Last year, I wrote about a mouse study that suggested UVB exposure suppressed a model of multiple sclerosis (MS) independent of vitamin D production. So I was excited to see media reports this week covering another study, this one epidemiological in nature, that supports this hypothesis.
The study by Lucas and colleagues analyzed data from The Ausimmune Study, of 282 patients who have had a first diagnosis of CNS demyelination (FCD) and of these, 216 had a first demyelinating event (FDE) (note this is not established multiple sclerosis. They chose these as MS patients would have altered more of their sun exposure behaviors). This is what they wanted to examine- if FDE incidence has any correlation with recent/past sun exposure. (note: 18 of the 282 were diagnosed with primary progressive MS, and 42 had an undiagnosed, possible historic event. For explanations of each diagnosis please google.) The subjects were from 4 regions of differing lattitude in Australia. Control subjects (395) were matched to the FDE subjects on age, sex, and region.
They estimated sun exposure with a questionnaire, which seems unreliable but has been verified in other research. The subjects estimated time in the sun from age 6 during weekends and holidays and in summer and winter, as well as reporting location of residence, and what their occupation was (or if schooling). This was validated as it correlated with a actinic skin damage score. Other data reported included: propensity to tan or burn, freckles as a teen, smoking history, education level, physical activity, a food frequency questionnaire, and use of vitamin D supplements.
Vitamin D (25OHD) concentration was taken and subjects were genotyped for SNPs that alter vitamin D binding proteins relevant to D concentration.
They found that: higher time in the sun (as reported on the questionnaire) in the 3 years prior to the interview AND higher leisure UV exposure from age 6 (also from questionnaire) correlated with a reduced FDE risk. This stayed true after adjustment for sun protection usage. Also, a higher actinic skin damage score was also correlated with a lower FDE risk.
They also found that FDE cases has lower 25OHD concentrations than controls and as those concentrations increased, FDE risk decreased. This held true after adjustment for melanin density, phenotypic variables, or the relevant SNPs that were genotyped. It is notable that no threshold effect was found (other vitamin D areas, especially the bone density studies suggest a threshold effect).
Importantly, mathematical modeling showed that both 25OHD concentrations (per 10 nmol/L) AND recent and lifetime UV exposure were independently associated with a reduced FDE risk. The researchers also verified that this was true in the full FCD sample (282 subjects) because the undiagnosed events in some of the subjects are not as likely to influence sun exposure behavior as they state.
As the latitude of the location differed in FDE incidence by 4-fold, their models showed that 25OHD, lifetime UV exposure, and melanin density separately or together accounted for 32.4% of difference in the FDE incidence.
In the discussion, the authors note previous research finding UV and vitamin D can “independently stimulate T-regulatory cells and secretion of IL-10, reduced levels of the proinflammatory cytokine IL-17, and dampen T-helper (Th)-1 immune function,” so there are logical mechanisms as to why these findings (and the animal study) may be true.
Reference
Lucas RM, Ponsonby AL, Dear K, Valery PC, Pender MP, Taylor BV, Kilpatrick TJ, Dwyer T, Coulthard A, Chapman C, van der Mei I, Williams D, & McMichael AJ (2011). Sun exposure and vitamin D are independent risk factors for CNS demyelination. Neurology, 76 (6), 540-8 PMID: 21300969
