J Clin Endocrinol Metab 99(9):3373–81Google Scholar
5.The D2-D3 Study is funded by the BBSRC DRINC Programme (Grant No. BB/I006192/1). LRW is a recipient of a BBSRC DRINC Studentship.Google Scholar
Figure 0

Table 1. Serum total 25OHD, 25OHD2 and 25OHD3 levels at baseline (wk0), after the 12-week D2-D3 intervention (wk12), and four weeks after the intervention ended (wk16) within each treatment group