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Sunlight, and plenty of it, may be the best method for reducing the risk of melanoma. An impressive piece of research on melanoma and sunlight appeared recently in the European Journal of Cancer.[1] Dr. Julia Newton Bishop and colleagues (thirteen scientists in all) researched sunlight exposure habits and compared those habits to the risk of melanoma in an English population. Among other notable findings was a considerable reduction in melanoma risk among those who received the highest summer sunlight exposure on weekends. Compared to those with the least exposure to sunlight on weekends, those who received 4-5 hours of sunlight during the weekends had a reduced risk of melanoma of 28%, and those who received more than 5 hours had a reduced risk of melanoma of 33%.
In general, the English have very light complexions—complexions that are known to be more susceptible to melanoma, a fact that makes the research even more interesting. One can only conclude from this information that regular sunlight exposure protects against melanoma. In reality, this result should come as no surprise; at least 16 studies have shown indoor workers are much more likely to contract melanoma than outdoor workers.[2] Other research points out that melanomas occur much more frequently on areas of the body that receive little or no exposure to sunlight.[3]
Finally, it is quite obvious that outdoor living has decreased dramatically since 1935. Based on materials furnished by the Department of Labor Statistics, I calculated that sunlight exposure has decreased by at least 83%..[4] Yet, the Melanoma International Foundation has stated, “Melanoma is epidemic: rising faster than any other cancer and projected to affect one person in 50 by 2010, currently it affects 1 in 75 . In 1935, only one in 1500 was struck by the disease.” In other words, as sunlight exposure has dropped profoundly, melanoma risk has increased by 3,000%! Based on those facts, the idea—that sunlight exposure is the cause of melanoma—is counterintuitive at best, and ludicrous at worst.
It is likely that vitamin D production in the skin, in response to sunlight, is a major player in reducing the risk of melanoma. Enzymes in melanoma cells form active vitamin D[5], which in turn can lead to melanoma cell death,[6] and in lab experiments, active vitamin D can destroy melanoma cells.[7] In fact, vitamin D works in many ways to reduce cancer. Here are just a few:
1. Vitamin D promotes apoptosis (normal cell death) so that cancer cells die normally.[8]
2. Vitamin D inhibits proliferation (out-of-control growth) of cancer cells.[9]
3. Vitamin D inhibits angiogenesis in cancerous tissue. Angiogenesis is the formation of blood vessels. It is a process that provides blood and nutrients to newly formed tissue. If angiogenesis in cancer cells can be stopped, the cells die. Vitamin D acts a selective angiogenesis inhibitor—it retards the growth of new, undesirable “feeder” blood vessels into cancer cells.[10]
4. Vitamin D inhibits metastasis (the spreading of cancer cells from the initial location of the disease to another location).[11]
The key to safe sunlight exposure is to avoid burning and to gradually develop a tan. Caution is always in order. To prevent melanoma, we need not to avoid the sunlight but safely embrace it!
[1] Newton-Bishop, J et. al. Relationship between sun exposure and melanoma risk for tumours in different body sites in a large case-control study in a temperate climate. European Journal of Cancer 2011; 4 7; 7 3 2 –7 4 1.
[2] Lee J. Melanoma and exposure to sunlight. Epidemiol Rev 1982;4:110–36.
Vågero D, Ringbäck G, Kiviranta H. Melanoma and other tumors of the skin among office, other indoor and outdoor workers in Sweden 1961–1979 Brit J Cancer 1986;53:507–12.
Kennedy C, Bajdik CD, Willemze R, De Gruijl FR, Bouwes Bavinck JN; Leiden Skin Cancer Study. The influence of painful sunburns and lifetime sun exposure on the risk of actinic keratoses, seborrheic warts, melanocytic nevi, atypical nevi, and skin cancer. Invest Dermatol 2003;120:1087–93.
Garland FC, White MR, Garland CF, Shaw E, Gorham ED. Occupational sunlight exposure and melanoma in the USA Navy. Arch Environ Health 1990; 45:261-67.
Kaskel P, Sander S, Kron M, Kind P, Peter RU, Krähn G. Outdoor activities in childhood: a protective factor for cutaneous melanoma? Results of a case-control study in 271 matched pairs. Br J Dermatol 2001;145:602-09.
Garsaud P, Boisseau-Garsaud AM, Ossondo M, Azaloux H, Escanmant P, Le Mab G. Epidemiology of cutaneous melanoma in the French West Indies (Martinique). Am J Epidemiol 1998;147:66-8.
Le Marchand l, Saltzman S, Hankin JH, Wilkens LR, Franke SJM, Kolonel N. Sun exposure, diet and melanoma in Hawaii Caucasians. Am J Epidemiol 2006;164:232-45.
Armstong K, Kricker A. The epidemiology of UV induced skin cancer. J Photochem Biol 2001;63:8-18
Crombie IK. Distribution of malignant melanoma on the body surface. Br J Cancer 1981;43:842-9.
Crombie IK. Variation of melanoma incidence with latitude in North America and Europe. Br J Cancer 1979;40:774-81.
Weinstock MA, Colditz,BA, Willett WC, Stampfer MJ. Bronstein, BR, Speizer FE. Nonfamilial cutaneous melanoma incidence in women associated with sun exposure before 20 years of age. Pediatrics 1989;84:199-204.
Tucker MA, Goldstein AM. Melanoma etiology: where are we? Oncogene 20f03;22:3042-52.
Berwick M, Armstrong BK, Ben-Porat L, Fine J, Kricker A, Eberle C. Sun exposure and mortality from melanoma. J Nat Cancer Inst 2005;97:95-199.
Veierød MB, Weiderpass E, Thörn M, Hansson J, Lund E, Armstrong B. A prospective study of pigmentation, sun exposure, and risk of cutaneous malignant melanoma in women. J Natl Cancer Inst 2003;95:1530-8.
Oliveria SA, Saraiya M, Geller AC, Heneghan MK, Jorgensen C. Sun exposure and risk of melanoma. Arch Dis Child 2006;91:131-8.
Elwood JM, Gallagher RP, Hill GB, Pearson JCG. Cutaneous melanoma in relation to intermittent and constant sun exposure—the western Canada melanoma study. Int J Cancer 2006;35:427-33
[3] Garland FC, White MR, Garland CF, Shaw E, Gorham ED. Occupational sunlight exposure and melanoma in the USA Navy. Arch Environ Health 1990; 45:261-67.
Rivers, J. Is there more than one road to melanoma? Lancet 2004;363:728-30.
Crombie, I. Racial differences in melanoma incidence. Br J Cancer 1979;40:185-93.
[4] Ian D. Wyatt and Daniel E. Hecker. Occupational changes in the 20th century. Monthly Labor Review, March 2006 pp 35-57: Office of Occupational Statistics and Employment Projections, Bureau of Labor Statistics.
[5] Chida K, Hashiba H, Fukushima M, Suda T, Kuroki T. Inhibition of tumor promotion in mouse skin by 1 alpha, 25-dihydroxyvitamin D3. J Cancer Res 1985;45:5426–30.
[6] Evans SR, Houghton AM, Schumaker L, Brenner RV, Buras RR, Davoodi F, et al. Vitamin D receptor and growth inhibition by 1, 25-dihydroxyvitamin D3 in human malignant melanoma cell lines. J Surg Res 1996;61:127–33.
[7] Seifert M, Diesel B, Meese E, Tilgen W, Reichrath J. Expression of 25-hydroxyvitamin D-1alpha-hydroxylase in malignant melanoma: implications for growth control via local synthesis of 1,25(OH)D and detection of multiple
splice variants. Exp Dermatol 2005;14:153–4.
[8] Diaz, G. et al. Apoptosis is induced by the active metabolite of vitamin D3 and its analogue EB1089 in colorectal adenoma and carcinoma cells: possible implications for prevention and therapy. Cancer Res 2000;60:2304-12.
Swamy, N. et al. Inhibition of proliferation and induction of apoptosis by 25-hydroxyvitamin D3-3beta-(2)-Bromoacetate, a nontoxic and vitamin D receptor-alkylating analog of 25-hydroxyvitamin D3 in prostate cancer cells. Clin Cancer Res. 2004;10:8018-27.
Miller, E. et l. Calcium, vitamin D, and apoptosis in the rectal epithelium. Cancer Epidemiology Biomarkers & Prevention 2005;14: 525-28.
[9] Swamy, N. et al. Inhibition of proliferation and induction of apoptosis by 25-hydroxyvitamin D3-3beta-(2)-Bromoacetate, a nontoxic and vitamin D receptor-alkylating analog of 25-hydroxyvitamin D3 in prostate cancer cells. Clin Cancer Res. 2004;10:8018-27.
[10] Mantell, D. et al. 1,25-Dihydroxyvitamin D3 inhibits angiogenesis in vitro and in vivo. Circulation Research. 2000;87:214.
[11] Nakagawa K. et al. 1alpha,25-Dihydroxyvitamin D(3) is a preventive factor in the metastasis of lung cancer. Carcinogenesis 2005;26:429-40.
El Abdaimi, K. et al. The vitamin D analogue EB 1089 prevents skeletal metastasis and prolongs survival time in nude mice transplanted with human breast cancer cells. Cancer Research 2000;60:4412-4418.
Lokeshwar B. et al. Inhibition of prostate cancer metastasis in vivo: a comparison of 1,23-dihydroxyvitamin D (calcitriol) and EB1089. Cancer Epidemiol Biomarkers Rev. 1999;8:241-48.
