Wrong about Vitamin D….?
Jacob Schor ND, FABNO
April 22, 2010
It looks we were wrong again. It’s not like we haven’t made similar mistakes in the past either. In our eagerness to simplify the world and reach quick and easy fixes, we jump to explanations that later come out to be false. We may have done this with vitamin D.
But vitamin D is certainly not the first example of hitching the cart to the wrong horse. The classic of course is ascorbic acid, the anti-scorbutic vitamin, what we call vitamin C. Ever since the Nobel Prize was awarded to Szent-Györgyi there have been recurring concerns that lime juice and other older treatments were more effective at treating scurvy than the new vitamin. Biology tends to be more complex than we would want it to be.
Then there was the whole betra-carotene fiasco. Eating lots of fruits and vegetables lowers the risk of lung cancer and these foods contain beta-carotene. Researchers, scientists and even naturopathic physicians were eager to believe that beta-carotene supplements would work as well. In the now infamous clinical trial, smokers who took daily betacarotene pills actually increased their risk of getting lung cancer. Now it appears we may be heading for a similar, though not quite so consequential, lesson with vitamin D.
We’ve long known that something about sunlight exposure decreases risk of getting multiple sclerosis (MS). The closer to the equator one lives, the lower the risk of getting MS. For example MS incidence is 5 cases per 100,000 people in Nigeria, 15 per 100,000 in Tunisia and 100 per 100,000 in Sweden.
The hypothesis that has become widely accepted over the last few years that MS and other diseases that share a similar latitudinal distribution, are related to vitamin D levels. The closer to the equator one lives, the more sunlight and ultraviolet light one is exposed to and correlated with this, the more vitamin D one makes and stores in the body. This makes so much sense that the lack of a direct cause-and-effect relationship study hasn’t bothered us overly much. A recent series of experiments performed by Hector DeLuca at the University of Wisconsin-Madison suggests we may have been too hasty.
Using mice in an experiment in which the MS like myelin damage was artificially triggered, the researchers exposed some of the animals to ultraviolet light (UV). The UV exposure as expected suppressed the MS-like disease even though the exposure was minimal, barely enough to change the animals’ vitamin D levels.
In another similar test, the scientists gave the mice varying doses of vitamin D but omitted the UV light exposure. The vitamin D failed to control the disease.
“We conclude that UV light is doing something beyond” making vitamin D was the conclusion reached by the team of scientists.
What else could be going on? Several years ago while reading the literature about tanning and sunscreen, we noticed an obscure paper that suggested the very first step in making melanin was an upregulation of the gene that makes the enzyme p53. Thus as the very first start of a tan, the body experiences a surge of p53 enzyme. This of course is the enzyme that communicates the level of internal damage within the cell and can trigger apoptosis, self-destruction, of the cell. Could this be the missing piece of the puzzle?
Even if it turns out that vitamin D alone isn’t as protective against MS as we had hoped, this does not mean it is without benefit against other diseases that are currently thought to be correlated with low vitamin D levels, disease such as cancer, heart disease and diabetes. Still, this information begs us to consider these assumptions more closely.
While we wait for the scientists to reach a consensus, it won’t hurt us to get a little extra sun this summer, work on our tans when we get the chance. Burning is bad for you, but a tan, well, it may be what the doctor ordered.
New Scientist April 24, 2010. “Sunlight may cut MS risk by itself: study complicates theories about the role of vitamin D. Nathan Seppa
Proc Natl Acad Sci U S A. 2010 Apr 6;107(14):6418-23.
UV radiation suppresses experimental autoimmune encephalomyelitis independent of vitamin D production.
Becklund BR, Severson KS, Vang SV, DeLuca HF.
Department of Biochemistry, University of Wisconsin, Madison, WI 53706, USA.
Although the exact cause of multiple sclerosis (MS) is unknown, a number of genetic and environmental factors are thought to influence MS susceptibility. One potential environmental factor is sunlight and the subsequent production of vitamin D. A number of studies have correlated decreased exposure to UV radiation (UVR) and low serum 25-hydroxyvitamin D(3) [25(OH)D(3)] levels with an increased risk for developing MS. Furthermore, both UVR and the active form of vitamin D, 1alpha,25-dihydroxyvitamin D(3), suppress disease in the experimental autoimmune encephalomyelitis (EAE) animal model of MS. These observations led to the hypothesis that UVR likely suppresses disease through the increased production of vitamin D. However, UVR can suppress the immune system independent of vitamin D. Therefore, it is unclear whether UVR, vitamin D, or both are necessary for the putative decrease in MS susceptibility. We have probed the ability of UVR to suppress disease in the EAE model of MS and assessed the effect of UVR on serum 25(OH)D(3) and calcium levels. Our results indicate that continuous treatment with UVR dramatically suppresses clinical signs of EAE. Interestingly, disease suppression occurs with only a modest, transient increase in serum 25(OH)D(3) levels. Further analysis demonstrated that the levels of 25(OH)D(3) obtained upon UVR treatment were insufficient to suppress EAE independent of UVR treatment. These results suggest that UVR is likely suppressing disease independent of vitamin D production, and that vitamin D supplementation alone may not replace the ability of sunlight to reduce MS susceptibility.
PMID: 20308557 [PubMed - in process]