Abstract
We are encouraged that our article [1] has inspired this response, and we thank Björn et al. for their recent comments [2].
Björn et al. said we assumed “the yield of vitamin D3 would be the same in (the) model as in real skin” (p. 139) [2]. However, we did not assume this and this was aside from the central aim of our research. Our aim was to demonstrate that the dose–response relationship between UV exposure and vitamin D3 (cholecalciferol) synthesis is non-linear over a physiologic range of UV doses, using our in vitro model. The non-linear relationship we found is attributable to the reciprocity law of vitamin D3 synthesis, where the production of other photoproducts increases at the expense of previtamin D3, as larger UV doses are given (as we discussed in [1]). This finding is confirmatory of work by previous researchers who showed that the production of previtamin D3 (which becomes vitamin D3 following a thermal isomerization [3]) was non-linear with larger doses of UV. In particular, this was first shown by Holick et al. in their landmark study in 1981 [4] and has been shown elsewhere since then [5]. Notwithstanding, in most of the previous studies including the study by Holick et al. in 1981 [4], the authors did not report the doses that were given; rather, the duration of exposure was reported as a proxy [5], [6], [7]. One notable exception is MacLaughlin et al. in 1982 [8], who reported the doses given (in units of J/cm2); however, the UV spectrum of the source was not given and only several samples were used. In our article, we have modeled the dose–response relationship over a larger number of samples and a wider range of doses. The doses were measured in erythemally weighted units (minimal erythemal dose, MED), administered using simulated solar UV, and calibrated to the NIST standard of irradiance [1]. The range of doses used was representative of those that humans receive in daily life [9]. Moreover, we measured vitamin D3 as the endpoint of the model (not previtamin D3). This had several methodological advantages (discussed in [1]), especially that other researchers could more easily replicate our findings with commercially available chemicals. These were the strengths of our work.
Björn et al. said we assumed “the yield of vitamin D3 would be the same in (the) model as in real skin” (p. 139) [2]. However, we did not assume this and this was aside from the central aim of our research. Our aim was to demonstrate that the dose–response relationship between UV exposure and vitamin D3 (cholecalciferol) synthesis is non-linear over a physiologic range of UV doses, using our in vitro model. The non-linear relationship we found is attributable to the reciprocity law of vitamin D3 synthesis, where the production of other photoproducts increases at the expense of previtamin D3, as larger UV doses are given (as we discussed in [1]). This finding is confirmatory of work by previous researchers who showed that the production of previtamin D3 (which becomes vitamin D3 following a thermal isomerization [3]) was non-linear with larger doses of UV. In particular, this was first shown by Holick et al. in their landmark study in 1981 [4] and has been shown elsewhere since then [5]. Notwithstanding, in most of the previous studies including the study by Holick et al. in 1981 [4], the authors did not report the doses that were given; rather, the duration of exposure was reported as a proxy [5], [6], [7]. One notable exception is MacLaughlin et al. in 1982 [8], who reported the doses given (in units of J/cm2); however, the UV spectrum of the source was not given and only several samples were used. In our article, we have modeled the dose–response relationship over a larger number of samples and a wider range of doses. The doses were measured in erythemally weighted units (minimal erythemal dose, MED), administered using simulated solar UV, and calibrated to the NIST standard of irradiance [1]. The range of doses used was representative of those that humans receive in daily life [9]. Moreover, we measured vitamin D3 as the endpoint of the model (not previtamin D3). This had several methodological advantages (discussed in [1]), especially that other researchers could more easily replicate our findings with commercially available chemicals. These were the strengths of our work.
| Original language | English |
|---|---|
| Pages (from-to) | 169-170 |
| Number of pages | 2 |
| Journal | Journal of Photochemistry and Photobiology B: Biology |
| Volume | 97 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 2 Dec 2009 |
| Externally published | Yes |