Do white British children and adolescents get enough sunlight?
BMJ 2005; 331 doi: https://doi.org/10.1136/bmj.331.7507.3 (Published 30 June 2005) Cite this as: BMJ 2005;331:3All rapid responses
Rapid responses are electronic comments to the editor. They enable our users to debate issues raised in articles published on bmj.com. A rapid response is first posted online. If you need the URL (web address) of an individual response, simply click on the response headline and copy the URL from the browser window. A proportion of responses will, after editing, be published online and in the print journal as letters, which are indexed in PubMed. Rapid responses are not indexed in PubMed and they are not journal articles. The BMJ reserves the right to remove responses which are being wilfully misrepresented as published articles or when it is brought to our attention that a response spreads misinformation.
From March 2022, the word limit for rapid responses will be 600 words not including references and author details. We will no longer post responses that exceed this limit.
The word limit for letters selected from posted responses remains 300 words.
Edmonton, Alberta, Canada at Latitude 52 degrees north was compared
with Boston by Horlick some years ago. We can make vitamin D in our skin
from April to September, during noon plus or minus 2 hours. During the
rest of the year, the angle of the sun is too low to allow adequate UV-B
radiation to reach the earth, being absorbed by the ozone layer and
particulate matter. At 2000 ft altitude and low humidity, we have
everything going for us, but it's not enough!
In a study 2 years ago in the first 10 days of April in our centre, 34% of
children between 3 years and 17 years had levels of circulating 25(OH)D
below 40 nmol/l, and only 1 had a level above 80, now considered to be a
more appropriate "lower limit of normal". Fortified milk (400 IU per
litre)was the major contributor to blood levels of 25(OH)D, while outside
exposure in "sunny Alberta" played no apparent role. Within that group,
69% of the boys 9 - 16 yrs had levels below 40. It is absolutely
impossible to make sufficient D in the skin during our winter months that
are far sunnier than those of the UK.
Our native population including the Inuit survived by eating fish and the
fat including bone marrow from animals that contained vitamin D. Neither
the English nor Canadians consume adequate amounts of oily fish to supply
their vitamin D needs (1/2 a pound of Salmon per day would supply roughly
1000 IU, still only 30% of our estimated daily burn rate for D, (see
letters above).
55 years ago, my father bought an ultra-violet light and my sister and I
sat, naked, in front of it with goggles on (near Cookham Dean). Lawyers
are not known as visionaries, but he was clearly on to something!
Adrian B. Jones MD FRCPC
Refs Daniel E. Roth MD , Pat Martz RD, Rochelle Yeo RD, Connie
Prosser PhD, Melissa Bell RD, Adrian B. Jones MD. Vitamin D insufficiency
is common in Canadian children and adolescents: national guidelines
provide insufficient vitamin D to maintain adequate blood levels. Can J
Public Health 2005 In press
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; 67:373-378.
Competing interests:
None declared
Competing interests: No competing interests
Vitamin D supplied through exposure to natural sunlight versus the
dangers of skin cancers ? It is interesting to note that Vitamin D is mass
produced by irradiation (!) of sterols present in dairy products, fish and
eggs.
Whether the thinking ought to be "away from exposure to sunlight" as
Dr. Goldberg asserts is an unanswered question for many.
Here in Australia, the "slip, slop, slap" campaign started in the mid
eighties and, vigorously promoted since, has witnessed a doubling of
melanoma incidence in the last 20 years. So much for the dangers of
sunlight (as the short answer).
Humans, of course, have enormous genetic variability, and adaptation
to various environments has always been a pre-requisite to successful
migration on the planet.
One can also view this from a different angle. Was migration driven
by factors that would likely improve the lot of the "nomads" ?
Asking a geneticist would probably result in being pointed toward the
writings of William Loomis, who proposed in 1967 that the white skin of
Europeans has come about because of a lack of intense sunlight in Northern
regions, thus making it impossible for the skin to produce enough Vitamin
D.
This is also known as the Vitamin D Theory of Light Skin Colour.
While some considerable controversy surrounds the Postulates of Loomis it
is widely recognised that sun exposure is an important if not essential
source of Vitamin D.
As to the children of England who are not keen to have their cod
liver oil or other food source of Vitamin D would the benefits of sun
exposure (and an annual trip to the shores of a tropical land)outweigh the
perceived dangers of UV radiation?
Evidence is emerging that conditions such as melanoma, other sun-
related damage to skin and such illnesses as macular degeneration may be
caused or partially caused by the excessive intake of polyunsaturated oils
(PUFA's). The thought occurs whether the intake of PUFA's might be
directly responsible or exert its influence by "crowding" out the animal
fats containing Vitamin D.
While the jury is not in on that question either, the vast majority
of fast food outlets in Queensland, Australia did switch from animal fats
to PUFA's 15-20 years ago.
Overall, I do not hold to the belief that Mother Nature can be seen
as the greatest bumbling idiot(esse) of all times, having created another
monster, and I still believe in the words rise and shine, by which I am
referring to the sun.
It seems to me that a dermatologist would tend to see the sunlight as
the enemy and might therefore even fall into the trap of recommending
PUFA's rich in Vitamin D (there aren't many).
If he also subscribes to the current dogma of low fat eating he could
compound the problem as poor fat absorption (or supply) may result in
Vitamin D deficiency.This deficiency is emerging as an important
contributor to heart disease, certain cancers and other modern
"nutritional diseases".
Good sources of Vitamin D are Dairy products, Cod Liver Oil, Fish and
many animal products.Last but not least, Vitamin D is a cousin to the
bogeyman cholesterol.
Competing interests:
None declared
Competing interests: No competing interests
The history of vitamin D deficiency in this country is long and
unfortunate. Rickets was endemic in mid-17th century England and remained
so for more than 250 years, during which time the primary factor in the
aetiology of the disease - sunlight deprivation - was overlooked. [1-3]
Following the belated recognition in 1921 that the sun's UV rays could
prevent and cure rickets [4], sunbathing was promoted as a form of
preventive medicine and parents were
encouraged to put their off-spring out in the sun. [5]
Today they are told not to and, unfortunately, vitamin D deficiency
has re-emerged as a global health problem
among infants; as it has amongst the elderly and other groups. [6,7]
Public health campaigns which focus on the dangers of sunbathing while
ignoring the benefits must have contributed to this. Certainly the
assertion that casual exposure to the sun in the summer provides
sufficient stores of the vitamin to last through the winter, and that
additional exposures will not confer further benefit, [8,9] appears to be
contrary to the facts. [10-16] The importance of solar UVR as the
principal source of vitamin D has been, and continues to be, greatly
underestimated. It seems that those who cannot learn from public health
disasters of the past are condemned to repeat them.
1. Glisson, F. A treatise of the rickets being a disease common to
children. London. 1668.
2. Findlay L et al. A study of social and economic factors in the
causation of rickets. Medical Research Committee
Special Report 20. Galston and Sons. London. 1918. p43.
3. Hess AF. Rickets. Henry Kimpton. London. 1930.
4. Hess AF and Unger LJ. The cure of infantile rickets by sunlight. J
Am Med Assoc 1921;77(1):39.
5. Park EA. The therapy of rickets. JAMA 1940;115(5):370-9.
6. Plehwe WE. Vitamin D deficiency in the 21st century: an
unnecessary pandemic? Clin Endocrinol 2003 Jul;59(1):22-4.
7. Richardson JP. Vitamin D deficiency - the once and present
epidemic. Am Fam Physician. 2005 Jan 15;71(2):241-2.
8. National Radiological Protection Board. Report of the Advisory
Group on Non-ionising Radiation (AGNIR): Effects of ultraviolet radiation
on human health. Documents of the NRPB 2002;13(1). p.214-5.
9. Ibid. p7.
10. Working Group of the Australian and New Zealand Bone and Mineral
Society, Endocrine Society of Australia and
Osteoporosis Australia. Vitamin D and adult bone health in Australia and
New Zealand: a position statement. Med J
Aust 2005 Mar 21;182(6):281-5.
11. Glerup H, Mikkelsen K et al. Commonly recommended daily intake of
vitamin D is not sufficient if sunlight
exposure is limited. J Intern Med 2000;247:260-268.
12. Barger-Lux MJ and Heaney RP. Effects of above average summer sun
exposure on serum 25-Hydroxyvitamin D
and calcium absorption. J Clin Endocrinol Metab 2002 Nov; 87(11):4952-6.
13. Heaney RP, Davies KM, Chen TC, Holick MF, Barger-Lux MJ. Human
serum 25-hydroxycholecalciferol response to
extended oral dosing with cholecalciferol. Am J Clin Nutr 2003
Jan;77(1):204-10.
14. Outila TA, Karkkainen MU, Seppanen RH, Lamberg-Allardt CJ.
Dietary intake of vitamin D in premenopausal,
healthy vegans was insufficient to maintain concentrations of serum 25-
hydroxyvitamin D and intact parathyroid
hormone within normal ranges during the winter in Finland. J Am Diet Assoc
2000;100(4):434-41.
15. Veith R, Cole DE, Hawker GA et al. Wintertime vitamin D
insufficiency is common in young Canadian women, and
their vitamin D intake does not prevent it. Eur J Clin Nutr 2001; 55:1091-
7.
16. Lehtonen-Veromaa M, Mottonen T, et al. Vitamin D intake is low
and hypovitaminosis D common in healthy 9- to 15-year old Finnish girls.
Eur J Clin Nutr 1999; 53(9): 74-76.
Competing interests:
None declared
Competing interests: No competing interests
I’ve been surfing in Australia(and currently in QLD) for about forty
years and my recent mole scan says I don’t have anything remotely
resembling a melanoma. My surfing “associates” don’t seem to have melanoma
either, though they spend hours everyday in the water getting sun
exposure, and do get health problems related to surfing[1]. Why aren’t
surfers in Queensland, the world’s melanoma capital, showing the highest
incidence of melanoma in the world?
My watch band skin is “white”[white people are really pink] in
contrast to my otherwise tanned skin. If I forget the watch, skin in that
area gets burned, while the tanned area remains completely comfortable,
seemingly protected by tan. Tan happens for a reason, not just because
God prefers dolphins over dermatologists.
[1] Hurst W, Bailey M, Hurst B. Prevalence of external auditory
canal exostoses in Australian surfboard riders. J Laryngol Otol. 2004
May;118(5):348-51.
Competing interests:
None declared
Competing interests: No competing interests
deaths are not
caused by melanoma, as per CancerResearchUK.org.uk. Should one
therefore not first determine if improved sun-derived vitamin D
status improves general health and reduces all-cause deaths and all-cause cancer mortality before
advocating sun avoidance?
The CancerResearchUK.org programme SunSmart.org
recognises this pesky factoid in a 'brief holding statement'
[sic]. Yet, and potentially doing harm first and their website looking
like an advertisement for hats, they advise sun avoidance between 11 and
3, and 'a high factor sunscreen when shade or clothing are not
practical options.'
Wasn't there a time when dogs and Englishmen were known for being out
in the midday sun when the 'natives' were already vitamin D replete? [ref.
Noel Coward, 1932: text
or sung]
Competing interests:
None declared
Competing interests: No competing interests
Brian Diffey(1) suggests that exposure of hands, arms and face to
the sun for a short time two or three times a week in autumn, spring or
summer may provide a person in the UK with enough vitamin D to last
throughout the year. However Diffey has used too low a figure for the
daily vitamin D requirement and has failed to budget for this requirement
on an annual basis, a procedure which is necessary because of seasonal
differences in vitamin D synthesis in the skin.
In fact it is not possible to obtain a sufficient, healthy, level of
vitamin D in the UK if Diffey’s recommendations, which are similar to
those of the SunSmart programme run by Cancer Research UK, are followed.
That is why I have suggested, as noted by Diffey in your editorial, that
the SunSmart programme should be abandoned(2,3).
Diffey reasons that weekly exposure of arms, hands and face may be
relied upon to produce a total of 1 MED per week (MED = minimal erythemal
dose – just enough sun exposure to redden the skin)(1). However in the UK
this is only possible in those weeks in which the sun is strong and the
sky is clear of cloud.
In the UK the sun is not strong enough between the end of September
and the end of March to produce any significant amount of vitamin D(4).
Furthermore many of the weeks when the sun is strong in the northern
hemisphere (beginning of April to the end of the September) will be cloudy
and overcast in the UK preventing any useful sunlight reaching ground
level. And even when the sun is strong people are often working and
unable to be outside. So over the period of a year a person in the UK
will be lucky to be exposed to strong sun for one week out of three or
four. If this is so then Diffey’s figure for adequate weekly exposure to
sunlight (when possible) should be multiplied by three or four to allow
for sunless weeks.
However another error enters Diffey’s calculations when he assumes
that 600 to 1000 IU vitamin D per week (supplied by 1 MED of sunlight
reaching hands, arms and face) provides enough vitamin D from the sun for
optimum health(1). Such a dose will do little more than prevent rickets
and gross osteomalacia and is likely to leave a person vulnerable to other
disease in particular cancer. Recent research by Heaney and others in
Omaha and Boston suggests that between 3,000 and 5,000 IU vitamin D is
needed daily by an adult for optimum health(5).
The human vitamin D requirement needs to be considered over the
period of a year because vitamin D is stored during the summer months in
the body and used in the winter. If we take Heaney’s lower figure of 3,000
IU as the optimum daily requirement of vitamin D then the requirement over
the period of a year is 1,095,000 IU. Diet can provide only a very small
portion of this, less than 200 IU per day or 73,000 IU per year(5). The
remainder, 1,022,000 IU, must be obtained from supplements or from the
sun.
Vitamin D supplements sold over the counter in the UK supply
relatively small quantities of the vitamin which are insufficient to
substantially increase blood levels. Prescription products for vitamin D
in the UK all consist of vitamin D2 (ergocalciferol) which has a potency
about one third that of vitamin D3(6). So prescription products prescribed
in recommended quantities in the UK are also likely to be ineffective in
raising blood levels of D substantially.
In sunny countries sun exposure is the easiest way to obtain the
major part of the vitamin D requirement. This is the natural way to obtain
vitamin D and the way that people like to obtain it if they are able to
and are not discouraged. The only other way is to buy high dose vitamin D
tablets through the internet.
But is it possible to obtain an optimum annual dose of vitamin D,
that is 1,022,000 IU or more, by sun exposure in the UK? The sun is
generally strong enough in South East England to provide at least some
useful vitamin D for 26 weeks between the first week of April and last
week of September. However April is generally too cold for sunbathing, and
throughout the summer cold winds or cloud frequently prevent sunbathing in
south east England. The summer season is substantially shorter in Scotland
where, in addition, the sun is less intense and there are more cold days.
Casual exposure of the hands, arms and face two or three times a
week, as suggested by Diffey using Holick’s criteria(1,7) might supply 1
MED to an adult in southern England, weather and time permitting. This
will supply up to 26,000 IU of vitamin D. If the casual exposure of hands,
arms and face could be increased from three to seven times per week then
61,000 IU could be obtained. This still leaves our subject with another
961,000 IU to find for optimum health.
In fact it makes no sense to try to increase vitamin D intake simply
by increasing exposure of hands, arms and face. Excessive sun exposure may
cause skin aging and so it is preferable, as in radiology, to spread the
dose. In this case the dose may be spread over all parts of the body by
active sunbathing while protecting the face which tends to get over-
exposed. Failure to recognise the advantage of spreading the UV dose over
the whole body is another flaw in the SunSmart programme.
Active sunbathing which exposes the whole body can supply up to
10,000 IU per day(7,8). To obtain something approaching the optimum annual
amount of vitamin D a person would have to sunbathe in a swimming suit on
about 100 sunny summer days. This is, for practical purposes, impossible
in the UK even for a dedicated nudist. There are about 182 days (26 weeks)
when the sun is potentially strong enough for sunbathing in the UK, but in
less than half of these will the sky be clear and the air warm enough for
sunbathing.
A British sunbather, who is able to take time off work when the sun
is shining brightly, might be able to sunbathe on 36 days in the year.
This would probably be enough to provide a sub-optimum, but possibly safe,
average blood level (higher in summer, lower in winter) of about 72 nmol/l
of 25-hydroxycholecalciferol, equivalent to a daily dose of 1000 IU
vitamin D.
Any discouragement from sunbathing in the middle of the day when
vitamin D production from the sun is most efficient will prevent
achievement of a safe blood level of vitamin D and is likely to have a
detrimental effect on health of people in the UK. So the SunSmart
programme, which forbids sun exposure in the middle of the day, is ill-
suited to our climate. SunSmart is based on an Australian model and may
possibly be suited to that climate but is completely unsuited to British
weather.
If the assumptions made here are correct, these figures illustrate
three points:
a) the SunSmart recommendation that 10 to 15 minutes of sun on the face,
arms and hands two or three times a week is sufficient for good health in
the UK does not even provide minimum requirements of vitamin D, b) in the
UK it is necessary to sunbathe whenever possible wearing as few clothes as
possible if an amount of vitamin D approaching the optimum requirement is
to be obtained, c) it is not possible for someone living in the UK to
obtain a fully optimum dose of vitamin D from the sun alone.
Northern Europe is an extreme climate for man. Human beings evolved
in tropical Africa where the sun shines strongly every day. The evolution
of white skin, which allows more rapid utilisation of UV rays from the sun
and greater synthesis of vitamin D, shows how important this vitamin is
for general health and Darwinian reproductive fitness. Furthermore the
cloudy maritime weather of the British Isles makes our climate one of the
most extreme in Europe so far as sun deprivation is concerned.
Telling people to avoid the sun in the middle of day and to avoid
tanning, which is an inevitable and normal consequence of sun exposure,
makes our climate even more extreme. Such advice, as provided by SunSmart,
will lead to insufficient levels of vitamin D unless a supplement is also
taken, or an Inuit diet is followed – that is a diet consisting of oily
fish or seal meat at every meal.
The low levels of vitamin D that may be expected to follow adherence
to the SunSmart advice carry potential risks(9). Increasing evidence
suggests that vitamin D plays a part in preventing a wide range of cancers
with particularly strong evidence showing that vitamin D protects against
the most common cancers, those of the breast, bowel, prostate and lymph
glands(10-16). There is also evidence that vitamin D is important in
protecting against multiple sclerosis(17-19), diabetes(20),
hypertension(21) and a multitude of other ills(3).
Further fortification of foods with vitamin D in the UK is desirable
but is not likely to happen in the near future and is unlikely ever to
provide the complete requirement of vitamin D. So in the UK sunbathing is
the easiest way to obtain levels of vitamin D that may protect against
these diseases.
The benefit of sunbathing must be set against any risks of sun
exposure. Skin cancer is very common in the UK, as elsewhere, but deaths
from skin cancer are relatively rare compared with deaths from other
cancers. Most skin cancer deaths are accounted for by melanoma which seems
to occur less frequently in people who work outdoors and have regular
exposure to the sun(22,23). Longer lifetime sun exposure has been found to
be associated with lower risk of melanoma(24). So the risk of melanoma
from sun exposure appears to be associated with irregular intense exposure
of unconditioned skin, and possibly burning, rather than regular exposure
to the sun which seems to be protective(25). Diet may also be a factor in
melanoma as it is in other cancers(26,27).
The risks of insufficient vitamin D, although difficult to quantify
exactly, would seem to far outweigh risks from excessive sun exposure(9).
Careful sunbathing, taking care to avoid burning, may carry very little
extra risk and may in fact protect against melanoma as well as other
cancers. Exposure to the sun is a part of life for people living in
traditional rural societies. Thus the onus is upon those who recommend
additional sun avoidance in our already highly artificial lifestyle to
show that the changes they recommend improve the balance of risks and
benefits. Those who have promoted the SunSmart programme in the UK have
yet to publish an adequate rationale for their policy.
Oliver Gillie BSc PhD
Health Research Forum
(www.healthresearchforum.org.uk)
68 Whitehall Park, London N19 3TN
Telephone: 020 7561 9677
References:
1. Diffey, B. Do white British children and adolescents get enough
sunlight? British Medical Journal 331, 3-4 (2005).
2. Gillie, O. Sunny D. The Independent on Sunday, Sunday Review, 8-12
(2004).
3. Gillie, O. Sunlight Robbery: Health Benefits of sunlight are
denied by current public health policy in the UK. Health Research Forum
Occasional Reports 1, 1-42 (2004).
4. 41-43 (Committee on Medical Aspects of Food Policy (COMA),
Department of Health, UK, London, 1998).
5. Heaney, R., Davies, K., Chen, T., Holick, M. & Barger-Lux, M.
Human serum 25-hydroxycholecalciferol response to extended oral dosing
with cholecalciferol. Am J Clin Nutr 77, 204-210 (2003).
6. Trang, H. M. et al. Evidence that vitamion D3 increases serum 25-
hydroxyvitamin D more efficiently than does vitamin D2. Am J Clin Nutr 68,
854-8 (1998).
7. Holick, M. F. Sunlight "D"ilemma: risk of skin cancer or bone
disease and muscle weakness. Lancet 357, 4-6 (2001).
8. Vieth, R. Vitamin D supplementation, 25-hydroxyvitamin D
concentrations, and safety. Am J Clin Nutr 69, 842-56 (1999).
9. Garland, C. F. More on preventing skin cancer: Sun avoidance will
increase overall cancer incidence. British Medical Journal 327, 1228
(2003).
10. Grau, M., Baron, J., Sandler, R. & al, e. Vitamin D, calcium
supplementation, and colorectal adenomas: results of a randomised trial. J
Natl Cancer Inst 95, 1765-71 (2003).
11. Peters, U., McGlynn, K., Chatterjee, N. & al, e. Vitamin D,
calcium, and vitamin D receptor polymorphism in colorectal adenomas.
Cancer Epidemiol Biomarkers Prev 95, 1267-71 (2001).
12. Emerson, J. & Weiss, N. Colorectal cancer and solar
radiation. Cancer Causes Control 3, 95-9 (1992).
13. Grant, W. & Garland, C. A critical review of studies on
vitamin D in relation to colorectal cancer. Nutr Cancer in press (2004).
14. Pritchard, R. S., Baron, J. A. & Gerhardsson de Verdier, M.
Dietary calcium, vitamin D, and the risk of colorectal cancer in
Stockholm, Sweden. Cancer Epidemiol Biomarkers Prev 5, 897-900 (1996).
15. White, E., Shannon, J. S. & Patterson, R. E. Relationship
between vitamin and calcium supplement use and colon cancer. Cancer
Epidemiol Biomarkers Prev 6, 769-74 (1997).
16. John, E. M., Schwartz, G. G., Dreon, D. M. & 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 8, 399-406 (1999).
17. Goldacre, M., Seagrott, V., Yeates, D. & al, e. Skin cancer
in people with multiple sclerosis: a record linkage study. J Epidemiology
Community Health 58, 142-4 (2004).
18. Willer, C., Dyment, D., Sadovnick, A., Rothwell, P. & Ebers,
G. Timing of birth influences multiple sclerosis susceptibility: the
Canadian Collaborative Study Group. manuscript (2004).
19. Embry, A., Snowdon, L. & Vieth, R. Vitamin D and seasonal
fluctuations of gadolinium-enhancing magnetic resonance imaging lesions in
multiple sclerosis. Ann Neurol 48, 271-2 (2000).
20. Boucher, B. J. Inadequate vitamin D status: does it contribute to
disorders comprising syndrome 'X'? British Journal of Nutrition 79, 315-
327 (1998).
21. Pfeiffer, M., Begerow, B., Minne, H. & al, e. Effects of a
short-term vitamin D3 and calcium supplementation on blood pressure and
parathyroid hormone levels in elderly women. Journal of Clinical
Endocrinology and Metabolism 86, 1633-1667 (2001).
22. Hakansson, N., Floderus, B., Gustavsson, P., Feychting, M. &
Hallin, N. Occupational sunlight exposure and cancer incidence among
Swedish construction workers. Epidemiology 12, 552-7 (2001).
23. Garland, F. C., White, M. R., Garland, C. F., Shaw, E. &
Gorham, E. D. Occupational sunlight exposure and melanoma in the U.S.Navy.
Archives of Environmental Health 45, 261-7 (1990).
24. Kennedy, C., Bajdil, C. D., Willemze, R., de Gruijl, F. R. &
Bavinck, J. N. B. The influence of painful sunburns and lifetime sun
exposure on the risk of actinic keratoses, seborrheic warts, melanocytic
nevi, atypical nevi, and skin cancer. Journal of Investigative Dermatology
120, 1087-1093 (2003).
25. Elwood, J. Melanoma and sun exposure. Seminars in Oncology 23,
650-666 (1996).
26. Shors, A. R., Solomon, C., McTiernan, A. & White, E. Melanoma
risk in relation to height, weight, and exercise (United States). Cancer
Causes Control 12, 599-606 (2001).
27. Kirkpatrick, C. S., White, E. & Lee, J. A. Case-control study
of malignant melanoma in Washington State. II. Diet, alcohol, and obesity.
Am J Epidemiol 139, 869-80 (1994).
Competing interests:
None declared
Competing interests: No competing interests
The editorial on sunlight [1] downplays a growing body of evidence
showing the health benefits of solar ultraviolet-B (UVB) irradiance in
reducing the risk of cancer, multiple sclerosis, and a number of other
diseases and conditions. This editorial appears to have been written to
defend advice on sunlight avoidance developed before recent evidence on
the health benefits of solar irradiance became well known. A new approach
is now needed that makes best use of solar irradiance for optimal health.
The author and Cancer Research UK (CRUK) need to be more aware of risks
associated with sun avoidance and that the current sunlight policy in the
UK (SunSmart programme) probably has a net negative effect on total
health.
So, what is this new evidence? Regarding cancer, many papers have
reported inverse correlations between solar UVB irradiance and vitamin D
and cancer mortality rates [2-7]. Some of those that did not were not
considering serum 25-hydroxyvitamin D (25(OH)D) levels high enough to have
a demonstrable effect on cancer risk [8]. In addition, there is
increasing evidence that vitamin D is very useful in increasing survival
rates once cancer has been discovered. Two studies in Norway found that
those whose cancer was discovered in summer or fall lived longer than
those whose cancer was discovered in winter or spring [9,10]. A study in
the U.S. of those diagnosed with non small-cell lung cancer found a factor
-of-2 difference in 5-year survival rate for low vs. high vitamin D index
[11].
There are also a number of papers showing similar effects for
multiple sclerosis [12-14].
While Prof. Diffey and CRUK may consider the evidence regarding UVB
irradiance and vitamin D and cancer weak, the evidence does satisfy the
criteria for causality in a biological system as stated by Sir Austin
Bradford Hill in 1965 [15]. The more important criteria are 1 - strength
of association, 2 - consistency among different populations, 3 - the
understanding of mechanisms, 4 - accounting for confounding factors, and 5
- generally a linear dose-response relationship. These criteria are well
satisfied for UVB/vitamin D and cancer: 1 – the strength is high in
studies where 25(OH)D levels were high enough [8]; 2 – similar effects
have been observed in Australia [5], Canada [16], Japan [17], Norway
[9,10], the USSR [18], and the US [3]; 3 – the mechanisms are well
understood, and include inhibition of angiogenesis around tumors and
metastasis [19,20]; 4 – confounding factors have now been included in the
analyses [4, 21, Grant and Garland, in prep]; and 5 – there are generally
quasi-linear dose response curves for almost all cancers except prostate
cancer, for which both low and high values of serum 25(OH)D are associated
with increased risk [22, 23]. What is lacking are large-scale prospective
studies and intervention studies. Such studies are very likely in
progress.
So, how much could higher levels of serum 25(OH)D in the UK reduce
cancer mortality rates? An analysis of the geographic variation of cancer
mortality rates in the U.S. indicates that there are about 50,000-60,000
premature cancer deaths per year due to insufficient UVB and/or vitamin D
[24, Grant, Garland, and Holick, submitted]. These numbers represent
about 10% of all cancer deaths. By looking at the latitudinal variation
of vitamin D-sensitive cancer mortality rates for eastern U.S. states,
Canada, France, Germany, Ireland, and the UK, it is estimated that 20% of
cancer deaths in the UK or about 30,000 deaths per year could be
considered premature due to insufficient vitamin D [Grant, unpublished].
In summary, there is strong scientific evidence that vitamin D is
associated with reduced risk of cancer death. Since serum 25(OH)D levels
in the UK tend to be lower than in the U.S. due to lower oral intake and
UVB irradiance, there is a great opportunity to improve the overall health
status of the British by public policies that seek to increase, rather
than decrease, the serum 25(OH)D levels since there are many health
benefits of vitamin D [25-27]. While Prof. Diffey and CRUK are correct
that UV irradiance is a risk factor for skin cancer and melanoma, the risk
of death from these cancers is much lower than the risk of death from
vitamin D-sensitive cancers such as bladder, breast, colorectal, gastric,
ovarian, prostate, and renal cancer.
My suggestion is that vitamin D be recognized as an important risk
reduction factor for cancer incidence and mortality, with vitamin D oral
intake or photoproduction required year round. Associated policy changes
would also entail fortifying foods such as bread and milk with vitamin D,
making 1000 I.U. (40 micrograms) vitamin D3 capsules available, and
promulgating reasonable solar UVB irradiance guidelines such as
recommending midday irradiance when UVB levels are highest and irradiance
times can be reduced, and publishing vitamin D production forecasts [28].
For UV irradiance, it is important to consider one’s skin type in deciding
an appropriate irradiance schedule, to avoid burning and excess tanning,
and strive for a good antioxidant status, e.g., low-fat, high fruit and
vegetable diet [29].
For more information on the health benefits of UVB and vitamin D,
please visit www.sunarc.org.
References
1. Diffey B. Do British children and adolescents get enough sunlight?
BMJ 2005;331:3-4.
2. Garland CF. More on preventing skin cancer: sun avoidance will
increase incidence of cancers overall. BMJ. 2003;327:1228.
3. Grant WB. An estimate of premature cancer mortality in the United
States due to inadequate doses of solar ultraviolet-B radiation. Cancer.
2002;94:1867-75.
4. 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.
5. Hughes AM, Armstrong BK, Vajdic CM, et al. Sun exposure may
protect against non-Hodgkin lymphoma: a case-control study. Int J Cancer.
2004;112:865-71.
6. Smedby KE, Hjalgrim H, Melbye M, et al. Ultraviolet radiation
exposure and risk of malignant lymphomas. J Natl Cancer Inst. 2005;97:199-
209.
7. John EM, Dreon DM, Koo J, Schwartz GG. Residential sunlight
exposure is associated with a decreased risk of prostate cancer. J Steroid
Biochem Mol Biol. 2004;89-90:549-52.
8. Grant WB, Garland CF. A critical review of studies on vitamin D in
relation to colorectal cancer. Nutr Cancer, 2004;48:115-23.
9. Robsahm TE, Tretli S, Dahlback A, Moan J. Vitamin D3 from sunlight
may improve the prognosis of breast-, colon- and prostate cancer (Norway).
Cancer Causes Control. 2004;15:149-58.
10. Moan J, Porojnicu AC, Robsahm TE, et al. Solar radiation, vitamin
D and survival rate of colon cancer in Norway. J Photochem Photobiol B.
2005;78:189-93.
11. Zhou W, Suk R, Liu G, et al. Vitamin D predicts overall survival
in early stage non-small cell lung cancer patients. Am. Assoc. Cancer Res.
Annual Meeting, Abstract LB-231, 2005.
12. Freedman DM, Dosemeci M, Alavanja MC. Mortality from multiple
sclerosis and exposure to residential and occupational solar radiation: a
case-control study based on death certificates. Occup Environ Med.
2000;57:418-21.
13. van der Mei IA, Ponsonby AL, Blizzard L, Dwyer T. Regional
variation in multiple sclerosis prevalence in Australia and its
association with ambient ultraviolet radiation. Neuroepidemiology.
2001;20:168-74.
14. Goldacre MJ, Seagroatt V, Yeates D, Acheson ED. Skin cancer in
people with multiple sclerosis: a record linkage study. J Epidemiol
Community Health. 2004;58:142-4.
15. Hill AB. The environment and disease: Association or causation?
Proc R Soc Med. 1965;58:295-300.
16. Gorham ED, Garland CF, Garland FC. Acid haze air pollution and
breast and colon cancer mortality in 20 Canadian cities. Can J Public
Health. 1989;80:96-100.
17. Mizoue T. Ecological study of solar radiation and cancer
mortality in Japan. Health Phys. 2004;87:532-8.
18. Gorham ED, Garland FC, Garland CF. Sunlight and breast cancer
incidence in the USSR. Int J Epidemiol. 1990;19:820-4.
19. van den Bemd GJ, Chang GT. Vitamin D and vitamin D analogs in
cancer treatment. Curr Drug Targets. 2002;3:85-94.
20. Lamprecht SA, Lipkin M. Chemoprevention of colon cancer by
calcium, vitamin D and folate: molecular mechanisms. Nat Rev Cancer.
2003;3:601-14.
21. Grant WB. Benefits of UVB exposure to reduce the risk of cancer –
ecologic studies of cancer mortality rates. Proceedings of the CIE
Symposium ’04; Light and Health: non-visual effects, 30 Sep.-2 Oct. 2004,
Commission International de L’Eclairage, Vienna, Austria, 2004:174-177.
22. Tuohimaa P, Tenkanen L, Ahonen M, et al. Both high and low levels
of blood vitamin D are associated with a higher prostate cancer risk: a
longitudinal, nested case-control study in the Nordic countries. Int J
Cancer. 2004;108:104-8.
23. Grant WB. Geographic variation of prostate cancer mortality rates
in the United States: Implications for prostate cancer risk related to
vitamin D. Int J Cancer. 2004;111:470-1.
24. Grant WB. Insufficient sunlight may kill 45,000 Americans each
year from internal cancer. J Cos Dermatol. 2004;3:176-8.
25. Holick MF. Sunlight and vitamin D for bone health and prevention
of autoimmune diseases, cancers, and cardiovascular disease. Am J Clin
Nutr. 2004;80:1678S-88S.
26. Ustianowski A, Shaffer R, Collin S, Wilkinson RJ, Davidson RN.
Prevalence and associations of vitamin D deficiency in foreign-born
persons with tuberculosis in London. J Infect. 2005;50:432-7.
27. Grant WB, Holick MF. Benefits and requirements of vitamin D for
optimal health: a review. Altern Med Rev. 2005;10:94-111.
28. Schmalwieser A, private communication (alois.schmalwieser@vu-
wien.ac.at)
http://i115srv.vu-wien.ac.at/uv/uv_online.htm (accessed July 1, 2005)
29. Millen AE, Tucker MA, Hartge P, et al. Diet and melanoma in a
case-control study. Cancer Epidemiol. Biomarkers Prev. 2004;13:1042-51.
Competing interests:
None declared
Competing interests: No competing interests
Is it not time for dermatologists stay out of the vitamin
D issue? One should realize that every cell type has vitamin D receptors
and therefore a vital need for this calcium, cell and DNA regulator that
protects us from heart disease and cancers, as well as assuring bone health.
To this humble observer, there may just be a reason there
are predominantly white hairless humans North of the 45th parallel since
our dark-skinned female ancestors moving North may have died off in child
birth from bone deformities --unless they had a fish-oil based source of
vitamin D.
Dermatologist Goldberg clearly misses the raison d'être
of 'light skinned' people he warns away from sun exposure: this is to allow
every cell type to get UV-B derived vitamin D, i.e. "sun damaged" cholesterol.
His suggestion for mankind to rely on fortified milk or
orange juice is bizarre since a safe and fee source of vitamin D (and of
which overdose has never been shown) is available to most of us. vos{at}health-heart.org
Competing interests:
None declared
Competing interests: No competing interests
Dietary vitamin D supplementation is so easy to achieve and innocuous
to administer, espescially in milk or orange juice. There is no advantage
to trying to supply vitamin D needs through sunlight exposure. The
regulation of this exposure is crude and difficult. Sunlight is inherently
dangerous in light skinned relatively sun-sensitive people. The thinking
must be away from sunlight towards dietary regulation.
Leonard H Goldberg FRCP
Goldb1@aol.com
Competing interests:
None declared
Competing interests: No competing interests
Is The Sub-Optimal Health Status Shifting to Chronic Diseases Pathway….?
Dear Editor,
The suboptimal health or sub-health status also known as sub-optimal health status (SHS)[1], is the physical state of people which is generally undiagnosed[2], however, some changes in psychological behavior or physical characteristics can be observed [3]. SHS is a new health dimension for translation medicine [4]. In fact, SHS is an intermediate state between health and disease condition [4], where no any organic lesions appear in the body, only characterized by persistent and recurrent fatigue, headaches, dizziness, anxiety, depression, as well as a series of symptoms including non-specific pain and sleep disorders [5]. It has approved that SHS is an intermediate state between health and disease, which is due to the physical, psychological, and social stress of an individual[2,5–8]. Due to that the overall coordination of the body system becomes imbalance and dysfunction, e.g. the nervous system, endocrine system, digestive system, and immune system which lead to the decline of physiological, psychological, and social functions, however, the body has not yet reached the disease stage[4,9]. Therefore, SHS is now regarded as a subclinical, reversible stage of pre-chronic diseases[1,4,10]. Similarly, SHS has also been recognized as a potential risk factor and close association for chronic diseases such as type-II diabetes mellitus, cardiovascular diseases and stroke [4,5,10,11]. Thus, SHS has been recognized as a public health challenge globally [5,7,11,12]
The number of studies have revealed that SHS mainly influence by lifestyle factors[2,6,13], these factors have a close relationship with psychological symptoms or behavior of individuals[8,14]. Over time, with the rapid development of technology and changes in the environment and lifestyles of people, the risk of SHS has consistently been increasing in society[5]. Besides, the scientist believes that the changes of the living environment, over work-load, interpersonal relationship, lack of sleep time, excessive psychological stress, unbalanced diet, and an inappropriate exercise may lead to the formation of SHS, where others reported that socio-cultural factors are the main determinants factors of SHS[5,6]. Moreover, there are various factors that have been influencing SHS for example; the society, unhealthy atmosphere, working burden, less physical and humanistic activities, negative family influences (divorce, frequent quarrels, etc)[8,14–16]. At the same time, people also bear the personal as well as family and social stress and faced various degrees of challenges (serious physical, psychological and emotional) [17,18]. During the health check-up of people do not find a definite clinical diagnosis of the diseases. The physical examination results are also normal but show varying degrees of conditions such as; reduced response capacity, decreased mobility, decline adaption capacity in the house or society, etc[19–21].
Conclusion
Staggeringly, early detection and treatment of SHS, reduce those potential risk factors and promote proactive factors of SHS, then significant improvements can be possible in their real life and also can reduce the burden of the subclinical stage for chronic diseases. Therefore, a person has to be aware of the SHS and its consequences, which is very important in this contemporary society to improve the quality of a healthy life. Although, the government, health agencies, and world health communities have been making greater efforts to improve health care and control non-infectious diseases in the country and achievements have also been made, but still, there is a long way to go.
Competing interests: No competing interests.
References:
1 Yan Y-X, Liu Y-Q, Li M, et al. Development and Evaluation of a Questionnaire for Measuring Suboptimal Health Status in Urban Chinese. J Epidemiol 2009;19:333–41. doi:10.2188/jea.JE20080086
2 Ma C, Xu W, Zhou L, et al. Association between lifestyle factors and suboptimal health status among Chinese college freshmen: a cross-sectional study. BMC Public Health 2018;18. doi:10.1186/s12889-017-5002-4
3 Li G, Xie F, Yan S, et al. Sub health: definition, criteria for diagnosis and potential prevalence in the central region of China. BMC Public Health 2013;13:446. doi:10.1186/1471-2458-13-446
4 Wang W, Yan Y. Suboptimal health: a new health dimension for translational medicine. Clin Transl Med 2012;1:28. doi:10.1186/2001-1326-1-28
5 Wang Y, Liu X, Qiu J, et al. Association between Ideal Cardiovascular Health Metrics and Suboptimal Health Status in Chinese Population. Scientific reports 2017;7:14975–14975. doi:10.1038/s41598-017-15101-5
6 Lolokote S, Hidru TH, Li X. Do socio-cultural factors influence college students’ self-rated health status and health-promoting lifestyles? A cross-sectional multicenter study in Dalian, China. BMC Public Health 2017;17:478. doi:10.1186/s12889-017-4411-8
7 Wang Y, Ge S, Yan Y, et al. China suboptimal health cohort study: rationale, design and baseline characteristics. Journal of translational medicine 2016;14:291–291. doi:10.1186/s12967-016-1046-y
8 Hou H, Feng X, Li Y, et al. Suboptimal health status and psychological symptoms among Chinese college students: a perspective of predictive, preventive and personalised health. EPMA Journal 2018;9:367–77. doi:10.1007/s13167-018-0148-4
9 Wang W, Zhou M, Wang L. The concept and characteristics of sub-health and its relationship with chronic fatigue syndrome. Chinese Journal of Behavioral Medicine and Brain Science 2010;19.
10 Wang W, Tan X. Suboptimal Health Status and Cardiovascular Deficits. In: Advances in Predictive, Preventive and Personalised Medicine. Springer Nature Switzerland AG: : Springer 2019. 287–315.
11 Adua E, Roberts P, Wang W. Incorporation of suboptimal health status as a potential risk assessment for type II diabetes mellitus: a case-control study in a Ghanaian population. The EPMA journal 2017;8:345–55. doi:10.1007/s13167-017-0119-1
12 Alzain MA, Asweto CO, Zhang J, et al. Telomere Length and Accelerated Biological Aging in the China Suboptimal Health Cohort: A Case–Control Study. OMICS: A Journal of Integrative Biology 2017;21:333–9. doi:10.1089/omi.2017.0050
13 Bi J, Huang Y, Xiao Y, et al. Association of lifestyle factors and suboptimal health status: a cross-sectional study of Chinese students. BMJ Open 2014;4. doi:10.1136/bmjopen-2014-005156
14 Yao Y, Wang L, Chen Y, et al. Correlation analysis of anxiety status and sub-health status among students of 13-26 years old. Int J Clin Exp Med 2015;8:9810–4.
15 Cao H, Cui W, Zhao H. Epidemiological analysis of the relationship between life events and sub-health in 1483 middle school students. Journal of Medical Science Yanbian University 2013;1:34–7.
16 Zhao S, Sun C, Wang D. Analysis of the status of body subhealth in 1324 middle school students. Journal of Qiqihar Medical College 2009;30:2169–71.
17 Ren L, Li J. Analysis of sub-health status and related factors of a high school student in Weinan City. China Science and Technology Information 2013;5:78–9.
18 Jiang C, Fu X, Yang H. Investigation on Health Risk Behavior of Middle School Students in Urban District of Hangzhou. Chinese Journal of School Health 2006;27:1037–8.
19 Wang W. Suboptimal health: a potential preventive instrument for non-communicable disease control and management. Journal of Translational Medicine 2012;10:A45–A45. doi:10.1186/1479-5876-10-S2-A45
20 Zhang L, Shao J, Chen M. Study on sub-health symptoms and health risk behaviors of college students in Chongqing. Chinese Health Care Management 2012;29:145–8.
21 Zhao R, Song Z. Research progress on sub-health problems. Foreign Medical Social Medicine 2002;19:10–3.
Competing interests: No competing interests