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Stephen F Hayes, Hospital Practitioner in dermatology Isle of Wight hospital trust
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Education about prevention and early detection of melanoma should be directed to groups known to be at most risk. People with type 1 and 2 skin phototypes are at significantly higher risk of melanoma and non melanoma skin cancers for a given level of sun exposure, patients with red hair and very large numbers of freckles are also at higher risk as are those with very large numbers of normal moles or dysplastic moles. Despite the fact that melanoma is now killing more people in the UK than cancer of the cervix, no screening is in prospect. Screening for breast and cervical cancer were introduced before there was good evidence of its efficacy or cost effectiveness. There is an argument for targeting education to primary health care workers to increase awareness of those groups of patients who are at increased risk of melanoma (over 150 moles, over 15 dysplastic moles, skin types 1 and 2, positive family history, severe sun exposure under age 15) and target advice about prevention and early detection at these people. Most such patients I advise are unaware of their and their children's increased risk. Giving these people this information opportunistically during the consultation may encourage them to protect themselves more effectively than simply leaving leaflets around the waiting room. Competing interests: None declared |
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Sergio Stagnaro, Specialist in Blood, Gastrointestinal, and Metabolic Diseases. Researcher in Biophysical Semeiotics. Via Erasmo Piaggio 23/8. 16037 Riva Trigoso (Genoa) Italy
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Sirs, In my opinion there is a fundamental bias in Alison Fry and Verne J.’s article. In fact, I think that because a congenital functional mitochondrial cytopathology is overlooked- "conditio sine qua non" of the most frequent and dangerous human disorders, including malignancies - all current oncological research are fundamentally biased. That is, such researchers do not consider the existence or assess the seriousness as well as the location of Congenital Acidosic Enzyme-Metabolic Histangiopathy (2, 3, 4). In fact, all environmental risk factors "could" influence some human biological functions and/or bring about different disorders, such as cancers, exclusively in relation to both the presence and intensity of CAEMH in a well-defined biological system, as CAEM-H is present always at the base of Oncological Terrain (See the site HONCode 233736, http://digilander.libero.it/semeioticabiofisica). Although overlooked(or worse, ignored), Oncological Terrain does really exist. 1) Fry A., Verne J.Preventing skin cancer. BMJ 2003;326:114-115 ( 18 January ). 2) Stagnaro S., Stagnaro-Neri M.Istangiopatia Congenita Acidosica Enzimo Metabolica. Gazz. Med. It.- Arch. Sci. Med. 144, 423, 1985. 3) Stagnaro S., Stagnaro-Neri M. Una patologia mitocondriale ignorata: la Istangiopatia Congenita Acidosica Enzimo-Metabolica. Gazz. Med. It. - Arch. Sci. Med. 149, 67 1990. 4) Stagnaro S., Istangiopatia Congenita Acidosica Enzimo-Metabolica condizione necessaria non sufficiente della oncogenesi. XI Congr. Naz. Soc. It. di Microangiologia e Microcircolaz. Abstracts, pg 38, 28 Settembre-1 Ottobre, Bellagio Competing interests: None declared |
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William B. Grant, Atmospheric Sciences, NASA Langley Research Center (this letter is not related to my NASA work) 12 Sir Francis Wyatt Place, Newport News, VA 23606-3660, USA
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The recent editorial on preventing skin cancer (1) is, in the author's opinion, too narrowly focused to accomplish the overriding goal of the editorial, namely, reducing death rates in the U.K., especially from cancer. Focusing the discussion of solar ultraviolet-B (UV-B) radiation (280-320 nm) only on skin cancer, especially melanoma, is a very narrow perspective (2). It is a narrow viewpoint since solar UV-B, which gives rise to tanning, sun burning, and, sometimes, skin cancer, is also the primary source of vitamin D for many people. Vitamin D has many mechanisms involved in reducing the risk of cancer, including increasing cell differentiation and apoptosis, reduction of metastasis and angiogenesis around tumors, and reduction of parathyroid hormone (3-6). A number of epidemiologic studies have shown an inverse correlation between solar UV-B doses for several types of cancer (7-16). The cancer mortality rates in the U.S. from 1970-94 (17), as well as the map of solar DNA-weighted UV-B (peaking near 300 nm) radiation for the U.S. in July (18), can be used to show that the 50% higher mortality rates for a dozen types of cancer in the NE U.S. compared to those in the SW U.S. are highly correlated with differences in solar UV-B doses for the two regions (16). It should be pointed out that while this study was conducted using only cancer mortality rates in (17) and solar UV-B radiation doses in (18), a more extensive study using additional factors such as diet, Hispanic heritage, other diseases, poverty, and smoking, has been completed and a manuscript on the findings will be submitted for publication shortly. In the new study, a much larger fraction of the cancer mortality rate distributions can be explained with the additional factors, but the fraction attributed to insufficient UV-B radiation and/or vitamin D remains very nearly the same. Total consumption of vitamin D (dietary plus supplements) is generally significantly inversely associated with cancer, such as colorectal cancer (19-23). Vitamin D also plays an important role in reducing the risk of or severity and progression of a number of other diseases including arthritis, multiple sclerosis, osteoporosis, and rickets (24,25). Vitamin D deficiency is a problem in the U.K., especially among non-European immigrants (26-28) and the elderly (29), as well as for Europeans in general (30,31). To put UV-B and cancer risk and risk reduction in perspective in the U.K., it is instructive to look at cancer incidence and mortality rates for cancers related to solar UV-B radiation (16). The data for the mid-to -late 1990s are available from (32). The data are based on the best available data as well as modeling efforts. The results are presented in Table 1. The sums of incidence for the cancers for which UV-B radiation and vitamin D are risk reduction factors (7-16) are about 25 times the incidence for melanoma, the predominant form of skin cancer, while the mortalities are 50 times those for melanoma. In the U.S., a conservative estimate is that 8% of the "premature" mortality rates for the sum of these cancers for males can be delayed, as well as 10% of those for females (16). However, the UV-B doses in the U.K. are equivalent to those at the northern boundary of the U.S. Thus, the fraction of premature mortality that can be attributed to insufficient UV-B and/or vitamin D in the U.K. could be 12% for males and 15% for females. These rates imply that the UV-B/vitamin D-preventable incidence of all non-melanoma cancer is 3.5 times the incidence of melanoma in the U.K., while the delay in mortality from all non-melanoma cancer is 7 times that for melanoma, assuming that incidence and mortality have the same relation to vitamin D. Going further, the increase in melanoma rates in the U.K. may be due only in part to increased UV exposure practices: it could also be due to increasing obesity. Obesity has been linked to melanoma in two studies (33,34). Increases in obesity rates have been reported in the U.K. (35). So, what should be the responsible policy guideline regarding solar UV-B exposure and vitamin D? First, enjoy the sun in moderation; avoid burning and excessive tanning. Second, consider supplementing with vitamin D, individually or at the population level. However, be careful not to have serum 25(OH)D3 levels rise too high (<50-60 ng/ml). Serum testing for 25(OH)D3 levels is now readily available. See (36) for thoughts on fortification of foods with vitamin D. References 1. Fry A, Verne J. Preventing skin cancer. BMJ. 2003;326:114-5 2. Dyer O. Sunlight prevents cancer, study says. BMJ 2002;324(7339):696. 3. Feldman D, Zhao XY, Krishnan AV. Editorial/mini-review: Vitamin D and prostate cancer. Endocrinology. 2000;141:5-9. 4. Mehta RG, Mehta RR. Vitamin D and cancer. J Nutr Biochem. 2002;13:252-64. 5. Van den Bemd CJCM, Chang GTG. Vitamin D and vitamin D analogs in cancer treatment. Current Drug Targets. 2002;3:85-94. 6. Ylikomi T, Laaksi I, Lou YR, et al. Antiproliferative action of vitamin D. Vitam Horm. 2002;64:357-406. 7. Garland CF, Garland FC. Do sunlight and vitamin D reduce the likelihood of colon cancer? Int. J. Epidemiol. 1980;9:227-31. 8. Hanchette CL, Schwartz GG. Geographic patterns of prostate cancer mortality. Cancer, 1992;70:2861-9. 9. Lefkowitz ES, Garland CF. Sunlight, vitamin D, and ovarian cancer mortality rates in U.S. women. Int. J. Epidemiol. 1994;23:1133-6. 10. Freedman DM, Zahm SH, Dosemeci M. Residential and occupational exposure to sunlight and mortality from non-Hodgkin's lymphoma: composite (threefold) case-control study. BMJ. 1997;314:1451-5. 11. Janowsky EC, Lester GE, Weinberg CR, et al. Association between low levels of 1,25-dihydroxyvitamin D and breast cancer risk. Public Health Nutr. 1999;2:283-91. 12. John EM, Schwartz GG, Dreon DM, Koo J. Vitamin D and breast cancer risk: the NHANES I Epidemiologic follow-up study, 1971-1975 to 1992. National Health and Nutrition Examination Survey. Cancer Epidemiol. Biomarkers Prev. 1999;8:399-406. 13. Luscombe CJ, Fryer AA, French ME, et al. Exposure to ultraviolet radiation: association with susceptibility and age at presentation with prostate cancer. Lancet. 2001;358:641-2. 14. Freedman DM, Dosemeci M, McGlynn K. Sunlight and mortality from breast, ovarian, colon, prostate, and non-melanoma skin cancer: a composite death certificate based case-control study. Occup. Environ. Med. 2002;59:257-62. 15. Grant WB. An ecologic study of dietary and solar UV-B links to breast cancer mortality rates. Cancer. 2002;94:272-81. 16. Grant WB. An estimate of premature cancer mortality in the United States due to inadequate doses of solar ultraviolet-B radiation. Cancer. 2002;941:867-75. 17. Devesa SS, Grauman DJ, Blot WJ, Pennello GA, Hoover RN, Fraumeni JF Jr. Atlas of Cancer Mortality in the United States, 1950-1994. NIH Publication No. 99-4564, 1999. http://cancer.gov/atlasplus/new.html (accessed January 16, 2003). 18. DNA spectral exposure (kJ/m2) for July 1992 (North America) http://toms.gsfc.nasa.gov/ery_uv/dna_exp.gif (accessed January 16, 2003). 19. Bostick RM, Potter JD, Sellers TA, et al. Relation of calcium, vitamin D, and dairy food intake to incidence of colon cancer among older women. The Iowa Women's Health Study. Am J Epidemiol. 1993;137:1302-17. 20. Kearney J, Giovannucci E, Rimm EB, et al. Calcium, vitamin D, and dairy foods and the occurrence of colon cancer in men. Am J Epidemiol. 1996;143, 907-17. 21. Martinez ME, Giovannucci EL, Colditz GA, et al. Calcium, vitamin D, and the occurrence of colorectal cancer among women. J Natl Cancer Inst 1996;88: 1375-82. 22. Marcus PM, Newcomb PA. The association of calcium and vitamin D, and colon and rectal cancer in Wisconsin women. Int J Epidemiol. 1998;27:788-93. 23. Grant WB, Garland CF, Evidence supporting the role of vitamin D in reducing the risk of cancer, Comments on "Prospects for chemoprevention of cancer" by RM Tamimi et al., J Intern Med 2002;251:286-300. J Intern Med, 2002;252:178-9. 24. Deluca HF, Cantorna MT. Vitamin D: its role and uses in immunology. FASEB J. 2001;15:2579-85. 25. Holick MF. Vitamin D: A millenium perspective. J Cell Biochem. 2003;88:296-307. 26. Iqbal SJ, Kaddam I, Wassif W, Nichol F, Walls J. Continuing clinically severe vitamin D deficiency in Asians in the UK (Leicester). Postgrad Med J. 1994;70:708-14. 27. Datta S, Alfaham M, Davies DP, et al. Vitamin D deficiency in pregnant women from a non-European ethnic minority population--an interventional study. BJOG. 2002;109:905-8. 28. Shaw NJ, Pal BR. Vitamin D deficiency in UK Asian families: activating a new concern. Arch Dis Child. 2002;86:147-9. 29. Bates CJ, Prentice A, Cole TJ, et al. Micronutrients: highlights and research challenges from the 1994-5 National Diet and Nutrition Survey of people aged 65 years and over. Br J Nutr. 1999;82:7-15. 30. van der Wielen RP, Lowik MR, van den Berg H, et al. Serum vitamin D concentrations among elderly people in Europe. Lancet. 1995;346:207-10. 31. Scharla SH. Prevalence of subclinical vitamin D deficiency in different European countries. Osteoporos Int. 1998;8(Suppl 2:S7-12. 32. J. Ferlay, F. Bray, P. Pisani and D.M. Parkin. GLOBOCAN 2000: Cancer Incidence, Mortality and Prevalence Worldwide, Version 1.0. IARC CancerBase No. 5. Lyon, IARCPress, 2001. Limited version available from: URL: http://www-dep.iarc.fr/globocan/globocan.htm Last updated on 03/02/2001. (accessed Jan. 16, 2003). 33. Kirkpatrick CS, White E, Lee JA. Case-control study of malignant melanoma in Washington State. II. Diet, alcohol, and obesity. Am J Epidemiol. 1994;139:869-80. 34. Shors AR, Solomon C, McTiernan A, White E. Melanoma risk in relation to height, weight, and exercise (United States). Cancer Causes Control. 2001;12:599-606. 35. Seidell JC. Obesity: a growing problem. Acta Paediatr Suppl. 1999;88:46-50. 36. Andersen R, Brot C, Ovesen L. Towards a strategy for optimal vitamin D fortification (OPTIFORD). Nutr Metab Cardiovasc Dis. 2001;11(4 Suppl):74-7. Table 1. Incidence and mortality for cancers linked to UV-B radiation as risk (melanoma, however, UV-A (320-400 nm also plays a very important role)) or risk reduction factors for the U.K. in the mid-to-late 1990s (30). Cancer Type Incid. Mortal. Incid. Mortal. Males (cases) Females (cases) Melanoma 2398 769 3375 795 Bladder 9593 3670 3837 1795 Breast 34,815 14,415 Colorectal 17,249 9341 15,924 9,047 Endometrial 5000 1112 Esophageal 4264 4212 2800 2640 Gastric 6178 5101 3579 3199 NHL 4402 2414 3760 2131 Ovarian 6138 4560 Prostate 21,301 10,062 Renal 3356 1891 2007 1179 Totals 66,343 36,691 77,896 40,078 Preventable through UV-B and/or vitamin D - USA rates (16) 5300 2900 7800 4,000 Preventable through UV-B and/or vitamin D - estimated UK rates 8000 4500 12,000 6,000 Competing interests: None declared |
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CEDRIC F. Garland, PROFESSOR UNIV OF CALIF SAN DIEGO SCH OF MEDICINE 9500 GILMAN DRIVE LA JOLLA CALIFORNIA 92093-0631 USA
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The authors correctly conclude that sunscreens may create a false sense of security and encourage overexposure to the sun (1). Sunscreens certainly should not be relied upon for prevention of melanoma, as typical sunscreens have extremely poor absorption of UVA, which is 95% of UV radiation and is nearly as carcinogenic for melanocytes as UVB. The typical protection factor for UVA is 2-4 for the usual UVA-related compounds in sunscreens (2). This is true even if the SPF is 50 or higher, as UVA is not included in calculation of the SPF. The author's advice to avoid the sun certainly would not be the best strategy for reducing overall incidence of cancer in the UK. A recommendation for moderate exposure to the sun would be far more prudent. Solar exposure is the overwhelmingly main source of vitamin D. Vitamin D and its metabolites reduce the risk of cancers of the colon (3-6), breast (7-9), and prostate (10-11), and recent studies suggest that vitamin D may reduce the risk of other cancers (12). Since it was proposed in 1980 that vitamin D reduces risk of colon cancer, there have been 1,021 scientific papers indexed in the US National Library of Medicine MEDLINE database on the role of vitamin D in cancer control and prevention, including analysis of the mechanisms. Since the UK is located at northern latitudes, supplementation of the adult diet with vitamin D would be helpful, in addition to encouraging moderate exposure to the sun. Individuals at the latitudes of the UK cannot synthesize vitamin D from November through March, like residents of the the US Northeast (13). The half-life of the storage form of vitamin D (25(OH)2D) is only 12-22 days, so people become deficient by December and become increasingly deficient until March, if not supplemented. Residents of the UK should aim for 10-15 minutes a day in the sun when the weather allows, without sunscreen, to allow adequate synthesis of vitamin D. Such moderate exposures are unlikely to adversely influence the risk of melanoma or other skin cancers, but are likely to reduce the incidence of cancers of the colon, breast and prostate, among other non-cutaneous cancers. Vitamin D supplementation of children age one year and older and adults at a level of 400 IU per day (10 micrograms) would also be appropriate, and consistent with guidelines for avoidance of toxicity from the US National Academy of Sciences (15). Individuals aged 71 and older should receive 600 IU (15 micrograms) per day, due to poorer absorption and synthesis of vitamin D at older ages (15). Sunscreens should be used with caution until products are available that block UVA with the same degree of protection as UVB, and SPF should not be relied upon as an indicator of the safety of sunscreens. Future sunscreens should perhaps contain a moderate amount of vitamin D to counteract their abolition of vitamin D synthesis References 1. Garland CF, Garland FC, Gorham ED. Rising trends in melanoma: an hypothesis concerning sunscreen effectiveness. Annals of Epidemiology 1993;3: 103-10. 2. Diffey BL, Farr PM. UVA filters in sunscreen preparationsLancet 1989; 2: 170-1. 3. Garland CF, Garland FC. Do sunlight and vitamin D reduce the likelihood of colon cancer? International Journal of Epidemiology 1980; 9: 227-31. 4. Garland CF, Shekelle RB, Barrett-Connor E, et al. Dietary vitamin D and calcium and risk of colorectal cancer: a 19-year prospective study in men. Lancet 1985; 1: 307-9. 5. Garland CF, Comstock GW, Garland FC, Helsing KJ, Shaw EK, and Gorham ED. Serum 25-hydroxyvitamin D and colon cancer: eight-year prospective study. Lancet 1989; 2: 1176-8. 6. Tangrea J, Helzlsouer K, Pietinen P, Taylor P, Hollis B, Virtamo J, Albanes D, Serum levels of vitamin D metabolites and the subsequent risk of colon and rectal cancer in Finnish men. Cancer Causes and Control 1997;8:615-25. 7. Garland FC, Garland CF, Gorham ED, Young JF, Jr. Geographic variation in breast cancer mortality in the United States: a hypothesis involving exposure to solar radiation. Prev Med 1990;19:619-22. 8. Janowski EC, Lester GE, Weinberg CR, Millikan RC, Schildkraut JM, Garrett PA, Hulka BS. Association between low levels of 1,25-dihydroxyvitamin D and breast cancer risk. Publ Hlth Nutr 1999;2:283-91. 9. John EM, Schwartz GG, Dreon DM, Koo J. Vitamin D and breast cancer risk: The NHANES I epidemiologic follow-up study, 1971-1975 to 1992. Cancer Epidemiol Biomark Prev 1998;8:399-406. 10. Hanchette CL, Schwartz G. Geographic patterns of prostate cancer mortality: evidence for a protective effect of ultraviolet radiation. Cancer 1992;70:2681-9. 11. Ma J, Stampfer MJ, Gann PH, Hough HL, Giovanucci E, Kelsey KT, Hennekens CH, Hunder DJ. Vitamin D receptor polymorphisms, circulating vitamin D metabolites, and risk of prostate cancer in United States physicians. Cancer Epidemiol Biomarkers Prev 1998;7:385-90. 12. Grant WB. An estimate of premature cancer mortality in the U.S. due to inadequate doses of solar ultraviolet-B radiation. Cancer 2002: 94: 1867-75. 13. Webb AR, Kline L, Holick MF. Influence of season and latitude on the cutaneous synthesis of vitamin D3: exposure to winter sunlight in Boston and Edmonton will not promote vitamin D3 synthesis in human skin. J Clin Endocrinol Metab 1988; 67:373-8. 14. Haddad, JG, Jr., Rojanasathit S. Acute administration of 25-hydroxycholecalciferol in man. J Clin Endocrinol Metab 1976;42:284-90. 15. National Academy of Sciences–Institute of Medicine–Food and Nutrition Board. Dietary reference intakes for calcium, phosphorus, magnesium, vitamin D, and fluoride. Washington DC: National Academy Press, 1997. Competing interests: None declared |
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John N Burry, Retired Dermatologist PO Box 7177 Hutt Street PO Adelaide 5000 South Australia Australia
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Editor--Messages should certainly emphasize the need to cover up and stay out of the sun if skin cancer is to be prevented.1 Messages should also emphasize the biology of the condition. The message that those chosen by Darwinian natural selection to live in Australia have black skins, which protect them against skin cancer and those chosen by Darwinian natural selection to live in Europe have no such protection when living in Australia, is a message which is not commonly given probably because it would be unpopular. However it could well be a most effective educational tool. The skin of northern Europeans distributed throughout continents for which it was not chosen by natural selection may not be effectively protected unless fully protected by clothing, the equivalent of black skin. John N Burry 1 Fry A, Verne J. Preventing skin cancer (editorial). BMJ 2003; 326: 114-115 Competing interests: None declared |
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James A R Willis, writer/lecturer retired GP 28 Borovere Lane, Alton, Hants, GU34 1PB
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The statement that the incidence of melanoma in the United Kingdom has doubled over twenty years is inadequate to justify the conclusion of this editorial. We need to see the frequency as well. Obviously, doubling from 100 cases per thousand would be a stronger reason to argue for a change in the recreational habits of the population than a doubling from, say, 0.1 cases per thousand. Obsessional sun-avoidance (especially as practiced by some parents and education authorities on children) and the unprecedented use of potent sun-blocking creams, may have long-term adverse effects. There are reasons for guessing this might apply particularly towards the end of a full life- time. It would have been reassuring to have seen some indication that these possibilities had occurred to Fry and Verne before they contributed to both trends with their advice. Meanwhile their article provides no justification for departing from the traditional wisdom: 'Everything in moderation - a little of what you fancy does you good.' Competing interests: None declared |
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Phillip J. Colquitt, Independent Technical Advisor Independent
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The emphasis in Australia and other such sunburnt countries, should be on providing shade. This to be used as required by a sun-educated population. Not to mention the illness approach of diagnosing and treating sun affected persons, and the preventative approach of hats, sun screen and clothing[1]. It is not going too far to legislate shade into existence, as part of town planning. A whole Australian Government Department of Shade would be nice - politicians would be supportive, as they enjoy shade like none other. Most Australian live in towns and cities, not in cowboy country, and it is enjoyable to be at the beach, using the sunny sky for scenery. You don’t have to do the Apache torture routine-staked out and sizzling. Most over-baked people I see in downtown Brisbane are sun starved European tourists. [1] Alison Fry and Julia Verne Preventing skin cancer. BMJ 2003; 326: 114-115 Competing interests: None declared |
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Peter M Lapsley, Chief Executive, Skin Care Campaign Hill House, Highgate Hill, Lpndon N19 5NA
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Dear Sir Your contributors’ say that strategies to prevent skin cancer in the United Kingdom have not resulted in a tanned appearance becoming less fashionable. That is misleading. The Health Education Authority (HEA) spent up to £500,000 per annum on the Sun Know How Campaign (SKHC) which they ran for six years from 1994 until the dissolution of the HEA in March 2000. Just before the programme ended, its Director gave a presentation to the All Party Parliamentary Group on Skin. In it, he was able to show clearly that the programme had brought about substantial and positive attitudinal and behavioural change. As a direct result of the programme, people had become significantly more aware of the risks associated with UV exposure and significantly less preoccupied with tanning. At that stage, the SKHC programme ceased although the website was maintained, residual posters and other promotional materials continued to be available through Health Promotion England and the DH continued to fund the Meteorological Office to provide UV information for public weather forecasts in the summer. In 2002, the total spent by the government was just £50,000. As a result of pressure from the Skin Care Campaign, the Department of Health has now found £100,000 with which to fund a UV health promotion campaign in 2003/04. It will be managed for them by Cancer Research UK who will add a further £40,000 from their own funds. While seeing some progress in this field as being better than none, we have serious doubts as to the adequacy of the total sum being allocated to the campaign and, although UV health promotion is necessarily a long-term business, we have yet to receive any assurance of government commitment to proper funding of the campaign over time. At least as alarming as the government’s failure to have run a continuous and coherent UV health promotion programme are the implications for dermatology services of the growth in the incidence of skin cancer. At present, with approximately 100,000 new cases a year, most consultant dermatologists spend as much as fifty percent of their time treating skin cancers. Current forecasts suggest that there will be 300,000 new cases per annum in ten years time. If that is so, and if there is not significant investment in training and a commitment fully to fund new consultant dermatologist posts, secondary care dermatology services will be unable even to deal with skin cancer, let alone to treat patients with other skin diseases. Yours sincerely Peter Lapsley
Competing interests: None declared |
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