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Vitamin D

Vitamin D

ABSTRACT: Integrative Oncology is the synthesis of mainstream care and nonpharmacologic, evidence-based complementary therapies for the control of cancer-related physical and emotional symptoms. This month, we consider supplementation with vitamin D, which has been examined as a preventive agent and as a treatment for cancer.


ALSO KNOWN AS: Calciferol, ergocalciferol, calcitriol, cholecalciferol

USES: To treat psoriasis, scleroderma, seasonal affective disorder, and to prevent osteoporosis and cancer

BACKGROUND: Vitamin D is a fat-soluble substance found in dairy products, fish, and mushrooms. Sunlight, the major source of vitamin D for humans, promotes the endogenous synthesis of its active form. Multivitamins and supplements with various amounts of vitamin D are commercially available. The two forms used in humans are ergocalciferol (D2) and cholecalciferol (D3)—they are bioequivalent, but D3 may be preferable because it has a longer half-life.

RESEARCH: Vitamin D was shown to improve bone density and prevent fractures,[1] but such benefits were not observed in the Women’s Health Initiative (WHI) study,[2] perhaps due to the use of inadequate doses. Vitamin D effectively treats psoriasis.[3] Its ability to improve seasonal affective disorder is unclear.[4] It has also been examined as a preventive agent and as a treatment for cancer. Observational, prospective, and retrospective studies suggest that it decreases the risk of developing cancer.[5] A recent double-blind, randomized controlled trial found that supplementation with vitamin D plus calcium significantly reduced cancer incidence.[6]

Conversely, a recent large prospective study showed that, with the exception of colorectal cancer, vitamin D did not protect against cancer,[7] and a study of Finnish smokers showed that subjects with higher 25(OH)D levels were at greater risk for pancreatic cancer compared with those with lower concentrations.[8] Controlled clinical trials studying vitamin D supplementation are required to determine optimal levels for cancer prevention.

ADVERSE REACTIONS: High doses of vitamin D can cause hypercalcemia.[9] Toxicity associated with elevated serum levels of vitamin D includes depression, headache, drowsiness, weakness, calcium and bone loss, and metastatic calcification of soft tissues in the kidney, heart, blood vessels, and lungs.[10]

 DR. CASSILETH: The recommendation to minimize sun exposure to prevent skin cancer has produced a pandemic of vitamin D deficiency. Vitamin D has generated considerable interest in the past decade, as accumulating evidence from both retrospective and prospective epidemiologic studies suggests an association between vitamin D deficiency and increased risk of autoimmune, infectious, and cardiovascular diseases, as well as cancer. Vitamin D supplementation assists repletion in deficient individuals. Major medical centers typically recommend 1,000 IU/d for an average adult.

Vitamin D maintains serum calcium and phosphorus levels by regulating their absorption and excretion. It is also important for bone formation, as deficiency can cause rickets and other bone disorders, is a potent antiproliferative agent, and a pro-differentiation hormone.

Currently, the level of the major circulating form of vitamin D, 25-hydroxyvitamin D—resulting from vitamin D metabolism in the liver—is used to measure vitamin D status. Optimal concentration, including that for cancer prevention, is not yet known. Vitamin D lowers the incidence of colorectal cancer but not that of other cancers. This plus the Finnish pancreatic cancer study suggest that response to vitamin D may vary by tissue type. Additional research is needed to fully understand the mechanism of action and optimal dosing of vitamin D.


1. Rodriguez-Martinez MA, García-Cohen EC: Pharmacol Ther 93:37-49, 2002.
2. Jackson RD, LaCroix AZ, Gass M, et al: N Engl J Med 354:669-683, 2006.
3. Kragballe K: J Am Acad Dermatol 27:1001-1008, 1992.
4. Gloth FM 3rd, Alam W, Hollis B: J Nutr Health Aging 3:5-7, 1999.
5. Garland CF, Garland FC, Gorham ED, et al: Am J Public Health 96:9-18, 2006.
6. Lappe JM, Travers-Gustafson D, Davies KM, et al: Am J Clin Nutr 85:1586-1591, 2007.
7. Freedman MD, Looker AC, Chang SC, et al: J Natl Cancer Inst 99:1594-1602, 2007.
8. Stolzenberg-Solomon RZ, Vieth R, Azad A, et al: Cancer Res 66:10213-10219, 2006.
9. Koeffler HP, Hirji K, Itri L: Cancer Treat Rep 69:1399-1407, 1985.
10. Pronsky ZM: Power’s and Moore’s Food-Medication Interactions, 11th ed. Pottstown, Pa; Food Medication Interactions; 2000.
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