Preventing skin cancer
BMJ 2003; 326 doi: https://doi.org/10.1136/bmj.326.7381.114 (Published 18 January 2003) Cite this as: BMJ 2003;326:114All rapid responses
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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
Chief Executive
Skin Care Campaign
Competing interests:
None declared
Competing interests: No competing interests
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
Competing interests: No competing interests
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
Competing interests: No competing interests
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
Retired Dermatologist
PO Box 7177, Hutt St. PO, Adelaide, 5000. South Australia.
Australia
1 Fry A, Verne J. Preventing skin cancer (editorial). BMJ
2003; 326: 114-115
Competing interests:
None declared
Competing interests: No competing interests
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
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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
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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
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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
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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
Competing interests: No competing interests
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="ng" ml.="ml." serum="serum" testing="testing" for="for" _25ohd3="_25ohd3" levels="levels" is="is" now="now" readily="readily" available.="available." see="see" _36="_36" thoughts="thoughts" on="on" fortification="fortification" of="of" foods="foods" with="with" vitamin="vitamin" d.="d." p="p"/> References
1. Fry A, Verne J. Preventing skin cancer. BMJ. 2003;326:114-5
2. Dyer O. Sunlight prevents cancer, study says. BMJ
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4. Mehta RG, Mehta RR. Vitamin D and cancer. J Nutr Biochem.
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5. Van den Bemd CJCM, Chang GTG. Vitamin D and vitamin D analogs in
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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
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18. DNA spectral exposure (kJ/m2) for July 1992 (North America)
http://toms.gsfc.nasa.gov/ery_uv/dna_exp.gif (accessed January 16,
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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.
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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.
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36. Andersen R, Brot C, Ovesen L. Towards a strategy for optimal
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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
Competing interests: Table 1. Incidence and mortality for cancers linked to UV-B radiationas 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 795Bladder 9593 3670 3837 1795Breast 34,815 14,415Colorectal 17,249 9341 15,924 9,047Endometrial 5000 1112Esophageal 4264 4212 2800 2640Gastric 6178 5101 3579 3199NHL 4402 2414 3760 2131Ovarian 6138 4560Prostate 21,301 10,062 Renal 3356 1891 2007 1179Totals 66,343 36,691 77,896 40,078Preventable through UV-B and/or vitamin D - USA rates (16) 5300 2900 7800 4,000Preventable through UV-B and/or vitamin D - estimated UK rates 8000 4500 12,000 6,000
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
Competing interests: No competing interests
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
Competing interests: No competing interests
Re: Preventing skin cancer
Causes of regional differences in breast cancer prevalence are largely unknown (1). However many recent studies have come out with some clue about unknown factor/s. Caucasion women have by far the highest incidence of breast cancer, virtually twice as high as Asians and hispanics. The incidence of breast cancer is significantly lower in Japan, Thailand, Nigeria, and India compared to Denmark, New Zealand, U.K. and the United States. The difference is attributed partly to reproductive behaviors, diet and culture. There have been reports of greater breast cancer incidence and mortality at northern compared with southern latitudes postulated to be related to vitamin D exposure.
Recent study Among 71,662 participants in the Women's Health Initiative Observational Study (WHIOS) explored between incident invasive postmenopausal breast cancer (n = 2,535), over ∼8.6 years follow-up, and the following: (a) region of residence at birth, age 15 years, age 35 years; (b) region of residence at WHIOS baseline; and (c) clinic center solar irradiance. Hazard ratios and 95% confidence intervals (CI) for breast cancer were estimated after adjustment for individual level confounders. There was no difference in breast cancer risk by region of earlier life, baseline residence, or solar irradiance measured in Langelys (gm-cal) per cm2. There was an observed 15% decreased risk among women residing in areas of low versus high solar irradiance. Conversely, women who reported spending on average <30 minutes versus >2 hours outside in daylight year round at WHIOS year 4 follow-up (n = 46,926), had a 20% increased risk of breast cancer (2 & 3).
Countries those are having large incidence of basal cell carcinoma of skin, curtsey ultraviolet radiation and sun exposure, naturally studies done there largely concentrate on sun protection. Countries like India, where skin cancer is so negligible that only case reports are published, and no measurable prevalence, should draft their own guidelines for cancer prevention, specially in case of breast cancer, in view of its geographical location and reported difference of prevalence of this condition on regional basis with role of sun exposure (4-6).
References:
1. Regional Differences in Known Risk Factors and the Higher Incidence of Breast Cancer in San Francisco. Anthony S. Robbins and Jennifer L. Kelsey. JNCI J Natl Cancer Inst (1997) 89 (13): 960-965.
2. Incident Invasive Breast Cancer, Geographic Location of Residence, and Reported Average Time Spent Outside. Amy E. Millen, Mary Pettinger, Jo L. Freudenheim et al. Cancer Epidemiol Biomarkers Prev 2009;18:495-507.
3. Serum 25(OH) vitamin D and risk of breast cancer: a nested case-control study from the French E3N cohort. Engel P, Fagherazzi G, Boutten A et al. Cancer Epidemiol Biomarkers Prev. 2010 Sep;19(9):2341-50.
4. Serum 25-hydroxyvitamin D concentrations and postmenopausal breast cancer risk: a nested case control study in the Cancer Prevention Study-II Nutrition Cohort. McCullough ML, Stevens VL, Patel R Breast Cancer Res. 2009;11(4):R64.
5. Meta-analysis: serum vitamin D and breast cancer risk. Yin L, Grandi N, Raum E, Haug U et al. Eur J Cancer. 2010 Aug;46(12):2196-205.
6. Joint effects of dietary vitamin D and sun exposure on breast cancer risk: results from the French E3N cohort. Engel P, Fagherazzi G, Mesrine S et al. Cancer Epidemiol Biomarkers Prev. 2011 Jan;20(1):187-98.
Competing interests: No competing interests