Blood test results this week came back showing Vitamin D levels seriously below normal limits, and Plasma Viscosity risen from two weeks ago. So I decided to research more about low Vit D as this is the first time it's been evident.
I'd be interested to hear comments from readers as to whether they have found any benefit from using A Light Box to counteract the deficiency? lumie.com for more information
Also, this paper below might be useful to you:
Evidence that abnormally large seasonal declines in vitamin D status may trigger SLE flare in non-African Americans
Cross-sectional studies have shown that low vitamin D (25-hydroxyvitamin D (25(OH)D)) is associated with increased systemic lupus erythematosus (SLE) activity. This study is the first to assess the temporal relationship between 25(OH)D levels and onset of SLE flare. This assessment was made possible because of the specimen bank and database of the Ohio SLE Study (OSS), a longitudinal study of frequently relapsing SLE that involved regular bimonthly patient follow-up. We identified for this study 82 flares from 46 patients that were separated by at least 8 months from previous flares. Serum 25(OH)D levels were measured at 4 and 2 months before flare, and at the time of flare (a flare interval). We found that for flares occurring during low daylight months (LDM, Oct-Mar), 25(OH)D levels were decreased at the time of flare, but only in non-African American (non-AA) patients (32% decrease at flare, compared to 4 months prior, p?<?0.001). To control for seasonal effects, we also measured 25(OH)D levels in the LDM “no-flare” intervals, which were intervals that matched to the same calendar months of the patients’ LDM flare intervals, but that didn’t end in flare (n?=?24). For these matches, a significant decrease occurred in 25(OH)D levels during the flare intervals (18.1% decrease, p?<?0.001), but not during the matching no-flare intervals (6.2% decrease, p?=?0.411). For flares occurring during high daylight months (HDM), 25(OH)D levels changed only in non-AA patients, increasing slightly (5.6%, p?=?0.010). Analysis of flare rates for the entire OSS cohort (n?=?201 flares) revealed a tendency for higher flare rates during LDM compared to HDM, but again only in non-AA patients (p?=?0.060). Flare rates were lower during HDM for non-AA patients compared to AA patients (p?=?0.028). In conclusion, in non-AA SLE patients, unusually large declines in 25(OH)D during LDM may be mechanistically related to SLE flare, whereas relatively high 25(OH)D levels during HDM may protect against flare.