| |
Vitamin D and UVB Radiation: How Much Is Necessary? "Exposure to a UVB dose of 1 SED every second week to ~88% body area is sufficient for maintaining summer 25(OH)D levels during the winter." - pdf attached
|
| |
| |
Download the PDF here
For individuals unable to benefit from supplements, ultraviolet B exposure every 2 weeks may be an alternative.
Adequate vitamin D levels are necessary for bone health and might prevent a variety of other diseases. Many individuals are able to maintain adequate circulating concentrations of this important molecule during the summer, when ambient ultraviolet B (UVB) from sunlight is greatest. However, during winter months, when terrestrial UVB is at its nadir, levels can drop precipitously, particularly in regions far from the equator. For most, vitamin D deficiency can be addressed by the administration of supplements. However, physician-monitored UVB treatments have been advocated as an alternative therapeutic approach.
Investigators in Denmark assessed how much artificial UVB is necessary to maintain summertime vitamin D concentrations. Every 1, 2, or 4 weeks during a 16-week period between October and February, 55 subjects received one standard erythemal dose (equivalent to 10 minutes of summer noonday sun exposure) to about 88% of total body area from a broadband UVB light source; a control group received no UVB.
UVB administered every 2 weeks was sufficient to maintain summertime vitamin D levels. Smaller changes were observed in those with higher concentrations at baseline and in older subjects, and greater changes were seen in those with higher body mass index and total body surface area.
Comment: For individuals resistant to or unable to take supplements, ultraviolet B exposure every 2 weeks may be an alternative method for maintaining summertime levels of vitamin D in winter. Narrowband UVB might be a better choice than the broadband UVB used in this study, because it may have fewer long-term adverse effects. It is important to emphasize that tanning beds do not emit the appropriate wavelengths and have been linked to melanoma and nonmelanoma skin cancers. Increasing UV exposure is not necessarily healthier; higher baseline vitamin D levels correlated with smaller increases in vitamin D concentrations.
A small suberythemal ultraviolet B dose every second week is sufficient to maintain summer vitamin D levels: a randomized controlled trial
British Journal of Dermatology
February 2012
Summary
Background It is known that ultraviolet (UV) B radiation increases serum 25-hydroxyvitamin D3 [25(OH)D] level. However, there is uncertainty about the relationship between the maintenance of vitamin D status and UVB.
Objectives To define the frequency of UVB exposure necessary for maintaining summer 25(OH)D levels during the winter.
Methods In total, 60 participants were included from October 2008 to February 2009 (16 weeks) and randomized for UVB exposure of 1 standard erythema dose (SED) to ~88% body area once a week (n = 15 completed), every second week (n = 14 completed) or every fourth week (n = 12 completed). The controls (n = 14 completed) had no intervention. Vitamin D was measured at baseline, every fourth week before exposure, and 2 days after the last UVB exposure.
Results The 25(OH)D levels (mean) after UVB exposure once a week increased significantly (from 71·9 to 84·5 nmol L-1) (P < 0·0001), whereas UVB exposure every second week maintained 25(OH)D levels (P = 0·16). A significant decrease in mean 25(OH)D levels (from 56·4 to 47·8 nmol L-1) (P < 0·0001) was found after UVB exposure once every fourth week and for the control group (from 64·8 to 40·1 nmol L-1) (P < 0·0001). The development in 25(OH)D levels during the 16-week study period were negatively correlated with baseline 25(OH)D (P < 0·0001). Further, the increase in 25(OH)D after the last UVB exposure was negatively correlated with the 25(OH)D level just before the last UVB exposure (P < 0·0001).
Conclusions Exposure to a UVB dose of 1 SED every second week to ~88% body area is sufficient for maintaining summer 25(OH)D levels during the winter.
Vitamin D is essential for bone structure. Recently, several studies have suggested that vitamin D plays a role in other diseases such as cancer, autoimmune disorders and other aspects of health.1-3 Ultraviolet (UV) B radiation (280-320 nm) is the only part of the solar UV radiation spectrum that causes formation of vitamin D.4 However, solar UVB is also known to be an aetiological factor in the development of skin cancer.5
Health campaigns recommend a few short sun exposures in a week to keep a sufficient vitamin D level, but the UVB exposure frequency necessary for maintaining summer 25-hydroxyvitamin D3 [25(OH)D] levels during winter is unknown.
Discussion
A full body exposure to 1 SED (~10 min of sun exposure at zenith in summertime in Denmark at 56°N) every second week is sufficient to maintain summer vitamin D levels. However, our UVB cabin irradiates full body area simultaneously, whereas people lying in the sun are irradiated only from above lying supine or prone; therefore, vitamin D production would take longer in sunlight. Health campaigns recommend a few short sun exposures (5-15 min) a week to guarantee a sufficient vitamin D level. It has been shown that significant vitamin D can be produced by a few minutes of sun exposure in the summer on ~25% body area.10 Our data show that a very small amount of UVB is sufficient to maintain summer vitamin D levels. We found a significant increase in 25(OH)D after weekly UVB exposure, but the 25(OH)D increase was reduced steadily during the course, suggesting a state of saturation in vitamin D production. In a recent study, saturation in vitamin D production was found for the higher UVB doses and body areas.10 This has also been reported in other studies.13,14 Our results were consistent with a linear model, which gave a strong correlation (r2 = 0·763) and may be due to relatively long intervals between every UVB exposure and the small UVB dose of 1 SED. However, the 25(OH)D increase might have reached a plateau for group 1 if the UVB exposures had continued. The fact that we found no significant increase in 25(OH)D for group 1 after the last UVB exposure supports this theory. The change in 25(OH)D levels during the 16 weeks and the increase in 25(OH)D after the last UVB exposure were significantly negatively correlated with baseline 25(OH)D levels. This finding is consistent with previous studies.11,15 The mechanisms are unknown, but 25(OH)D may act as a negative feedback to 25-hydroxylase in the liver, which prompts the hydroxylation of vitamin D3 to 25(OH)D. In conclusion, a suberythemal UVB dose of 1 SED every second week to ~88% body area is sufficient for maintaining summer 25(OH)D levels during winter.
What's already known about this topic?
· · Previous studies have shown that vitamin D insufficiency is common, especially during winter.
· · However, relatively few studies exist on the photobiology of vitamin D, and the exposure frequency for maintenance of summer vitamin D status during winter remains to be clarified.
What does this study add?
· · This study clarifies the frequency of ultraviolet (UV) B exposure necessary to maintain summer vitamin D levels during winter: a small UVB dose of 1 standard erythema dose every second week maintains summer vitamin D levels during winter.
Materials and methods
Design
A randomized, controlled trial was conducted from October 2008 to February 2009. The ethics committee approved the protocol (H-C-2008-072), which was carried out in accordance with the Declaration of Helsinki. ClinicalTrials.gov identifier: NCT01101243.
Participants
Of 60 participants included, 55 completed. Five were unable to comply with scheduled visits. Weight, height and body mass index (BMI) were recorded and total body area was calculated.6 Inclusion criteria were age 18-65 years; avoidance of sunbed exposure; travelling south of 45°N; and vitamin D supplementation. Exclusion criteria were pregnancy; skin or psychiatric disease; drug addiction; previous skin cancer; and intake of statins or photosensitive medicine.
Intervention
The participants were randomized to a UVB dose of one standard erythema dose (SED) to ~88% body surface area (full body except underwear)7 once a week (17 UVB exposures, group 1, n = 15), every second week (nine UVB exposures, group 2, n = 14) or every fourth week (five UVB exposures, group 3, n = 12). The controls (group 4, n = 14) had no interventions. One standard erythema dose is defined as 100 J m-2 at 298 nm using CIE (Commission Internationale de l'Eclairage) erythema action spectrum.8 The UVB source was a Waldmann UV-6 cabin (Waldmann, Villingen-Schwenningen, Germany) (Fig. 1). Pigment protection factor (range 1·0-24·0) was measured on back and buttocks at baseline and 2 days after last UVB exposure by remittance spectroscopy (Chromo-Light, Espergarde, Denmark).9 This method has been described previously.10 Blood samples were analysed for 25(OH)D at baseline and every month in all four groups. In the intervention groups (groups 1-3), the 25(OH)D was analysed a few minutes before irradiation and approximately 48 h after last UVB exposure. Parathyroid hormone, total calcium, total cholesterol and alkaline phosphatase were assessed at baseline. The analyses have been described previously.11 Skin type according to Fitzpatrick was registered.12
Randomization, sample size and statistics
We used a computer-generated randomization list for sealed envelopes containing notes distributing the participants into four groups. Given a significance level of 5% and an assumed SD of 9 nmol L-1 for 25(OH)D analysis at 50 nmol L-1, the study was designed to show a difference of at least 12 nmol L-1 between the groups with a power of 80% if a minimum of nine subjects per group completed.
SPSS 18.0 was used (SPSS Inc., Chicago, IL, U.S.A.). The correlations between the development in 25(OH)D level after UVB during the 16 weeks and the personal and biochemical baseline data were examined using analysis of variance. For all significant analyses (P < 0·05), linear regressions were performed.
Results
Baseline data
Baseline data are shown in Table 1. At baseline, 34 (62%) were vitamin D sufficient [25(OH)D > 50 nmol L-1] and 21 (38%) were vitamin D insufficient [25(OH)D < 50 nmol L-1]. The baseline 25(OH)D (mean) was 66·6 nmol L-1. There were no significant differences in age, skin type or baseline 25(OH)D level between the groups.
Development of 25-hydroxyvitamin D3 levels during the 16 weeks
The 25(OH)D (mean) after UVB exposure once a week, measured a few minutes before irradiation and approximately 48 h after last UVB exposure, increased significantly from 71·9 to 84·5 nmol L-1 (P < 0·0001), whereas UVB exposure every second week maintained 25(OH)D with no significant change during the 16 weeks (P = 0·16). The mean 25(OH)D after UVB exposure every fourth week decreased significantly from 56·4 to 47·8 nmol L-1 (P < 0·0001). The mean 25(OH)D for the control group decreased significantly from 64·8 to 40·1 nmol L-1 (P < 0·0001) (Table 2, Fig. 2a). The groups were analysed together in one combined linear regression model which includes different slopes for each group (r2 = 0·763). Figure 2a is based on true data for each participant and Figure 2b shows the change in 25(OH)D (mean) during the 16 weeks adjusted for baseline 25(OH)D (mean 66·6 nmol L-1). The changes in 25(OH)D during the 16 weeks were negatively correlated with baseline 25(OH)D (P < 0·0001; r2 = 0·763) and age (P < 0·0001) in all groups. A significant positive relation was found between the change in 25(OH)D during the 16 weeks and weight (P = 0·02), BMI (P = 0·04), total body area (P = 0·02) and serum alkaline phosphatase (P = 0·002).
Analyses of the increase in 25-hydroxyvitamin D3 after the last ultraviolet B exposure
We found a significant negative correlation between the 25(OH)D level before the last UVB exposure and the increase in 25(OH)D measured approximately 48 h after the UVB treatment (P = 0·001; r2 = 0·252). We found no significant increase in 25(OH)D for group 1 (P = 0·6). However, 25(OH)D increased significantly for group 2 (P = 0·03) and group 3 (P = 0·017), by 4·4 and 6·9 nmol L-1, respectively.
| |
| |
| |
|
|
|
