National Institute of Water & Atmospheric Research, NIWA Lauder, PB 50061, Omakau, Central Otago, 9352, New Zealand.
Photochem Photobiol Sci. 2012 Jul;11(7):1174-85. doi: 10.1039/c2pp05403e. Epub 2012 Mar 13.
We investigate the relationship between blood serum 25-hydroxyvitamin D (25(OH)D) and UV exposure from two artificial sources. We then use the results to test the validity of the action spectrum for vitamin D production, and to infer the production from summer and winter sunlight. The results are based on a two-arm randomised clinical trial of biweekly UV exposure for 12 weeks using two different types of dermatological booths: one emitting primarily UV-A radiation, and the other emitting primarily UV-B radiation (booth A and booth B respectively). In terms of the vitamin D production per unit erythema, one of the booths mimics summer noon sunlight, while the other mimics winter noon sunlight. Blood samples were taken before and after the exposures. For all participants, the phototherapy booth treatments arrested the usual wintertime decline in 25(OH)D, and for most the treatments from either booth resulted in significant increases. The increases were highly non-linear and there was a high degree of variability in 25(OH)D and its response to UV from person to person. By the end of the 12 week period, the mean increase was >30 nmol l(-1) from a cumulative exposure of 17 SED from the UV-A booth, and twice that for the UV-B booth for which the cumulative exposure was 268 SED. Assuming a logarithmic relationship between UV and vitamin D, the results for the two booths show no obvious inconsistency in the action spectrum for pre-vitamin D production. However, further measurements with similar exposures from each booth are required to confirm its validity. A model was developed to describe the increases in serum 25(OH)D resulting from the UV exposures, which differed markedly between the two booths. The deduced initial rate of increase of 25(OH)D was approximately 5 nmol l(-1) per SED. From the large increases in 25(OH)D from each booth, along with knowledge of the spectral distribution of sunlight and assuming the currently-accepted action spectrum for photo-conversion to pre-vitamin D, we infer that the production of 25(OH)D from sunlight should be possible throughout the year, although in winter the exposures necessary to maintain optimal levels of 25(OH)D would be impractically long. This finding is at variance with the commonly-held view that no vitamin D is produced at mid-latitudes in the winter. Further work is needed to resolve that inconsistency.
我们研究了血清 25-羟维生素 D(25(OH)D)与两种人工来源的紫外线暴露之间的关系。然后,我们使用结果来测试维生素 D 产生的作用光谱的有效性,并推断来自夏季和冬季阳光的产生。结果基于一项为期 12 周、每两周进行一次紫外线暴露的双臂随机临床试验,使用两种不同类型的皮肤科 booth:一种主要发射 UV-A 辐射,另一种主要发射 UV-B 辐射(分别为 booth A 和 booth B)。就单位红斑产生的维生素 D 而言,其中一个 booth 模拟了夏季中午的阳光,而另一个模拟了冬季中午的阳光。在暴露之前和之后采集了血液样本。对于所有参与者,光疗 booth 治疗阻止了冬季通常的 25(OH)D 下降,并且对于大多数人来说,来自任何一个 booth 的治疗都导致了显著的增加。增加是非线性的,人与人之间的 25(OH)D 及其对 UV 的反应存在高度的可变性。在 12 周的治疗期结束时,来自 UV-A booth 的累积 17 SED 的暴露导致 25(OH)D 增加超过 30 nmol l(-1),而对于累积暴露 268 SED 的 UV-B booth 则增加了两倍。假设 UV 与维生素 D 之间存在对数关系,两个 booth 的结果表明,前维生素 D 生产的作用光谱没有明显的不一致。然而,需要使用每个 booth 进行类似的暴露进一步测量以确认其有效性。开发了一个模型来描述来自 UV 暴露的血清 25(OH)D 的增加,这在两个 booth 之间有明显的差异。推断出的 25(OH)D 的初始增加率约为 5 nmol l(-1) per SED。从每个 booth 中 25(OH)D 的大量增加,以及对阳光光谱分布的了解,并假设目前接受的光转换为前维生素 D 的作用光谱,我们推断,全年都应该有可能从阳光中产生 25(OH)D,尽管在冬季,维持最佳 25(OH)D 水平所需的暴露时间将不切实际地长。这一发现与人们普遍认为在冬季中纬度地区不会产生维生素 D 的观点不一致。需要进一步的工作来解决这一不一致。