Sunscreen and related thoughts for NDNR

 

Jacob Schor, ND

April 3, 2007

 

 

With summer approaching, the sunscreen displays in our local retail stores are popping up like mushrooms after a week of rain or like warts on a ten year old. There is little doubt that using these topical sunscreens prevent sunburn, but little convincing evidence argues that they prevent skin cancer. In fact, some evidence suggests the opposite; sunscreen use may increase cancer risk.

 

In 1999, Martin Weinstock published the results of a meta-analysis of 13 epidemiological studies on the relation of sunscreen use to melanoma risk. Three showed a decreased risk of melanoma. Four showed an increased risk and six were inconclusive. [i] A 2002 review published in the British Journal of Dermatology yielded no more assurance that sunscreen is protective. The authors described their results as ‘discordant.' To quote their abstract: “Two case-control studies show a protective effect of sunscreen use, while three studies showed a significant risk associated with sunscreen use..” They found excuses to explain away results suggestive of sunscreen increasing risk but the authors still appear to be on the defensive. [ii]

 

 

There is something about sunlight that is good for us and protective against cancer. Some researchers think it is the vitamin D produced in the skin by sunlight. William Grant, an atmospheric physicist who works for NASA, was one of the first to suggest that vitamin D is protective against cancer. Mortality from many common cancers, including colon, breast and prostate, is 150% higher in the northeastern United States than in the southwest. Grant recognized that a map of cancer rates looks similar to one depicting geographical variations in ultraviolet exposure. Grant realized that these regional cancer variations can be explained by varying levels of vitamin D in the populations of these different areas.

 

 

Given the quantity of in-vitro research on vitamin D and cancer that has been published in recent years, Grants assumption that it is vitamin D that is protective appears to be a valid assumption.

 

Grant currently estimates that vitamin D deficiency causes 100,000 people to develop cancer each year and that these cancers result in 40,000 deaths per year. To put this in perspective, skin cancer accounts for just less than 10,000 deaths per year. [iii] Since 2002, Grant has published more than a dozen papers on this subject all easily found on www.Pubmed.gov or on his website www. SunArc.org.

 

 

Grant has posted some of these maps on his website.

Breast Cancer Map: http://sunarc.org/breastcancer.htm

Colon Cancer Map: http://sunarc.org/coloncancer.htm

Ovarian Cancer Map: http://sunarc.org/ovarycancer.htm

 

 

 

DNA Spectral Exposure for North America for July 1992

Skin tanning predicts prostate cancer risk. In a study on prostate cancer published in 2005, researchers measured forehead skin pigmentation comparing it to inner arm pigmentation, figuring that forehead pigmentation was a good measure of lifetime sun exposure and inner arm a baseline of skin coloration. The ratio of these two measurements allowed them to rate a man's lifetime sun exposure. Comparing the measurements of 450 white men with advanced prostate cancer against 455 matched controls without disease, produced striking data. Men with the most sun exposure were 49% less likely to develop prostate cancer than those with the palest forehead pigmentation. The assumption is that total sun exposure would predict vitamin D status over a lifetime. In the US there are currently 240,000 new prostate cancers diagnosed each year. In theory, providing adequate D through supplementation could prevent 120,000 prostate cancers a year. [iv]

Along the same lines, Cedric Garland and his colleagues at the University of California , San Diego have concluded that 1,000 IU of vitamin D a day, decreases risk of colorectal cancer by half. Garland calculated that this would prevent 28,000 colon cancer deaths a year. [v] Looking at the total cancers that might be prevented by vitamin D, Garland calculates that spending a billion dollars to provide 1,000 IU of vitamin D a day to every one in Europe and North America will save between $16-25 billion dollars in cancer care costs. [vi]

Sunscreen blocks vitamin D production.

Sunscreen is designed on purpose to block UV penetration into the skin. That is why it prevents sunburn. That is also why it prevents production of vitamin D. Even relatively weak sunscreens labeled SPF-8 will block UV and stop vitamin D production. [vii]

 

Remember Betacarotene?

Because carrots are protective against cancer and carrots are loaded with betacarotene, researchers, and many of us, assumed betacarotene would work as well. Biology unfortunately is often messy and more complicated than we want. In the studies on betacarotene, smoking and lung cancer, supplemental betacarotene was far from protective. I have begun to wonder if this protective effect from sunlight might be a little more complex than our early assumptions would lead us to believe.

In these calculations mentioned, the researchers all make the assumption that sun exposure and vitamin D are exactly the same thing. Maybe they are not synonymous.

This past March, an article in Nature Immunology suggested that the protective effect from sunlight was more complex than we first thought. Eugene Butcher at Stanford University in California and his colleagues were able to show that immune cells in the skin known as dendritic cells convert inactive vitamin D3 into its active form. This active form of vitamin D then causes T-cells to change their surface receptors so that they migrate to the upper levels of the skin. Recall that T-cells are the immune cells that destroy damaged and infected cells, and regulate other immune cells. It starts to sound as if it isn't just the total amount of vitamin D one has inside the body, but it is the formation and location in the skin that enables vitamin D to help repair sun-induced damage and fight off pathogens. [viii]

In other words, staying out of the sun or using sunscreen and then replacing the vitamin D one did not make by way of oral supplementation may not do quite the same thing. It may be necessary to actually make the vitamin D in the skin to trigger and attract immune protection to the skin and maybe elsewhere. Of course, it might be possible to apply vitamin D topically to duplicate the effect of sunlight. Maybe.

A study published in the March 9, 2007 issue of Cell, suggests that some of our basic assumptions about sunlight, vitamin D and cancer rates may have been too hasty. This study discloses that the tumor suppressor gene, p53, is the gene responsible for initiation of tanning.

Tanning is a reaction in the skin to ultraviolet light exposure. Melanin pigment production is increased and the melanin is then concentrated in skin cells. The skin gets darker. Melanin blocks UV penetration, protecting skin cells from DNA damage. Up until March, Researchers had already explained most of the chemistry of this tanning process but not what triggered the initial steps. This current paper reveals that UV light activates production of p53 enzyme, which in turn activates the tanning pathway. Skin cells without the p53 gene will not tan.

If this p53 business sounds vaguely familiar, it is because we read about it frequently in relation to cancer. This is the gene cells use to trigger apoptosis (cellular suicide) when they detect an insurmountable level of genetic damage. Let me repeat myself, the p53 enzyme is how cells kill themselves when they realize they are on the way to becoming cancerous. Cells without active p53 cannot protect themselves against cancer. Cells with working p53 enzymes will usually kill themselves if they become cancerous. Turning on the p53 gene through sun exposure may also turn on the cancer fighting potential of both the skin and the body. [ Cell vol 128, p 853]

Some of the cancer protection that we assume is due to vitamin D from UV exposure may actually be the result of stimulating p53. It is too early to tell. The relation to UV exposure and cancer prevention may only be partly due to resulting vitamin D production. It may have something to do with the more obvious reaction to sun. Our skin gets tan. Before writing off Vitamin D having a role in cancer prevention though, let's be serious; there is little doubt in my mind that vitamin D plays a major role in fighting cancer. At the time of this writing a Pubmed search yields 4,459 hits on ‘vitamin D and cancer'.

We know that sun exposure protects skin against cancer by stimulating vitamin D production and attracting immune protection. Sun exposure may also protect against skin cancer by stimulating p53 activity. Sunscreen blocks both effects. The evidence does not support the idea that sunscreen protects against skin cancer. Putting these pieces of information together, could bring one to a rather heretical position.

Recall that not too far in the distant past, naturopathic doctors and the nature cure proponents who preceded the development of our profession, all held great store in therapeutic sunbathing. Here in Denver the architects of our original hospitals included sunbathing facilities primarily for the treatment of tuberculosis patients. Our fear of the sun is a recent phenomenon. Generations have thought getting a good tan as both healthy and therapeutic. Perhaps it is time to reconsider our current opinion on sunlight, sunscreen and tanning.

Our desire to find a simple solution to complex problems has once again clouded our ability to see and remember the big picture. Sunscreen may not be the magic salve that prevents skin cancer. Sun damage is oxidative damage and there are clear studies which show that stuff that acts as antioxidants can reduce oxidative damage due to UV radiation providing protection against skin cancer. [ix] Radiation damage increases generation of reactive oxygen species in the skin cells. Various phenolic compounds and flavonoids that we are already familiar with which quench these oxidative species can be used protectively. [x]

Following the sunscreen model of topical application, researchers have experimented and shown that various topical versions of supplements we typically use orally effectively protect the skin. An article from 2004 in the Journal of Cosmetic Dermatology reports that:

“There are two great advantages in applying an active formulation of topical antioxidants to the skin. First, the skin attains far higher levels of each antioxidant than can be achieved by only taking these vitamins orally. The level of vitamin C attained in the skin by topical application is 20-40 times that achievable with oral vitamin C. With topical application, the concentration of vitamin E in the skin increases by a factor of 10.6 and selenium by a factor of 1.7. Second, topical application arms the skin with a reservoir of antioxidants that cannot be washed or rubbed off, a protection which stays in the skin for several days after application.” [xi]

Rather than topical sunscreen, we should consider using topical antioxidants. There is already good research supporting the use of Vitamin E, selenium, [xii] lutein, [xiii] green tea, [xiv] [xv] pomegranate, [xvi] curcumin, resveratrol, and silymarin. [xvii] How hard would it be to open a few capsules already on our shelves and mix them into a simple salve?

Life on our planet would not be possible without sunlight. People, no matter how primitive a culture they may live in, have understood this for millenia. It is peculiar than to consider that in recent years sunlight, at least in our modern culture, has become something we fear and seek protection from. It is this belief and the fact that people are so willing to believe it that we should really worry about.

 

 

 

 

[i] Weinstock MA. Do sunscreens increase or decrease melanoma risk: an epidemiologic evaluation. J Investig Dermatol Symp Proc. 1999 Sep;4(1):97-100.

[ii] Bastuji-Garin S, and Diepgen TL Cutaneous malignant melanoma, sun exposure, and sunscreen use: epidemiological evidence. Br J Dermatol. 2002 Apr;146 Suppl 61:24-30.

[iii] Grant WB. An estimate of premature cancer mortality in the U.S. due to inadequate doses of solar ultraviolet-B radiation. Cancer. 2002 Mar 15;94(6):1867-75.

[iv] .John EM, Schwartz GG, Koo J, Van Den Berg D, Ingles SA. Sun exposure, vitamin D receptor gene polymorphisms, and risk of advanced prostate cancer. Cancer Res. 2005 Jun 15;65(12):5470-9.

[v] Gorham ED, et al Optimal vitamin D status for colorectal cancer prevention: a quantitative meta analysis. Am J Prev Med. 2007 Mar;32(3):210-6.

[vi] Grant WB. An estimate of cancer mortality rate reductions in Europe and the US with 1,000 IU of oral vitamin D per day. Recent Results Cancer Res. 2007;174:225-34.

[vii] http://ods.od.nih.gov/factsheets/vitamind.asp

[viii] Sigmundsdottir H, Pan J, Debes GF, Alt C, Habtezion A, Soler D, Butcher EC. DCs metabolize sunlight-induced vitamin D3 to 'program' T cell attraction to the epidermal chemokine CCL27. Nat Immunol. 2007 Mar;8(3):285-93. Epub 2007 Jan 28.

[ix] Sies H, Stahl W. Nutritional protection against skin damage from sunlight. Annu Rev Nutr. 2004;24:173-200.

[x] Svobodova A, et al. Natural phenolics in the prevention of UV-induced skin damage. A review.

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2003 Dec;147(2):137-45.

[xi] Burke KE. Photodamage of the skin: protection and reversal with topical antioxidants. J Cosmet Dermatol. 2004 Jul;3(3):149-55.

[xii] Burke KE, Clive J, Combs GF Jr, Nakamura RM. Effects of topical L-selenomethionine with topical and oral vitamin E on pigmentation and skin cancer induced by ultraviolet irradiation in Skh:2 hairless mice. J Am Acad Dermatol. 2003 Sep;49(3):458-72.

[xiii] Lee EH, et al. Dietary lutein reduces ultraviolet radiation-induced inflammation and immunosuppression. J Invest Dermatol. 2004 Feb;122(2):510-7.

[xiv] Yusuf N, et al. Photoprotective effects of green tea polyphenols.Photodermatol Photoimmunol Photomed. 2007 Feb;23(1):48-56.

[xv] .Katiyar SK. Skin photoprotection by green tea: antioxidant and immunomodulatory effects Curr Drug Targets Immune Endocr Metabol Disord. 2003 Sep;3(3):234-42.

[xvi] Afaq F, et al. Pomegranate fruit extract modulates UV-B-mediated phosphorylation of mitogen-activated protein kinases and activation of nuclear factor kappa B in normal human epidermal keratinocytes paragraph sign . Photochem Photobiol. 2005 Jan-Feb;81(1):38-45.

[xvii] Lao CD,et al Targeting events in melanoma carcinogenesis for the prevention of melanoma.Expert Rev Anticancer Ther. 2006 Nov;6(11):1559-68.