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Vitamin D and Cancer

Vitamin D and Cancer

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Published by: Dancebp4 on Oct 14, 2009
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05/17/2012

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Rebecca Willis4/1/09
Vitamin D and Cancer 
Introduction:
Vitamin D, or 1,25(OH)
2
D
3,
while initially labeled as a vitamin, is in fact a steroid "synthesized in the body as a result of ultraviolet radiation (UVR) exposure."(2) While vitamin D can be found in the diet, itscontribution is almost negligible. (2) The article "Vitamin D" stated that vitamin D is "essential for normalskeletal development and maintenance of calcium homeostasis."(2) It is also needful for proper musclefunction.(2) In addition, as asserted in Francis P. Boscoe's article, many studies have shown that vitamin D "has benefits against a variety of cancer types,"(1) even skin cancer.(2) In the article, "In Vivo," Dixon concededthat UVR exposure may result in skin carcinogenesis, however his studies have shown that vitamin D "reducedthe level of UVR-induced cell death in human skin cells" and reduces damage in surviving cells by a raidresponse pathway. (3) Its presence in irradiated skin decreased cyclobutane pyrimidine dimers (CPD) andimmunosuppression, which contributes to skin cancer development, and vitamin D decreased cell death of sunburned cells.(3)
 Objectives:
To prove that vitamin D was "inversely correlated with cancer mortality and survival" in manyinternal cancer sites and to prove it has potential for therapeutic use in the prevention of skin cancer. (1,2,3)Further, the objective was to prove that "where you live determines your sun exposure."(1)
Materials and Methods:
Boscoe and Schymura used "cancer incidence and mortality data... from 3,108 counties" in theUnited States totaling nearly 7 million cases and deaths. (1) The data was acquired from the North AmericanAssociation of Central Cancer Registries. White non-Hispanics were the group in study while the black  population was used as the comparison group because they are much less able to absorb vitamin D from thesun. Age groups were divided up by tens and ranged from 35 to 85+. The data was further analyzed on the basis of gender. The study was even more thorough by collecting solar UV-B exposure data taken of different areas of the United States by NASA's Total Ozone Mapping Spectrometer (TOMS). (1) Dixonirradiated 69 human neonatal foreskins (in vitro) which were pretreated with vitamin D analogs, and albino,hairless mice (in vivo) which were given several different treatments immediately following irradiation. (3)The treatments included: vehicle, 1,25(OH)
2
D
3,
and low calcemic, rapid-acting analog JN. Skin samplesfrom the mice and the human samples were analyzed for sunburn, CPD, and immunosuppression. (3)
Results:
Boscoe and Schymura found that sun exposure was inversely related to cancer sites: "bladder,colon, Hodgkin Lymphoma, myeloma, other biliary, prostate, rectum, stomach, uterus, and vulva, maleesophagus, female gallbladder" and less so in "female breast, kidney, leukemia, non-Hodgkin lymphoma, pancreas, small intestine, female esophagus and thyroid, and male gallbladder."(1) The particular county inthe US had considerable effect on UV-B rays in relation to cancer incidences or lack thereof. Dixon'sresults were "based on quadruplicates of each treatment from experiments performed at least twice withsimilar results."(3) Dixon found that those samples treated with 1,25(OH)
2
D
3
or JN had "reduced cellloss...to 15.4%" after irradiation that those treated with vehicle which had 37% cell loss. Sunburned cellswere reduced significantly when treated with 1,25(OH)
2
D
3
or JN. Finally, "1,25(OH)
2
D
3
and JNsignificantly reduced levels of UVR-induced immunosuppression in mice."(3) All were decreased by atleast 50% with the application of 1,25(OH)
2
D
3
or JN.(3) Thus, vitamin D had inhibitory effects on skinand several internal cancers.
Summery and Discussion:
Boscoe and Schymura's study discussed the effect of sun exposure as it relates to vitamin Dsynthesis and cancer prevention. They found that in most cancer sites studied, sun exposure was negativelycorrelated with incidences of cancer. In Dixon's study, the consistent decrease in carcinogenic effectors proved the photoprotective effect of 1,25(OH)
2
D
3
, by the rapid pathway.(3) That conclusion was drawn because JN had similar photoprotective effects as 1,25(OH)
2
D
3
while conformationally limited to the rapid pathway. Finally, because repair of CPD damage reduces skin cell apoptosis and prevents UVR-inducedmutation and immunosuppression and because vitamin D provided said photoprotective effect, it wasconcluded that vitamin D is protective against skin cancer by at least 50%.

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