Hi, in cancer there is hypercalemia, calcium metabolism affected by vitamin D levels. Thus they are related.

Vitamin D has a definite role in sequential differentiation and orderly progression of keratinocytes from the basal layer of the epidermis. Also, a variety of malignant cells express vitamin D receptors (VDR). Vitamin D has been shown to have an anti-proliferative and pro-differentiating effect on many cell types. This is possibly modulated through stimulation of cell cycle inhibitors p21 and p27, this in turn affects E-cadherin and beta-catenin.

There was an interesting article on the role of vitamin D in colorectal carcinoma in the NEJM in 2006. I am sure that article would be informative.

thanks Vasant Chinnabhandar it was very helpful information i will share it with my colleges specially the article by Jean Watchweski and thank you Nandini you are the first one answering my question

take a look a the presentations on www.vitamind3world.com and www.vitaminDcouncil.com

Vitamin D, or more correctly the active 1,25 dihydroxy vitamin D3 inhibits proliferation and enhances differentiation of colonic epithelial cells. These cells express the 1alpha hydroxylase, the enzyme that converts the precursor, 25-D3 into the active form, therefore in colon cancer, serum 25D3 levels are relevant for the preventive effect. Additionally to the mechanisms described by Vasant Chinnabhandar, vitamin D can also inhibit the Wnt pathway and prostaglandine E2 signalling (COX2). It has not only anti-proliferative but also anti-inflammatory effects. There are several very good reviews on the role of vitamin D in colorectal carcinogenesis.

Case-Control Studies or Cohort Studies would be approaches for this, but the question can be addressed from several points of view, from medical statistics and epidemiology, to end results reporting, to lab techniques for measuring things, it can be more complex than imagined, and each approach may have its corresponding books and articles references

You could do a cross-sectional study, too (similar to a case-control): you take all the people who have colonoscopy during 1 year, and measure their vitamin D. You could assess an eventual gradient between vitamin d concentration and degree of differentiation of the tumour, eventually no cancer / premalignant (adenoma) / malignant (argument for causality). With the weaknesses of such a study (compared to a cohort one) - e.g. which was first, low vitamin d or cancer?

At least 57 studies have already been made for Vitamin D and Colon Cancer

You can see an overview of them and links to details at

is.gd/vitdcolon

Thanks dr. That was very helpfull

I wrote my thesis on vitamin D and CRC in the late 80's at St Marks and the Hammersmith in London, as has been pointed out above the hormone 1,25 OH2 D3 has powerfully effects on the colorectal cell cycle and apopotosis. here are some of my/our references which also go through some of the evedence

Vitamin D and its metabolites inhibit cell proliferation in human rectal mucosa and a colon cancer cell line MG Thomas, S Tebbutt & RCN Williamson Gut 1992; 33:1660-1663

Oral calcium inhibits rectal epithelial proliferation in familial adenomatous polyposis MG Thomas, JPS Thomson & RCN Williamson Br J Surg 1993; 80:499-501 

  Divergent effects of epidermal growth factor and calcipotriol on human rectal cell proliferation. MG Thomas, GR Brown, MR Alison & RCN Williamson Gut 1994; 35:1742-1746

 The steroid vitamin D3 reduces cell proliferation in human duodenal epithelium. MG Thomas, RP Sturgess & M Lombard Clin Sci 1997; 92: 375-377.

 Vitamin D3 receptor expression in colorectal cancer M G Thomas, P A Sylvester, P Newcomb, R Longman. J.Clin Path 1999; 52: 181-183

Apoptosis is induced by the active metabolite of vitamin D3 and its anaologue EB1089 in colorectal adenoma and carcinoma cells. Possible implications for prevention and therapy. G D Diaz, C Parakeva, M G Thomas, L binderup, A Hague. Cancer Res 2000; 60: 2304-2312.

This a review, focused on CRC, perhaps it can be of help.

Ragrads. Salut +

Cancer Epidemiol Biomarkers Prev. 2011 May;20(5):1003-16. doi:

10.1158/1055-9965.EPI-10-1141. Epub 2011 Mar 4.

Meta-analyses of vitamin D intake, 25-hydroxyvitamin D status, vitamin D receptor

polymorphisms, and colorectal cancer risk.

Touvier M(1), Chan DS, Lau R, Aune D, Vieira R, Greenwood DC, Kampman E, Riboli

E, Hercberg S, Norat T.

Author information:

(1)Department of Epidemiology and Biostatistics, School of Public Health, Imperial

College London, London, UK. [email protected]

BACKGROUND: Our objective was to conduct a systematic review and meta-analysis of

prospective studies on colorectal cancer (CRC) and vitamin D intake and

25-hydroxyvitamin D status, as part of the World Cancer Research Fund Continuous

Update Project. We also aimed at conducting meta-analysis of all studies on CRC

and vitamin D receptor (VDR) single-nucleotide polymorphisms.

METHODS: Relevant studies were identified in PubMed (up to June 2010). Inclusion

criteria were original and peer-reviewed publications with a prospective design

(for studies on vitamin D intake or status). Random effects of dose-response

meta-analyses were performed on cancer incidence.

RESULTS: We observed inverse associations of CRC risk with dietary vitamin D

[summary relative risk (RR) per 100 IU/day = 0.95, 95% CI: 0.93-0.98; 10 studies;

range of intake (midpoints) = 39-719 IU/day] and serum/plasma 25-hydroxyvitamin D

(RR per 100 IU/L = 0.96, 0.94-0.97; 6 studies; range = 200-1,800 IU/L), but not

with total vitamin D (5 studies). Supplemental (2 studies; range = 0-600 IU/day)

and total (4 studies; range = 79-732 IU/day) vitamin D intake and

25-hydroxyvitamin D status (6 studies; range = 200-1,800 IU/L) were inversely

associated with colon cancer risk. We did not observe statistically significant

associations between FokI, PolyA, TaqI, Cdx2, and ApaI VDR polymorphisms and CRC

risk. The BsmI polymorphism was associated with a lower CRC risk (RR = 0.57,

0.36-0.89 for BB versus bb, 8 studies).

CONCLUSIONS: These meta-analyses support the evidence of an inverse association

between vitamin D intake, 25-hydroxyvitamin D status, and the BsmI VDR

polymorphism and CRC risk.

IMPACT: Improving vitamin D status could be potentially beneficial against CRC

incidence.

©2011 AACR.

PMID: 21378269 [PubMed - indexed for MEDLINE]