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Heliophobia: Fear of the sun Jacob Schor, ND April 3, 2007
Beach Season: Here in Colorado, the month of May is when we go to the Beach. By Beach, we mean the parking lot at the base of Arapahoe Basin Ski Area, commonly called The Basin. By long tradition, a day of spring skiing at the Basin requires a lounge chair, barbecue, ice chest and a few end of season ski runs, but the emphasis is to work on your tan. It's a party lasting from sun up to sun down. Between the warm weather, the high altitude and the late spring sun reflecting off the snow covered peaks, the Beach turns into a magnificent ultraviolet reflector oven. Sunscreen should be mandatory but this year I'm wondering if this really is a good idea
Medical authorities encourage us to use more and more sunscreen every year. As friends are having bits of their faces frozen cut, and burned off, there is little wonder that we become fearful of skin cancer and growing conscientious about applying sunscreen. Yet reading the research on skin cancer and sun exposure raises questions about this approach; are we doing the right thing?
Over the last half dozen years, scientists have established a link between sun exposure, vitamin D production and cancer prevention. Sunscreen, by blocking ultraviolet light penetration into the skin, limits vitamin D production. Thus, sunscreen and the precautions people take to prevent sun exposure and lower risk of skin cancer, increase the risk for other cancers.
A Map reading Man William Grant was one of the first to report the link between vitamin D and cancer. Grant is as an atmospheric ozone physicist with NASA. He noticed that mortality from many common cancers, including colon, breast and prostate, is higher in the north-east US than in the rest of the country. The standard explanation for this phenomenon is that people in colder areas eat more fat. This explanation wasn't adequate for Grant to account for the 150% difference in cancer rates from northeast to southwest. He recognized that a map of cancer incidence looked similar to one depicting geographical variations in ultraviolet exposure. Grant realized the regional cancer variations were better explained by varying levels of vitamin D in the populations of these different areas as a result of varying UV exposure. (see Maps).
Further Maps:
In his early calculations, Grant figured that at least 23,600 Americans die of cancer every year through lack of sunshine (Cancer, vol 94, p 1867). To put that into perspective, about 9800 die each year from skin cancer. He has since increased his estimate to 100,000 people developing cancer and 40,000 deaths per year result from vitamin D deficiency, or four times the death rate of skin cancer. Prostate Cancer: The classic risk factors for developing prostate cancer, being old, black and living in the northern latitudes, all point to vitamin D deficiency. In an elegant study published in 2005, researchers measured the skin pigmentation on a person's forehead and on the inner arm, 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. In other words adequate sun exposure or vitamin D levels cut prostate cancer by half. In the US there are currently 240,000 new prostate cancers diagnosed each year. In theory, providing adequate D could prevent 120,000 prostate cancers a year. [ Cancer Research (vol 65, p5470)]
Colorectal Cancer: 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. [Journal of Steroid Biochemistry and Molecular Biology , vol 97, p 179]
Sun exposure may be worth the risk of skin cancer. Yet sun exposure isn't needed to make vitamin D, it can be taken as an oral supplement. Using sunscreen and taking vitamin D in pill form could lower colon, prostate and other cancer rates while still providing skin cancer protection. That is if life were simple. There are a few problems with this idea.
In February, a short summary of a recent article in Nature Immunology raised some interesting questions:
This new information suggests that oral vitamin D may not suffice, at least in preventing skin cancer. The Vitamin D made in the skin as a result of sun exposure attracts immune protection to the skin. One possible solution is to enrich sunscreens and other topical lotions with high doses of vitamin D. To match the natural vitamin D production that a day's use of sunscreen blocks, thousands of IUs of vitamin D per dollop of sunscreen should be considered. p53 the tanning Trigger Even this might not be adequate. What may be even more relevant news comes from a study published in the March 9, 2007 issue of Cell, which discloses that the tumor suppressor gene called p53, is the gene responsible for initiation of tanning. Tanning is a reaction to ultraviolet light exposure. Melanin pigment production is increased and the melanin concentrated in skin cells. Melanin then protects skin cells from DNA damage caused by UV exposure. Researchers had explained most of this tanning process already but not what initiated tanning. This current paper reveals that UV light activates the p53 gene, which in turn activates the tanning pathway. Skin cells without the p53 gene will not tan. We typically think of the p53 gene in relation to cancer protection and as the trigger to apoptosis (cellular suicide) of cancer cells. Cells without p53 genes can't protect themselves against cancer. Cells with a working p53 gene 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] Sun exposure protects our skin against cancer by stimulating vitamin D production. Sun may also protect against skin cancer by stimulating p53 activity. Sunscreen blocks both effects. How sure are we that sunscreen offers protection against skin cancer? It seems not as sure as we have been led to believe
Does Suncreen Prevent Skin Cancer? Martin Weinstock, has studied this question for years. In 1999, he published the results after he reviewed 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 asked the same question and yielded no more convincing an answer. 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..” At least they don't think sunscreen causes melanoma even if the data appears to suggest it: “….. the lack of dose-effect relationship and the numerous biases, especially the uncertainty that exposure (sunscreen use) preceded melanoma do not suggest a causative association between sunscreen use and melanoma.” [ii] Telling us that sunscreen doesn't cause melanoma hardly convinces this reader that it prevents melanoma. I need to say this. There is no strong research that say using sunscreen prevents skin cancer. Smarter options: There may be a smarter approach to preventing skin cancer. Ultraviolet light increases the reactive oxygen species in skin cells and the resultant oxidative damage may be to blame for causing skin cancer. A number of plant extracts with strong antioxidant action that reduces ROS damage from UV light have been shown to prevent skin cancer in animals. [iii] [iv] Green tea extracts [v] and pomegranate extracts [vi] are two examples. Using topical antioxidants along instead of or along with sunscreen might go a long way in preventing cancer.
What about people who don't tan? An interesting paper appeared last fall that suggests the supplement forskolin can help induce a tan. Here is a Science News summary:
Does sunscreen protect us from cancer or does it cause cancer. Probably the truth is somewhere in between. If using sunscreen, my choice is to use one loaded with vitamin D and plant antioxidants. Who sells this sunscreen? No one that I've found. We may have to make it ourselves. If this thought interests you, check out the website http://skinactives.com/products/productlist1.htm
This company sells a wide range of ingredients that you can use to make your own skin creams. Say you want a skin cream enriched with ellagic acid, resveratrol, betulinic acid and green tea, well this is the source for all your ingredients. At this point they don't sell vitamin D-3. My solution is to empty our tubes of sunscreen, mix in several 100,000 IUs of vitamin D and then figure out how to put all the goop back into the tube. I'll keep you posted.
References [i] J Investig Dermatol Symp Proc. 1999 Sep;4(1):97-100. Links Do sunscreens increase or decrease melanoma risk: an epidemiologic evaluation.• Weinstock MA . Dermatoepidemiology Unit , VA Medical Center , Providence , Rhode Island 02908-4799, USA . maw@brown.edu Ultraviolet adiation is an important cause of melanoma, so the use of sunscreen lotions has been advocated for melanoma prevention. Several arguments have been raised in opposition to this inference. Sunscreen use may interfere with cutaneous vitamin D synthesis, which some have hypothesized may lower melanoma risk. Sunscreen users may compensate for their sunscreen use by staying out much longer in the sun, or may use sunscreen lotions inconsistantly. Published melanoma case-control studies have not consistantly demonstrated a protective effect of sunscreens; however, these studies do not provide strong evidence, ultraviolet radiation is a known cause of melanoma, and ultraviolet B may be particularly potent, so on balance the evidence supports continued advocacy of sunscreen lotion use as part of an overall sun-protection regimen. Uncertainty will remain, however, until the action spectrum of melanoma is convincingly demonstrated or the methodologic limitations of existing epidemiologic evidence are overcome. The latter may require another decade or more of experience with sunscreen use.
[ii] Br J Dermatol. 2002 Apr;146 Suppl 61:24-30. Links Cutaneous malignant melanoma, sun exposure, and sunscreen use: epidemiological evidence.• Bastuji-Garin S , • Diepgen TL . Public Health Department, Paris XII University, Henri-Mondor Hospital, 51 avenue du Marechal de Lattre de Tassigny, 94000 Creteil, France. sylvie.bastuji-garin@hmn.ap-hop-paris.fr BACKGROUND: Cutaneous malignant melanoma is the most serious form of skin cancer and accounts for about three-quarters of all skin cancer deaths. Over the last few decades the incidence and mortality rates of melanoma have been increasing worldwide. The risk of melanoma is higher in individuals with both phenotypic susceptibility and a history of sun exposure. Therefore, recommended sun protection behaviours include wearing long-sleeved clothing, seeking shade, avoiding the sun when it is strongest, and using sunscreen lotion with a sun protection factor of 15 or higher. It has been reported, however, that the use of sunscreens does not protect against melanoma and seems to increase the duration of recreational sun exposure. METHODS: Published epidemiological studies examining sunscreen use and melanoma have been reviewed from an epidemiological point of view, taking into account potential biases. We have classified case-control studies into four categories: (1) inconclusive studies because of major bias in control population and/or the lack of multivariate analysis; (2) no association between sunscreen use and melanoma after controlling for confounders; (3) negative association (i.e. protective effect of sunscreen); and (4) positive association. Various other epidemiological studies were also analysed. RESULTS: These results are controversial. Two case-control studies show a protective effect of sunscreen use, while three studies showed a significant risk associated with sunscreen use. However, the discordant results, the low relative risks, the lack of dose-effect relationship and the numerous biases, especially the uncertainty that exposure (sunscreen use) preceded melanoma do not suggest a causative association between sunscreen use and melanoma. Several hypotheses could partly explain these contradictory results. PMID: 11966729 [PubMed - indexed for MEDLINE]
[iii]
Photodermatol
Photoimmunol Photomed. 2003 Apr;19(2):56-72. Photochemoprevention of skin cancer by botanical agents.• F'guyer S , • Afaq F , • Mukhtar H . Department of Dermatology, University of Wisconsin , Madison 53706 , USA . Photochemoprevention has become an important armamentarium in the fight against ultraviolet radiation (UVR)-induced damage to the skin. Among many UVR-induced damages, skin cancer is of the greatest concern as its rates have been steadily increasing in recent years and the same trend is expected to continue in the future. Ultra-violet radiation increases oxidative stress in skin cells by causing excessive generation of reactive oxygen species (ROS), leading to cancer initiation and promotion. Antioxidants have the capability to quench these ROS and much recent work shows that some of these can inhibit many UVR-induced signal transduction pathways. Thus, identifying nontoxic strong antioxidants--capable of preventing UVR-induced skin cancer--has become an important area of research. The use of botanical antioxidants in skin care products is growing in popularity. A wide range of such agents has been shown to prevent skin cancer in animal model systems. New agents are constantly being investigated; however, only a few have been tested for their efficacy in humans. Animal model and cell culture studies have clarified that antioxidants act by several mechanisms at various stages of skin carcinogenesis. This review focuses on skin cancer photochemopreventive effects of selected botanical antioxidants. PMID: 12945805 [PubMed - indexed for MEDLINE]
[iv]
Exp
Dermatol. 2006 Sep;15(9):678-84. Botanical antioxidants in the prevention of photocarcinogenesis and photoaging.• Afaq F , • Mukhtar H . Department of Dermatology, University of Wisconsin , Madison , 53706, USA . Exposure of the skin to ultraviolet (UV) radiation, particularly its UV-B component (280-320 nm), from the sun results in erythema, edema, hyperplasia, hyperpigmentation, sunburn cells, immunosuppression, photoaging, and skin cancer. Amongst these various adverse effects of UV-B radiation, skin cancer and photoaging are of great concern. More recent changes in lifestyle have led to a significant increase in the amount of UV-B radiation people receive leading to a surge in the incidence of skin cancer and photoaging. As these trends are likely to continue in the foreseeable future, the adverse effect of UV-B has become a major human health concern. Therefore, development of novel strategies to reduce the occurrence of skin cancer and delay the process of photoaging are highly desirable goals. One approach to reduce their occurrence is through photochemoprevention, which we define as the use of agents capable of ameliorating the adverse effects of UV-B on the skin. Photochemoprevention via use of botanical antioxidants, present in the common diet of human have gained considerable attention as photochemopreventive agents for human use. Many such agents have also found a place in skin care products. This review will focus on the effects of selected botanical antioxidants in the prevention of photocarcinogenesis and photoaging. PMID: 16881964 [PubMed - indexed for MEDLINE]
[v] : Curr Drug Targets Immune Endocr Metabol Disord. 2003 Sep;3(3):234-42. Links Skin photoprotection by green tea: antioxidant and immunomodulatory effects.• Katiyar SK . Department of Dermatology, University of Alabama at Birmingham , Birmingham , AL 35294 , USA . skatiyar@uab.edu Because of a characteristic aroma and health benefits, green tea is consumed worldwide as a popular beverage. The epicatechin derivatives, commonly called polyphenols, present in green tea possess antioxidant, anti-inflammatory and anti-carcinogenic properties. The major and most highly chemopreventive constituent in green tea responsible for the biochemical or pharmacological effects is (-)-epigallocatechin-3-gallate (EGCG). Epidemiological, clinical and biological studies have implicated that solar ultraviolet (UV) light is a complete carcinogen and repeated exposure can lead to the development of various skin disorders including melanoma and nonmelanoma skin cancers. We and others have shown that topical treatment or oral consumption of green tea polyphenols (GTP) inhibit chemical carcinogen- or UV radiation-induced skin carcinogenesis in different laboratory animal models. Topical treatment of GTP and EGCG or oral consumption of GTP resulted in prevention of UVB-induced inflammatory responses, immunosuppression and oxidative stress, which are the biomarkers of several skin disease states. Topical application of GTP and EGCG prior to exposure of UVB protects against UVB-induced local as well as systemic immune suppression in laboratory animals, which was associated with the inhibition of UVB-induced infiltration of inflammatory leukocytes. Prevention of UVB-induced suppression of immune responses by EGCG was also associated with the reduction in immunosuppressive cytokine interleukin (IL)-10 production at UV irradiated skin and draining lymph nodes, whereas IL-12 production was significantly enhanced in draining lymph nodes. Antioxidant and anti-inflammatory effects of green tea were also observed in human skin. Treatment of EGCG to human skin resulted in the inhibition of UVB-induced erythema, oxidative stress and infiltration of inflammatory leukocytes. We also showed that treatment of GTP to human skin prevents UVB-induced cyclobutane pyrimidine dimers formation, which are considered to be mediators of UVB-induced immune suppression and skin cancer induction. The in vitro and in vivo animal and human studies suggest that green tea polyphenols are photoprotective in nature, and can be used as pharmacological agents for the prevention of solar UVB light-induced skin disorders including photoaging, melanoma and nonmelanoma skin cancers after more clinical trials in humans.
[vi] J Med Food. 2003 Fall;6(3):157-61. Links Chemopreventive effects of pomegranate seed oil on skin tumor development in CD1 mice.• Hora JJ , • Maydew ER , • Lansky EP , • Dwivedi C . Department of Pharmaceutical Sciences, College of Pharmacy, South Dakota State University, Brookings, SD 57007, U.S.A. Pomegranate seed oil was investigated for possible skin cancer chemopreventive efficacy in mice. In the main experiment, two groups consisting each of 30, 4-5-week-old, female CD(1) mice were used. Both groups had skin cancer initiated with an initial topical exposure of 7,12-dimethylbenzanthracene and with biweekly promotion using 12-O-tetradecanoylphorbol 13-acetate (TPA). The experimental group was pretreated with 5% pomegranate seed oil prior to each TPA application. Tumor incidence, the number of mice containing at least one tumor, was 100% and 93%, and multiplicity, the average number of tumors per mouse, was 20.8 and 16.3 per mouse after 20 weeks of promotion in the control and pomegranate seed oil-treated groups, respectively (P <.05). In a second experiment, two groups each consisting of three CD(1) mice were used to assess the effect of pomegranate seed oil on TPA-stimulated ornithine decarboxylase (ODC) activity, an important event in skin cancer promotion. Each group received a single topical application of TPA, with the experimental group receiving a topical treatment 1 h prior with 5% pomegranate seed oil. The mice were killed 5 h later, and ODC activity was assessed by radiometric method. The experimental group showed a 17% reduction in ODC activity. Pomegranate seed oil (5%) significantly decreased (P <.05) tumor incidence, multiplicity, and TPA-induced ODC activity. Overall, the results highlight the potential of pomegranate seed oil as a safe and effective chemopreventive agent against skin cancer. PMID: 14585180 [PubMed - indexed for MEDLINE]
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