Ways you can increase vitamin D levels, even if you have cancer

The following includes some of the analysis by Dr. Cannell at the Vitamin D Council

The enzyme that activates vitamin D is 1-hydroxyase

The enzyme that deactivates vitamin D is 24-hydroxylase

Colon Cancer decreases Vitamin D

Destroys 1-hydroxylase which is bad
Increases 24-hydroxylase which is bad

Low levels of Calcium also decreases vitamin D by

Increasing 24-hydroxylase which is bad

Thus, as of May 2012, it appears the ways to increase vitamin D include:

Take more vitamin D and/or have more time in the sun without sunscreen
- Note: If your gut is functioning poorly, there is a form of vitamin D supplement for you
Add Estrogen which facilities 1-hydroxyase (however, adding Estrogen seems to cause problems)
Add folate and soy to reduce 24-hydroxylase which is good
Increase bioavailability of vitamin D supplements
- Increase monosaturated fats (such as almonds)
- Vitamin K2 increases D
- Increase Magnesium intake
- Decrease fast foods (many of which reduce Magnesium intake)
- Boron
Have some, but not too much
- Vitamin A
- Calcium
Do not smoke
Do not have soft drinks – which reduce Calcium, which reduced Vitamin D
Reduce taking drugs, such as statins, which reduce/consume vitamin D (which may not be possible)
- It may help to not take those drugs at the same time as vitamin D

Chemotherapy warning: CLICK HERE for more information

Beware of increasing your vitamin D if you are unable to decrease the amount of some kinds of Chemotherapy

Vitamin D increases the effectiveness of many chemotherapies

Which is good, as you may only need 1/2 as much chemotherapy drug to kill the cancer while doing less damage to the rest of the body
Which is bad if you cannot change the type or decrease the amount chemotherapy,
- Vitamin D increases the effectiveness of some chemo so much as to become fatal.

Dr. Cannell’s description of the enzyme paper is behind a $5 paywall

Can vitamin D be increased inside a cell? May 2012

His description of enzymes is in part based on the following paper

Colonic vitamin D metabolism: implications for the pathogenesis of inflammatory bowel disease and colorectal cancer.

Mol Cell Endocrinol. 2011 Dec 5;347(1-2):70-9. Epub 2011 Jul 27.

Cross HS heide.cross@meduniwien.ac.at, Nittke T, Kallay E.

Department of Pathophysiology, Medical University of Vienna, Austria.

In epidemiological studies serum levels below 30 nM of 25-OHD(3), the precursor of the active vitamin D metabolite 1,25-(OH)(2)D(3), were consistently associated with incidence of colorectal cancer. The active vitamin D metabolite possesses antimitotic, prodifferentiating and proapoptotic capacity in vivo and in vitro. The intestinal autocrine/paracrine vitamin D system, which is the main source of local 1,25-(OH)(2)D(3) plays a critical role in maintaining both mucosal immunity and normal growth of epithelial cells. It has been hypothesized that the VDR-mediated signaling antagonizing TNF-? and IL-6 receptor-activated pro-inflammatory and proliferative intracellular pathways, may prevent development of IBD and colitis-associated colorectal cancer. Conversely, any situation that impairs the efficiency of the 1,25-(OH)(2)D(3)/VDR signaling system at the level of the gut mucosa, e.g. vitamin D insufficiency, may increase risk for the development of IBD and colorectal cancer. Therefore, not only adequate serum levels of the precursor 25-OHD(3) are essential, but also optimal expression of the 1?-hydroxylating enzyme CYP27B1. The 1,25-(OH)(2)D(3) catabolizing hydroxylase CYP24A1 is increasingly expressed during colon cancer progression, indicating that colonocytes are released from normal growth control by the steroid hormone. Securing adequate levels of calcitriol by inhibition of catabolism and support of 1?-hydroxylation by calcium, phytoestrogens and folate could be a valid approach to control, at least in part, IBD and CRC pathogenesis.

PMID: 21801808