Dr Daniel Bikle of the San Francisco VA Medical Center and University of California at San Francisco recently reviewed the biochemical and physiological evidence that vitamin D may prevent skin cancer.
Dr. Bikle writes,
“The ability of the epidermis to make its own vitamin D and (activated vitamin D) is likely to be of great importance for epidermal physiology and pathology. It is not at all clear, for example, whether the oral administration of vitamin D, various analogs, and/or circulating levels of vitamin D has a major impact on processes within the skin—they may or they may not. Sun avoidance may reduce one’s risk of developing skin cancer, but this practice frequently results in suboptimal levels of vitamin D in the body, not to mention the epidermis. As pointed out in a recent analysis, the global disease burden due to UVR pales in comparison to the disease burden due to vitamin D deficiency, and although the latter can be prevented with vitamin D supplementation, the skin remains for most of the world’s population the major site of vitamin D availability.”
Dr. Bikle reported the following:
- Over one million skin cancers occur annually in the United States, 80% of which are basal cell carcinomas (BCC), 16% squamous cell carcinomas (SCC), and 4% melanomas, making skin cancer by far the most common cancer afflicting humankind.
- The idea that vitamin D protects against skin cancer took off when it was discovered that 85% of mice without vitamin D receptors developed skin tumors within two months following application of a topical carcinogen.
- The belief that vitamin D may prevent skin cancer focuses on the role of vitamin D signaling in skin development and growth. In particular, activated vitamin D suppresses two pathways that affect proliferation and differentiation. These are called hedgehog and wnt/β-catenin pathways.
- Vitamin D is also involved in signaling in the immune system of the skin. Activated vitamin D promotes innate immunity (ready to go at a moment’s notice) while suppressing adaptive immunity (antibody formation). Ultraviolet B irradiation – which makes you produce vitamin D – likewise promotes innate immunity and suppresses adaptive immunity. It is not clear how these effects, which can be profound, affect tumor formation.
- The third mechanism by which vitamin D may affect tumor growth is via DNA repair. The skin of mice with no vitamin D receptors show impaired DNA damage repair following ultraviolet irradiation. In addition, activated vitamin D accelerates DNA repair by increasing production of DNA repair enzymes.
Dr. Bikle summarizes, “Thus, by these mechanisms one can conclude that the skin has evolved protective mechanisms against UVR induced carcinogenesis, and that these mechanisms involve vitamin D.”
It is important to note that Dr. Bikle states that it is not at all clear that oral supplementation can produce the same beneficial effects in the skin as sunlight does. His warning is a good reason to get some safe sensible sun exposure this summer.
