More Research on Multiple Sclerosis (MS): Highest Sunlight Exposure as a Teenager predicts later Age of Onset of MS.
By Marc Sorenson, EdD, Sunlight Institute
Although several of my posts on the Sunlight Institute have discussed sunlight and MS, this post will provide the results of the most recent paper that I am aware of, and it reviews some of the most important investigations showing that sunlight exposure is absolutely essential for preventing or mitigating the disease.
MS is a disease in which the myelin sheaths (nerve coverings and insulators) are destroyed, leaving nerves bare and susceptible to “short circuiting.” This process is known as demyelination. New research, which should surprise no one, demonstrates that teenagers who have the greatest exposure to sunlight have a delayed onset of MS as adults. The study involved 1,161 Danish patients with MS who were given questionnaires regarding their sun-exposure habits and body-mass index (BMI) as teenagers. BMI is a measure of obesity (or the lack thereof). Besides sunlight, other vitamin-D predicting measures were also used to determine the probable cause of MS.
Interestingly, only sunlight exposure and lower BMI were associated with later age at the onset of the disease; other serum vitamin D predictors such as fish consumption did not show any association with MS. The authors still seemed to feel that vitamin D was the reason for the extended time before disease onset; however, that is unlikely, since other predictors of higher vitamin D levels showed no association. And, it has been shown that sunlight exposure has profoundly protective effects against MS, independently of vitamin D. Researchers determined to find the mechanism by which sunlight exposure suppressed the disease and found that UV light selectively inhibits spinal cord inflammation and demyelination. In that study, they performed an investigation in which ultraviolet radiation (UVR)—the same radiation that is found in sunlight and tanning beds—was administered to animals who suffered from experimental autoimmune encephalomyelitis (EAE). EAE is MS that has been deliberately induced in animals in a laboratory setting. The researchers found that the UVR treatments stopped inflammation and demyelination of the spinal cord by inhibiting a chemical known as a chemokine, also known as a cytokine. Chemokines are the cause of the inflammation and autoimmune attacks that result in MS. The MS-ameliorating effects in the study were directly initiated by UVR, independent of vitamin D.
Stunningly, another study by some of these same investigators determined that vitamin D was actually necessary for EAE to take place! Mice that lacked the vitamin D receptor, which causes vitamin D deficiency, had a markedly lower risk of developing EAE. In those mice that had receptors but were simply vitamin D deficient, the development of EAE was also partially suppressed. I do not look on this research as proving that vitamin D sufficiency leads to MS, but it certainly indicates that sunlight exposure, independent of vitamin D, is absolutely critical to prevent and ameliorate this frightening disease.
The bottom line? Be sure to get plenty of non-burning sun exposure!
 Julie Hejgaard Laursen, MD, PhD, Helle Bach Søndergaard, MSc, PhD, Per Soelberg Sørensen, MD, DMSc, Finn Sellebjerg, MD, PhD and Annette Bang Oturai, MD, PhD. Association between age at onset of multiple sclerosis and vitamin D level–related factors. Neurology 2015, Published online before print October 7, 2015.
 Becklund BR, Severson KS, Vang SV, DeLuca HF. UV radiation suppresses experimental autoimmune encephalomyelitis independent of vitamin D production. Proc Natl Acad Sci U S A. 2010;107:6418-23.
 Wang Y, Marling SJ, Beaver EF, Severson KS, Deluca HF. UV light selectively inhibits spinal cord inflammation and demyelination in experimental autoimmune encephalomyelitis. Arch Biochem Biophys. 2015 Feb 1;567:75-82.
 Wang Y, Marling SJ, Zhu JG, Severson KS, DeLuca HF. Development of experimental autoimmune encephalomyelitis (EAE) in mice requires vitamin D and the vitamin D receptor. Proc Natl Acad Sci U S A. 2012 May 29;109(22):8501-4.