New Roles of Vitamin D

Vitamin D is a fat-soluble vitamin commonly
associated with maintaining blood levels of calcium and the prevention of
rickets. The “sunshine vitamin” is generally acquired by the body in
two ways: sun exposure and dietary intake. Foods of animal origin are primary
food sources, including liver, beef, veal, eggs, vitamin D-fortified foods and
saltwater fish.1 Food sources contain relatively low levels of vitamin D.
Exposure to sunlight is our primary method of receiving vitamin D. People living
in areas with less sunlight due to geographic location, cloud cover and other
factors should consider vitamin D supplements. Those who receive enough sun
exposure for adequate vitamin D production must not receive overexposure, which
carries its own health risks.

New research suggests that vitamin D may play roles
in the prevention of infections, cancer and multiple sclerosis (MS). Several
epidemiological studies demonstrate a higher risk of several health ailments in
populations with reduced exposure from the sun.


Vitamin D
acts as an innate immune system modulator.5 The innate immune system is the
first line of defense against infection. Humans encounter potential
disease-causing agents called pathogens regularly, but seldom do they cause
disease. Most pathogens are destroyed by the innate immune system within minutes
or hours after contact as it provides broad-spectrum (non-specific),
short-lasting protection.6



The most important known role of vitamin D in
innate immunity involves its ability to stimulate the expression of
cathelicidin, an antimicrobial peptide produced in immune cells and the
epithelial cells lining the respiratory tract.7,8 Cathelicidin expression is
generally associated with inflammation.9,10 A study published in August 2006
demonstrated for the first time that vitamin D-induced cathelicidin expression
produced innate antimicrobial activity independent of the release of
pro-inflammatory molecules and did not result in inflammation.11


Vitamin D
supplementation is most needed in the fall and winter months when we get the
least sun exposure and when infections are most prevalent. Unfortunately,
sufficient human studies examining the correlation of vitamin D status and
infections have not been done. However, two papers published between 1949 and
1956 suggest that vitamin D may lessen the frequency and duration of the flu in
animal models.12,13 Recent attention to vitamin D should prompt further
investigation.



Good epidemiological evidence supports the
theory that living at latitudes closer to the equator decreases the risks of
many cancers such as prostate, colon, breast, endometrial, skin and
pancreatic.14 Observations over the last 65 years have shown an increased
association between sufficient sun exposure and cancer risks.15 In 1941,
researchers noticed that people living at latitudes farther from the equator had
an overall greater risk of dying from cancer than men and women of similar ages
living at lower latitudes. This observation began to gain more attention in the
1980s when it was reported that risks of colon and breast cancers increased in
higher-latitude populations.16



One study examining the amounts of vitamin
D-producing UV light in seven different areas of the U.S. showed a clear
difference during the winter months (November through February) based on
latitude. At higher latitude locations (>25 degrees N), vitamin D-producing
UV decreased dramatically compared to the eight warmer months. The lower
latitude locations (<25 degrees N) showed no difference between the winter
and warm months.17 A prospective study revealed that in populations with less
vitamin D being formed from UV exposure, low levels of vitamin D in the blood
increase the risk of cancer two-fold. Men and women with higher blood levels of
vitamin D are also less likely to die prematurely as a result of cancer.16


We do not
completely understand how vitamin D works as an anti-carcinogenic. Several
mechanisms are known, such as promoting programmed cell death in abnormal cells
(apoptosis), promoting cell differentiation, inhibition of cell proliferation in
malignant cell lines, inhibition of blood vessel growth, stimulating the mutual
adherence of cells, and enhancing cellular communication through gap
junctions.2,18 (Gap junctions are intercellular channels that allow for the
transfer of ions and other small molecules from cell to cell.) In the initial
stages of carcinogenesis, mutagenic changes may occur that result proliferation
of cells unable to communicate through gap junctions. Lack of mutual cell
adherence and communication through gap junctions inhibits apoptotic,
growth-suppressing and cell-differentiating signals from neighboring cells.19 A
recently published study of malignant breast epithelial cells in culture
demonstrated vitamin D’s promotion of apoptosis and differentiation, as
well as inhibition of proliferation.20 The effectiveness of vitamin D has been
found to be dose-dependant.2



Multiple sclerosis (MS) is an autoimmune
disease involving inflammation that leads to the destruction of the myelin
sheaths that surround and protect nerve fibers of the central nervous system
(CNS).19 This disease occurs most frequently in geographic areas farthest from
the equator, which suggests that vitamin D may protect against it.20-22 Very few
treatments or particular diets have been shown to effectively counter MS.
However, certain deficiencies in nutrients like vitamin D may potentially worsen
MS symptoms.23



Very little information is available regarding
the role of vitamin D in brain development. The white matter and branching cells
called oligodendrocytes in the brain have been shown to be responsive to vitamin
D and contain vitamin D receptors. It has been suggested that low levels of
vitamin D during the development of oligodendrocytes may cause unnecessary death
of these cells.20 Death of oligodendrocytes is devastating to the CNS, since
these cells are known to form myelin.



Although the relationship between the
increased frequencies of MS in populations most susceptible to vitamin D
deficiencies has been observed for more than 25 years, it has not yet been
thoroughly examined. A number of epidemiological studies have confirmed that
both exposure to sunlight during early life and vitamin D supplementation reduce
the prevalence of MS in women.20 Another study involving rats with experimental
autoimmune encephalomyelitis (EAE), which is the animal model of MS, used a
vitamin D treatment that reduced and even prevented the disease.21,22 In a
recent study, researchers looked at 12 years of blood samples from US Army and
Navy personnel and examined vitamin D levels and reported cases of MS in the
Army physical disability database. The results showed clearly a reduced risk of
MS in Caucasians with increasing blood levels of vitamin D. 24


More
well-designed clinical trials are needed in order to determine if vitamin D
deficiency increases risks of infections and if vitamin D supplements can be
cancer-and MS-preventive. Supplemental vitamin D may offer a cost-effective and
practical way to reduce the occurrence and symptoms of several diseases in the
future. Other new areas of vitamin D research include type I diabetes,
inflammatory bowel disease, rheumatoid arthritis, lupus and cardiovascular
disease.



References


1. Groff JL and Gropper SS. Advanced Nutrition
and Human Metabolism: 3rd Edition. Wadsworth ©

2000.
2.
PDR
for
Herbal Medicines 2nd Edition
2000 Medical
Economics Co. Inc.

3. Wang TT, Nestel FP,
Bourdeau V, Nagai Y, Wang Q, Liao J, Tavera-Mendoza L, Lin R, Hanrahan JW,

Mader S, and White JH. “Cutting edge:
1,25-dihydroxyvitamin D3 is a direct inducer of antimicrobial

peptide gene expression.” J Immunol.
2004 Nov 15;173(10)

4. Unknown Authors.
http://bioweb.wku.edu/courses/Biol328/Innate.htm. Access date December 4, 2006.

5. Lee PH, Ohtake T, Zaiou M, Murakami M,
Rudisill JA, Lin KH, and Gallo RL. “Expression of an

additional cathelicidin antimicrobial peptide
protects against bacterial skin infection” Immunology.

2005 Mar; 102(10):3750-3755.

6. Cannell JJ, Vieth R, Umhau JC, Holick MF,
Grant WB, Madronich S, Garland CF, and Giovannucci E.

“Epidemic influenza and vitamin
D.” Epidemiol Infect. 2006 Dec;134(6):1129-40.

7. Beisswenger C andBals R.
“Antimicrobial peptides in lung inflammation.” Antimicrobial
peptides in

lung inflammation. Chem Immunol
Allergy. 2005;86:55-71.

8. Wehkamp J, Schauber
J, Stange EF. “Microbial-epithelial cell crosstalk during inflammation:
the host

response.” Ann N Y Acad Sci.
2006 Aug;1072:313-20.

9. Schauber J, Dorschner
RA, Yamasaki K, Brouha B, Gallo RL. “Control of the innate epithelial

antimicrobial response is cell-type specific
and dependent on relevant microenvironmental stimuli.”

Immunology. 2006 Aug;118(4):509-19.

10. Young GA Jr, Underdahl NR, and Carpenter
LE. “Vitamin D intake and susceptibility of mice to

experimental swine influenza virus
infection.” Proc Soc Exp Biol Med. 1949 Dec;72(3):695-7.

11. Underdahl NR and Young GA. “Effect
of dietary intake of fat-soluble vitamins on intensity of

experimental swine influenza virus infection
in mice.” Virology. 1956 Jun;2(3):415-29.

12. Schwartz GG and Skinner HG. “Vitamin
D status and cancer: new insights.” Curr Opin Clin Nutr

Metab Care. 2007 Jan; 10(1):6-11.

13. Heany RP. “Long-latency deficiency
disease: insights from calcium and vitamin D.” Am J Clin Nutr.

2003; 78:912-9.

14. Holick MF. “Sunlight and vitamin D
for bone health and prevention of autoimmune diseases, cancers,

and cardiovascular disease.” Am J Clin
Nutr. 2004 Dec; 80(6):1678-88.

15. Kimlin MG,
Olds WJ, and Moore MR. “Location and vitamin D synthesis: Is the
hypothesis validated

by geophysical
data?” J Photochem Photobiol B. 2006 Dec 1 (Not printed yet)

16. Daniells S. “Low vitamin D status
may raise cancer risk, say scientists.”

www.nutraingredients.com/news/ng.asp?n=72441&m=1NIEN30&c=
wlpuaxndraentjv. Access date

November 30,
2006.

17. Unknown Author.
http://www.bioportfolio.com/LeadDiscovery/PubMed-020301.html. Adapted from

Upham et al, 2003 Int J Cancer 2003 Mar
10;104(1):12-18 Access date December 19, 2006.

18. Garland CF, Garland FC, Gorham ED, Lipkin
M, Newmark H, Mohr SB, and Holick MF. “The role of

vitamin D in cancer prevention.” Am J
Public Health. 2006 Feb; 96(2):252-61

19.
Unknown Author. http://ww2.wfaa.com/global/story.asp?s=1230548. Access date
December 28, 2006.

20. Chaudhuri A.
“Why we should offer vitamin D supplementation in pregnancy and childhood
to

prevent multiple sclerosis.” Med
Hypotheses. 2005; 64(3):608-18.

21. Van
Amerongen BM, Dijkstra CD, Lips P, and Polman CH. “Multiple sclerosis and
vitamin D: an

update.” Eur J Clin Nutr.
2004 Aug; 58(8):1095-109.

22. Hayes CE.
“Vitamin D: a natural inhibitor of multiple sclerosis.” Proc Nutr
Soc. 2000 Nov; 59(4):531-

5.

23. Schwartz S and Leweling H. “Multiple
sclerosis and nutrition.” Mult Scler. 2005 Feb; 11(1):24-32.

24. Munger KL, Levin LI, Hollis BW, Howard NS,
and Ascherio A. “Serum 25-hydroxyvitamin D levels

and risk of multiple sclerosis.” JAMA.
2006 Dec 20; 296(23):2832-8.


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