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Dermatoendocrinol. 2009 Jul-Aug; 1(4): 207–214.
PMCID: PMC2835876

In defense of the sun

An estimate of changes in mortality rates in the United States if mean serum 25-hydroxyvitamin D levels were raised to 45 ng/mL by solar ultraviolet-B irradiance


Emerging scientific evidence strongly supports the beneficial role of vitamin D in reducing the risk of incidence and death from many chronic and infectious diseases. This study estimates increases in melanoma and nonmelanoma skin cancer mortality rates and decreases in chronic and infectious disease mortality rates in the US from the standpoint of approximately doubling population doses of solar UVB to increase mean serum 25-hydroxyvitamin D levels from 16 ng/mL for black Americans and 25 ng/mL for white Americans to 45 ng/mL. The primary benefits are expected to come from reductions in cancer and cardiovascular diseases. Although a few thousand excess deaths per year might occur from melanoma and skin cancer, the avoided premature death rate could be near 400,000/ year, with most of the avoided deaths coming late in life. While oral sources of vitamin D could be used instead of UVB or when UVB irradiance is not available, public health policies do not yet recommend the 3,000–4,000 IU/day required to raise serum 25-hydroxyvitamin D levels to the levels required for optimal health, which would be required before vitamin D fortification levels in food can be raised. Until then, moderate solar UVB irradiance remains an import source, and the health benefits greatly outweigh the risks.

Key words: cancer, cardiovascular diseases, melanoma, respiratory infections, skin cancer, vitamin D, ultraviolet-B


Solar UVB (290–315 nm) irradiance correlates with reduced risk of about 14 types of cancer.14 It is hypothesized to explain the latitudinal variation of multiple sclerosis,5 the seasonality of epidemic influenza,6 the epidemiology of septicemia,7 and case fatality rates during the 1918–1919 influenza pandemic.8 The beneficial effect of ultraviolet irradiance (UVR) arises from production of vitamin D. Serum 25-hydroxyvitamin D [25(OH) D] level also inversely correlates with incidence and/or mortality rates of other diseases such as type 2 diabetes mellitus,9,10 coronary heart disease (CHD)11 and congestive heart failure.12

Let us put vitamin D production into the context of human history on Earth. The human species originated in the eastern portion of tropical Africa. Skin pigmentation in that region was very dark to protect against the adverse effects of solar UVR, primarily free radical production and DNA damage leading to melanoma and other skin cancer.13 Because UVB doses were high and clothes were not worn, sufficient UVB penetrated the epidermis to produce adequate vitamin D. As people migrated poleward from the tropics, skin pigmentation lightened to become very pale in northern Europe because those with dark skin had lower survival rates because of rickets and both chronic and infectious diseases.14

One underlying reason for concern about skin cancer and melanoma today is that many people with skin that has adapted for life at high latitudes are now living at lower latitudes, where their skin pigmentation does not afford adequate protection against the adverse effects of solar UV. Conversely, many with dark skin have moved poleward and have chronically low serum 25(OH)D levels and, as a result, higher disease rate.15,16

This report will estimate the health benefits and risks of increasing solar UVB irradiance and oral intake of vitamin D to increase mean serum 25-hydroxyvitamin D levels from 16 ng/mL for black Americans and 25 ng/mL for white Americans17,18 to 45 ng/mL, a level that seems to be in the range required for optimal health,19,20 which requires the production from UVB irradiance or oral intake of about 3,600 IU/day.21,22 The indices used for this study are mortality rates for diseases affected by either vitamin D or UVR leading to death. Although incidence and prevalence rates and the economic burden could also be used, they should yield similar results.


The index used to estimate the changes in health due to increased serum 25(OH)D levels is mortality rates of UV- and vitamin D-sensitive diseases. It is assumed that raising mean serum 25(OH)D levels for white Americans from 25 ng/mL to 45 ng/mL would take 2–2.5 times the current solar UVB irradiance and that the increase in serum 25(OH)D is achieved through increased time in the sun. The only adverse effects of increased UVR listed in Tables 14,23 are melanoma mortality rates. However, NMSC mortality rates would also increase. In 2009, the American Cancer Society estimates that 8,650 melanoma deaths will occur and 2,940 NMSC deaths (34% as many as for melanoma).24 To first order, total UVR-related deaths for white Americans could increase by a factor of 1.34 times the 2009 mortality rates. However, some of the increase in serum 25(OH)D can be achieved by exposing more body surface area and by taking supplements, so this value should be considered an upper limit.

Table 1
Death rates, white males, 200523
Table 4
Death rates, black females, 200523

The beneficial effects of increasing serum 25(OH)D levels from a population mean of 25 ng/mL to 45 ng/mL for white Americans and from 15 ng/mL to 45 ng/mL for black Americans as a function of age range are estimated based on the data presented in Table 5. The values are given as a column in Tables 1 and and22 for white Americans and Tables 3 and and44 for black Americans. The values used in this study are similar to those used in a study of vitamin D deficiency in western Europe.31 However, the estimate for CHD is somewhat lower than in that study. The reason is that the epidemiological studies on vitamin D and CHD and precursor metabolic disease to date are primarily cross-sectional3234 or observational11,3537 in nature, with no ecological studies and limited randomized controlled trials (RCTs), but with low vitamin D doses.38 The lack of ecological studies showing an inverse correlation with UVB indices for CHD indicates that other factors such as diet, genetics and smoking are more important risk factors for incidence and mortality than vitamin D. Several proposed mechanisms explain the beneficial roles of vitamin D for CHD, such as reduced risk of calcification of the arteries,39 negative influence on the renin-angiotensin-aldosterone system,40 and increased insulin sensitivity.41 On the other hand, there are many non-vitamin D risk-modifying factors for cancers, yet ecological studies have usefully demonstrated links to UVB.4244 Again, many proposed mechanisms seem to explain the beneficial role of vitamin D in reducing the risk of cancer.45,46 This study assumes a 15% reduction for CHD for whites and 20% for blacks. Until results of RCTs with sufficient vitamin D doses are reported, considerable uncertainty persists in these values.

Table 2
Death rates, white females, 200523
Table 3
Death rates, black males, 200523
Table 5
Recent results from the literature regarding disease outcome with measures of serum 25(OH)D or oral intake of vitamin D

Tables 14 give estimates of the changes in mortality rates for those aged 20–24 to 71–74 years. For white males and females, the ratio of avoided deaths to melanoma deaths rises from a factor of 2.8 for males and 4.2 for females in the 25- to 29-year age range to a factor of 28.4 for males and 52.4 for females in the 80- to 84-year age range. No estimates are given for black Americans because of lack of data for melanoma at various ages; they have lower melanoma rates than white Americans but comparable NMSC mortality rates.47

The data in Tables 14 along with Census Bureau data could be used to estimate the total avoided death rates. However, it is also possible to use total mortality rate for each vitamin D-sensitive disease. Work in progress estimates that increasing mean serum 25(OH)D levels in the US to 45 ng/mL would avoid 400,000 premature deaths per year, with cancers and cardiovascular diseases providing the largest shares (Grant et al. in preparation).


The health benefits of solar UVB are much larger than the adverse effects represented by melanoma and NMSC mortality rates. This study’s conclusion is similar to that in a report commissioned by the World Health Organization: “UVR exposure is a minor contributor to the world’s disease burden, causing an estimated annual loss of 1.6 million DALYs; i.e., 0.1% of the total global disease burden. A markedly larger annual disease burden, 3.3 billion DALYs, might result from reduction in global UVR exposure to very low levels.”48

Interestingly, although the estimated benefits for females are lower than for males, the ratio of avoided premature death rates to melanoma and NMSC death rates is higher for females. That outcome could be due to males spending more time in the sun in both occupational and nonoccupational activities. Nature has recognized that women need more vitamin D than males for pregnancy and lactation49 in that skin pigmentation is lighter for females than for males in all ethnic groups.13

The estimates for melanoma and skin cancer mortality rates are considered to be an upper bound. For one reason, UVA, not UVB, is the primary spectral region of risk for melanoma, and chronic solar UV irradiance is protective against melanoma.50,51 The reasons why chronic UV irradiance can be associated with reduced risk of melanoma incidence and mortality rates is probably threefold: production of vitamin D;52,53 tanning and thickening of the stratum corneum to reduce penetration of UVA to the lower epidermis;54 and generation of elastosis, which is associated with slower growth of melanoma.55 Also, people need increase UVB only enough to produce sufficient vitamin D, which could be a few minutes a day near solar noon in summer.56,57 The shadow rule favored by dermatologists,58,59 is designed to reduce the risk of erythema. However, the ratio of UVB to UVA increases with solar elevation angle, so solar UVR near solar noon is most favorable for vitamin D production.60 The time required for erythema to occur could be about 15 minutes for fair skinned individuals in midlatitude midday summer solar irradiance.59,61

In addition, skin cancer screening efforts could be increased. The combined mortality rate for melanoma and NMSC has more than tripled for males between 1950–1954 and 1990–1994 (3.30x) while declining slightly for females (0.96x).62 Evidently increased sun avoidance and use of sunscreen reduced NMSC rates, whereas the same plus increased travel increased melanoma rates. Thus, the factor of 1.34 times combined melanoma and NMSC mortality rates is considered a reasonable estimate of the increased mortality rate.

A few additional caveats are involved in relying on solar UVB irradiance for vitamin D production. First, those with red hair and freckles should generally avoid any intense solar UV irradiance because of their increased risk of developing melanoma and limited ability to tan.63 Second, vitamin D production rate decreases with age, with those older than 60 years requiring three to four times longer in the sun than those younger than 20 years.64 Because solar UV also destroys vitamin D at wavelengths between 290 and 330 nm, spending more time in the sun does not produce more vitamin D after a certain point. Third, those with very dark skin require about five times as long to produce vitamin D as those with fair skin.57 Fourth, it might be advisable to wear a brimmed hat when in the sun as the head and hands are generally exposed when in the sun and since UVB is highly scattered by the atmosphere, there is much diffuse UVR hitting the face.65 Finally, avoid erythema by limiting time in the sun without protection as much of the risk of melanoma is probably due to sunburning.66 Recent studies found that about 30% of adults become sunburned each year,67 with sunburn frequency rising to 61% for those aged 18–24 years.68

Although the ratio of avoided deaths to increased melanoma deaths is low at younger ages, it does not mean that people should avoid moderate UV irradiance from the sun in early life. A European study found that the number of sunburns, but not the age at which they occurred, was an important risk factor for melanoma69-recently repeated in another study.66 On the other hand, nevi, which develop in early childhood from UV irradiance, 7072 are an important risk factor for melanoma.73,74 No evidence has been presented that use of artificial UV sources generates nevi, although the possibility does exist. Vitamin D has important health benefits at all ages, and several studies report early-life UVB irradiance associated with significant reduction for diseases later in life (e.g., multiple sclerosis75 and prostate cancer76).

Because most modern sunbeds have spectral outputs with 3%–5% of the energy in the UVB spectral region, and raise serum 25(OH)D levels,7779 sunbed use should afford the same benefit-risk results as solar UVR. In fact, a recent study in Sweden found that women using sunbeds more than three times per year reduced their hazard ratio (HR) of endometrial cancer by 50% (0.5, 95% CI 0.3–0.9) and those women who were sunbathing during summer reduced their risk by 20% (HR, 0.8; 95% CI, 0.5–1.5) compared with women who did not expose themselves to the sun or to sunbeds.80 If white Americans were to obtain their vitamin D through use of artificial UVB sources in the US, such as in winter, when producing vitamin D from solar UVB is often impossible,57,60 using them once a week would produce 10,000–15,000 IU, sufficient to raise serum 25(OH)D levels by 6–15 ng/mL, so it would take about two visits per week to increase by 20 ng/mL.

For sunbed use, there are other caveats. First, the lamps used should have about 3%–5% of the UV in the UVB range. Second, the time required to produce 10,000–20,000 IU with whole-body UVB irradiance in a sunbed can be as short as a one to a very few minutes depending on the luminosity of the bulbs. In the US, bulbs are several times brighter than midlatitude midday solar UV; however, in Europe, lamp intensity is limited to midday Mediterranean solar UV, and the UVB to UVA ratio may be lower than in the US. Third, for sunbeds that employ high-pressure lamps near the head, the head should be covered. These bulbs emit only UVA, which oxidizes and darkens melanin; UVB and slightly longer wavelengths induce production of melanin. Ideally, these UVA lamps should be removed. Covering the groin area might also be advisable. Those with red hair and freckles and the type 1 Fitzpatrick skin phenotype should avoid using sunbeds.

Although an increase in melanoma and NMSC mortality rates from increased UVR is lamentable, the mortality benefit-risk ratio for all age groups combined is approximately 5–10 for males and 12–24 for females. The advantage of solar UVB is that it is free and not subject to government regulation. Supplements would be the most efficient way to obtain vitamin D, but obtaining high-dose vitamin D in European countries is difficult, and many people do not take supplements. Food can be fortified with vitamin D. In the US people obtain 250–300 IU/day of vitamin D from dietary sources.81 The US National Academy of Sciences’ Institute of Medicine has convened a Vitamin D and Calcium Dietary Requirements Committee to evaluate and revise the guidelines; 82 however, the committee seems to be restricting its sources of evidence unduly to clinical trials, downgrading observational and ignoring ecological studies in an attempt at evidence based medicine, i.e., RCT data,83 of which there are very few with 1,000 IU/day or more. Until the recommended guidelines are changed, vitamin D fortification of food is highly unlikely to change.

Materials and Methods

The estimates of reductions in mortality rates are based on the available ecological, observational and cross-sectional studies and, where available, RCTs that used more than 400 IU/day of vitamin D. Table 5 lists the studies used in these determinations. Although many of these studies are considered nondefinitive (only RCTs seem to be considered definitive for vitamin D), those for many types of cancer are considered generally reliable, generally satisfying Hill’s criteria for causality in a biological system.84 Additional analysis of the evidence for a beneficial effect of vitamin D in reducing the risk of cancer is presented in ref. 85. Those for CHD are either observational or cross-sectional, with some laboratory support for mechanisms, and are considered less reliable currently.

The values for white Americans in this study are similar to those used in deriving an estimate for the economic benefit of higher serum 25(OH)D levels for western Europe. The values for black Americans are based on increasing serum levels from 15 ng/mL to 45 ng/mL, so they are higher than those for white Americans.

One can use the following approach to estimate the increased risk of melanoma from increased UV irradiance. In the US, about 90% of vitamin D is derived from solar UVB irradiance, with dietary sources providing about 250–300 IU/day.81 The mean serum 25(OH)D for white Americans is about 25 ng/mL,17,18 which decreased by 1–10 ng/mL between the early 1990s and the early 2000s. Similar effects have been found in Australia86 and the UK.87 The likely reason is increased fear of skin cancer and melanoma88–90 and increased use of sunscreen. The role of sunscreen use in reducing serum 25(OH)D levels was recently disputed,91 but the paper was based on insufficient serum 25(OH) D levels (<20 ng/mL) in sunny countries and did not consider the trends in these three countries. In addition, use of sunscreen has been linked to increased risk of melanoma at latitudes above 40, with the likely reason that sunscreens provide little protection against UVA, the spectral region of greatest risk for melanoma.92 Casual irradiance in summer by those aged 45 years in the UK is sufficient to increase serum 25(OH)D from the winter value of 15 ng/mL to the summertime value of 30 ng/mL in a nearly sinusoidal manner.93 Thus, raising mean serum 25(OH)D levels for white Americans from 25 ng/mL to 45 ng/mL would take 2–2.5 times the current solar UVB irradiance—less in the Southern states, more in the northern states, less in summer, more in winter, although there is a vitamin D winter for several months above the latitude of about 35° N,57 in which either artificial UVB or supplements would have to be used to obtain vitamin D. Doubling UVB irradiance could involve simple steps such as going into the sun at midday, exposing more skin area to the sun, and not applying sunscreen until after 10–20 minutes of solar UVB irradiance.

Summary and Conclusion

The analysis presented here finds that the health benefits of increasing mean population serum 25(OH)D levels in the US to 45 nm/mL solely through natural or artificial ultraviolet irradiance that contains 3%–5% of the UV in the UVB spectral region (290–315 nm) could reduce the rate of premature deaths by about 400,000/year while increasing the death rate from melanoma and skin cancer by at most 12,000/year. The beneficial role of UVB irradiance for mortality rates outweighs the risks in terms of melanoma and NMSC mortality rates at all ages considered. Although more research is required to evaluate the findings in this study, the message that UVR should be avoided is counterproductive.

The public health policies regarding solar UV irradiance and vitamin D have swung back and forth like a pendulum. In the 1920s and 1930s, public health policies supported both measures as a means to reduce the burden of disease,94 but starting in the 1970s and 1980s, concerns regarding the risk of skin cancer turned public health policies against UVB irradiance.95 The rapidly expanding scientific evidence of health benefits of vitamin D are pushing the pendulum back towards favoring solar UVB irradiance.

It seems worthwhile to reiterate a statement by Jörg Reichrath: “Well-balanced recommendations on sun protection have to ensure an adequate vitamin D status, thereby protecting people against adverse effects of strict sun protection without significantly increasing the risk of developing UV-induced skin cancer.”96


The author receives funding from the UV Foundation (McLean, VA), the Vitamin D Society (Canada), the Sunlight Research Forum (Veldhoven), and Bio-Tech-Pharmacal (Fayetteville, AR).


Previously published online as a Dermato-Endocrinology E-publication:


A paper was recently published by Martin Weinstock from Brown University, chair of the American Cancer Society’s Skin Cancer Advisory Committee with Arnold M. Moses, in which the need for vitamin D was recognized.97 They pointed out that while solar UVB is the natural source of vitamin D, those with light skin should consider obtaining vitamin D from supplements, and that as a public health measure, food fortification should be increased. This paper represents an important step forward for the US dermatological community and, hopefully, the American Cancer Society.


1. Grant WB. An estimate of premature cancer mortality in the U.S. due to inadequate doses of solar ultraviolet-B radiation. Cancer. 2002;94:1867–1875. [PubMed]
2. Garland CF, Garland FC, Gorham ED, Lipkin M, Newmark H, Mohr SB, et al. The role of vitamin D in cancer prevention. Am J Public Health. 2006;96:252–261. [PubMed]
3. Grant WB, Garland CF. The association of solar ultraviolet B (UVB) with reducing risk of cancer: multifactorial ecologic analysis of geographic variation in age-adjusted cancer mortality rates. Anticancer Res. 2006;26:2687–2699. [PubMed]
4. Grant WB. An ecologic study of cancer mortality rates in Spain with respect to indices of solar UVB irradiance and smoking. Int J Cancer. 2007;120:1123–1128. [PubMed]
5. Grant WB, Holick MF. Benefits and requirements of vitamin D for optimal health: a review. Altern Med Rev. 2005;10:94–111. [PubMed]
6. Cannell JJ, Vieth R, Umhau JC, Holick MF, Grant WB, Madronich S, et al. Epidemic influenza and vitamin D. Epidemiol Infect. 2006;134:1129–1140. [PubMed]
7. Grant WB. Solar ultraviolet-B irradiance and vitamin D may reduce the risk of septicemia. Dermato-Endocrinology. 2009;1:25–30. [PMC free article] [PubMed]
8. Grant WB, Giovannucci E. The possible roles of solar ultraviolet-B radiation and vitamin D in reducing case-fatality rates from the 1918–1919 influenza pandemic in the United States. Dermato-Endocrinology. 2009. p. 1. [PMC free article] [PubMed]
9. Pittas AG, Dawson-Hughes B, Li T, Van Dam RM, Willett WC, Manson JE, et al. Vitamin D and calcium intake in relation to type 2 diabetes in women. Diabetes Care. 2006;29:650–656. [PubMed]
10. Knekt P, Laaksonen M, Mattila C, Harkanen T, Marniemi J, Heliovaara M, et al. Serum vitamin D and subsequent occurrence of type 2 diabetes. Epidemiology. 2008;19:666–671. [PubMed]
11. Giovannucci E, Liu Y, Hollis BW, Rimm EB. 25-hydroxyvitamin D and risk of myocardial infarction in men: a prospective study. Arch Intern Med. 2008;168:1174–1180. [PubMed]
12. Pilz S, Tomaschitz A. Vitamin D deficiency and myocardial dysfunction. J Am Coll Cardiol. 2009;53:2011. [PubMed]
13. Jablonski NG, Chaplin G. The evolution of human skin coloration. J Hum Evol. 2000;39:57–106. [PubMed]
14. Chaplin G, Jablonski NG. Vitamin D and the evolution of human depigmentation. Am J Phys Anthropol. 2009;139:451–461. [PubMed]
15. Grant WB. Lower vitamin-D production from solar ultraviolet-B irradiance may explain some differences in cancer survival rates. J Natl Med Assoc. 2006;98:357–364. [PMC free article] [PubMed]
16. Harris SS. Vitamin D and African Americans. J Nutr. 2006;136:1126–1129. [PubMed]
17. Looker AC, Pfeiffer CM, Lacher DA, Schleicher RL, Picciano MF, Yetley EA. Serum 25-hydroxyvitamin D status of the US population: 1988-1994 compared with 2000–2004. Am J Clin Nutr. 2008;88:1519–1527. [PMC free article] [PubMed]
18. Ginde AA, Liu MC, Camargo CA., Jr. Demographic differences and trends of vitamin D insufficiency in the US population, 1988–2004. Arch Intern Med. 2009;169:626–632. [PMC free article] [PubMed]
19. Holick MF. Optimal vitamin D status for the prevention and treatment of osteoporosis. Drugs Aging. 2007;24:1017–1029. [PubMed]
20. Cannell JJ, Hollis BW. Use of vitamin D in clinical practice. Altern Med Rev. 2008;13:6–20. [PubMed]
21. Heaney RP. Calcium intake and disease prevention. Arq Bras Endocrinol Metabol. 2006;50:685–693. [PubMed]
22. Aloia JF, Patel M, Dimaano R, Li-Ng M, Talwar SA, Mikhail M, et al. Vitamin D intake to attain a desired serum 25-hydroxyvitamin D concentration. Am J Clin Nutr. 2008;87:1952–1958. [PubMed]
23. Center for Disease Control (CDC), authors Worktable 210R. Death rates for 113 selected causes, alcohol-induced causes, drug-induced causes, and injury by firearms, by 5-year age groups, race and sex: United States, 2005. 2008; 141. 2008;141
24. Jemal A, Siegel R, Ward E, Hao Y, Xu J, Thun MJ. Cancer statistics, 2009. CA Cancer J Clin. 2009;59:225–249. [PubMed]
25. Jeng L, Yamshchikov AV, Judd SE, Blumberg HM, Martin GS, Ziegler TR, et al. Alterations in vitamin D status and anti-microbial peptide levels in patients in the intensive care unit with sepsis. J Transl Med. 2009;7:28. [PMC free article] [PubMed]
26. Lappe JM, Travers-Gustafson D, Davies KM, Recker RR, Heaney RP. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. Am J Clin Nutr. 2007;85:1586–1591. [PubMed]
27. Crew KD, Gammon MD, Steck SE, Hershman DL, Cremers S, Dworakowski E, et al. Association between plasma 25-hydroxyvitamin D and breast cancer risk. Cancer Prev Res (Phila Pa) 2009;2:598–604. [PMC free article] [PubMed]
28. Gorham ED, Garland CF, Garland FC, Grant WB, Mohr SB, Lipkin M, et al. Optimal vitamin D status for colorectal cancer prevention: a quantitative meta analysis. Am J Prev Med. 2007;32:210–216. [PubMed]
29. Pilz S, Dobnig H, Nijpels G, Heine RJ, Stehouwer CD, Snijder MB, et al. Vitamin D and mortality in older men and women. Clin Endocrinol (Oxf) 2009. [PubMed]
30. Aloia JF, Li-Ng M. Re: epidemic influenza and vitamin D. Epidemiol Infect. 2007;135:1095–1096. [PubMed]
31. Grant WB, Cross HS, Garland CF, Gorham ED, Moan J, Peterlik M, et al. Estimated benefit of increased vitamin D status in reducing the economic burden of disease in western Europe. Prog Biophys Mol Biol. 2009. [PubMed]
32. Scragg R, Jackson R, Holdaway IM, Lim T, Beaglehole R. Myocardial infarction is inversely associated with plasma 25-hydroxyvitamin D3 levels: a community-based study. Int J Epidemiol. 1990;19:559–563. [PubMed]
33. Martins D, Wolf M, Pan D, Zadshir A, Tareen N, Thadhani R, et al. Prevalence of cardiovascular risk factors and the serum levels of 25-hydroxyvitamin D in the United States: data from the Third National Health and Nutrition Examination Survey. Arch Intern Med. 2007;167:1159–1165. [PubMed]
34. Kendrick J, Targher G, Smits G, Chonchol M. 25-Hydroxyvitamin D deficiency is independently associated with cardiovascular disease in the Third National Health and Nutrition Examination Survey. Atherosclerosis. 2009;205:255–260. [PubMed]
35. Dobnig H, Pilz S, Scharnagl H, Renner W, Seelhorst U, Wellnitz B, et al. Independent association of low serum 25-hydroxyvitamin d and 1,25-dihydroxyvitamin d levels with all-cause and cardiovascular mortality. Arch Intern Med. 2008;168:1340–1349. [PubMed]
36. Reis JP, von Muhlen D, Miller ER, 3rd, Michos ED, Appel LJ. Vitamin D Status and Cardiometabolic Risk Factors in the United States Adolescent Population. Pediatrics. 2009. [PubMed]
37. Wang TJ, Pencina MJ, Booth SL, Jacques PF, Ingelsson E, Lanier K, et al. Vitamin D deficiency and risk of cardiovascular disease. Circulation. 2008;117:503–511. [PMC free article] [PubMed]
38. Trivedi DP, Doll R, Khaw KT. Effect of four monthly oral vitamin D3 (cholecalciferol) supplementation on fractures and mortality in men and women living in the community: randomised double blind controlled trial. BMJ. 2003;326:469. [PMC free article] [PubMed]
39. Matias PJ, Ferreira C, Jorge C, Borges M, Aires I, Amaral T, et al. 25-Hydroxyvitamin D3, arterial calcifications and cardiovascular risk markers in haemodialysis patients. Nephrol Dial Transplant. 2009;24:611–618. [PubMed]
40. Li YC, Kong J, Wei M, Chen ZF, Liu SQ, Cao LP. 1,25-Dihydroxyvitamin D(3) is a negative endocrine regulator of the renin-angiotensin system. J Clin Invest. 2002;110:229–238. [PMC free article] [PubMed]
41. Teegarden D, Donkin SS. Vitamin D: emerging new roles in insulin sensitivity. Nutr Res Rev. 2009;22:82–92. [PubMed]
42. Garland CF, Mohr SB, Gorham ED, Grant WB, Garland FC. Role of ultraviolet B irradiance and vitamin D in prevention of ovarian cancer. Am J Prev Med. 2006;31:512–514. [PubMed]
43. Mohr SB. A brief history of vitamin D and cancer prevention. Ann Epidemiol. 2009;19:79–83. [PubMed]
44. Grant WB, Mohr SB. Ecological Studies Of Ultraviolet B, Vitamin D And Cancer Since 2000. Ann Epidemiol. 2009. [PubMed]
45. Ingraham BA, Bragdon B, Nohe A. Molecular basis of the potential of vitamin D to prevent cancer. Curr Med Res Opin. 2008;24:139–149. [PubMed]
46. Garland CF, Grant WB, Boucher BJ, Cross HS, Garland FC, Gillie O, et al. Open Letter to IARC Director Christopher P. Wild: Re IARC Working Group Report 5-Vitamin D and Cancer. Dermato-Endocrinology. 2009;1:119–120. [PMC free article] [PubMed]
47. Devesa SS, Grauman DJ, Blot WJ, Pennello GA, Hoover RN, Fraumeni JFJ. Atlas of Cancer Mortality in the United States, 1950–1994. (NIH Publication No 99-4564: National Institute of Health 1999).
48. Lucas RM, McMichael AJ, Armstrong BK, Smith WT. Estimating the global disease burden due to ultraviolet radiation exposure. Int J Epidemiol. 2008;37:654–667. [PubMed]
49. Hollis BW. Vitamin D requirement during pregnancy and lactation. J Bone Miner Res. 2007;22:39–44. [PubMed]
50. Kennedy C, Bajdik CD, Willemze R, De Gruijl FR, Bouwes Bavinck JN. The influence of painful sunburns and lifetime sun exposure on the risk of actinic keratoses, seborrheic warts, melanocytic nevi, atypical nevi and skin cancer. J Invest Dermatol. 2003;120:1087–1093. [PubMed]
51. Berwick M, Armstrong BK, Ben-Porat L, Fine J, Kricker A, Eberle C, et al. Sun exposure and mortality from melanoma. J Natl Cancer Inst. 2005;97:195–199. [PubMed]
52. Osborne JE, Hutchinson PE. Vitamin D and systemic cancer: is this relevant to malignant melanoma? Br J Dermatol. 2002;147:197–213. [PubMed]
53. Gandini S, Raimondi S, Gnagnarella P, Dore JF, Maisonneuve P, Testori A. Vitamin D and skin cancer: a meta-analysis. Eur J Cancer. 2009;45:634–641. [PubMed]
54. Sheehan JM, Potten CS, Young AR. Tanning in human skin types II and III offers modest photoprotection against erythema. Photochem Photobiol. 1998;68:588–592. [PubMed]
55. Grant WB. The effect of solar UVB doses and vitamin D production, skin cancer action spectra, and smoking in explaining links between skin cancers and solid tumours. Eur J Cancer. 2008;44:12–15. [PubMed]
56. Webb AR, Engelsen O. Calculated ultraviolet exposure levels for a healthy vitamin D status. Photochem Photobiol. 2006;82:1697–1703. [PubMed]
57. Webb AR, Engelsen O. Ultraviolet exposure scenarios: risks of erythema from recommendations on cutaneous vitamin D synthesis. Adv Exp Med Biol. 2008;624:72–85. [PubMed]
58. Downham TF., 2nd The shadow rule: a simple method for sun protection. South Med J. 1998;91:619–623. [PubMed]
59. Sliney DH, Wengraitis S. Is a differentiated advice by season and region necessary? Prog Biophys Mol Biol. 2006;92:150–160. [PubMed]
60. Webb AR. Who, what, where and when-influences on cutaneous vitamin D synthesis. Prog Biophys Mol Biol. 2006;92:17–25. [PubMed]
61. McKenzie RL, Liley JB, Bjorn LO. UV radiation: balancing risks and benefits. Photochem Photobiol. 2009;85:88–98. [PubMed]
62. National Cancer Institute, authors. Cancer Mortality Maps and Graphs, 5 year rates. 2009.
63. Bastiaens M, ter Huurne J, Gruis N, Bergman W, Westendorp R, Vermeer BJ, et al. The melanocortin-1-receptor gene is the major freckle gene. Hum Mol Genet. 2001;10:1701–1708. [PubMed]
64. MacLaughlin J, Holick MF. Aging decreases the capacity of human skin to produce vitamin D3. J Clin Invest. 1985;76:1536–1538. [PMC free article] [PubMed]
65. Parisi AV, Green A, Kimlin MG. Diffuse solar UV radiation and implications for preventing human eye damage. Photochem Photobiol. 2001;73:135–139. [PubMed]
66. Dennis LK, Vanbeek MJ, Beane Freeman LE, Smith BJ, Dawson DV, Coughlin JA. Sunburns and risk of cutaneous melanoma: does age matter? A comprehensive metaanalysis. Ann Epidemiol. 2008;18:614–627. [PMC free article] [PubMed]
67. (CDC) CfDCaP, authors. Sunburn prevalence among adults—United States, 1999, 2003 and 2004. Morb Mortal Wkly Rep. 2007;56:524–528. [PubMed]
68. Brown SE. Vitamin D and fracture reduction: an evaluation of the existing research. Altern Med Rev. 2008;13:21–33. [PubMed]
69. Pfahlberg A, Kolmel KF, Gefeller O. Timing of excessive ultraviolet radiation and melanoma: epidemiology does not support the existence of a critical period of high susceptibility to solar ultraviolet radiation-induced melanoma. Br J Dermatol. 2001;144:471–475. [PubMed]
70. Dulon M, Weichenthal M, Blettner M, Breitbart M, Hetzer M, Greinert R, et al. Sun exposure and number of nevi in 5- to 6-year-old European children. J Clin Epidemiol. 2002;55:1075–1081. [PubMed]
71. Bauer J, Buttner P, Wiecker TS, Luther H, Garbe C. Risk factors of incident melanocytic nevi: a longitudinal study in a cohort of 1,232 young German children. Int J Cancer. 2005;115:121–126. [PubMed]
72. Harrison SL, MacLennan R, Buettner PG. Sun exposure and the incidence of melanocytic nevi in young Australian children. Cancer Epidemiol Biomarkers Prev. 2008;17:2318–2324. [PubMed]
73. Tucker MA. Melanoma epidemiology. Hematol Oncol Clin North Am. 2009;23:383–395. [PMC free article] [PubMed]
74. MacKie RM, Hauschild A, Eggermont AM. Epidemiology of invasive cutaneous melanoma. Ann Oncol. 2009;20:1–7. [PMC free article] [PubMed]
75. van der Mei IA, Ponsonby AL, Dwyer T, Blizzard L, Simmons R, Taylor BV, et al. Past exposure to sun, skin phenotype and risk of multiple sclerosis: case-control study. BMJ. 2003;327:316. [PMC free article] [PubMed]
76. Gilbert R, Metcalfe C, Oliver SE, Whiteman DC, Bain C, Ness A, et al. Life course sun exposure and risk of prostate cancer: population-based nested case-control study and meta-analysis. Int J Cancer. 2009;125:1414–1423. [PMC free article] [PubMed]
77. Tangpricha V, Turner A, Spina C, Decastro S, Chen TC, Holick MF. Tanning is associated with optimal vitamin D status (serum 25-hydroxyvitamin D concentration) and higher bone mineral density. Am J Clin Nutr. 2004;80:1645–1649. [PubMed]
78. Porojnicu AC, Bruland OS, Aksnes L, Grant WB, Moan J. Sun beds and cod liver oil as vitamin D sources. J Photochem Photobiol B. 2008;91:125–131. [PubMed]
79. Cicarma E, Porojnicu AC, Lagunova Z, Dahlback A, Juzeniene A, Moan J. Sun and sun beds: inducers of vitamin D and skin cancer. Anticancer Res. 2009;29:3495–3500. [PubMed]
80. Epstein E, Lindqvist PG, Geppert B, Olsson H. A population-based cohort study on sun habits and endometrial cancer. Br J Cancer. 2009;101:537–540. [PMC free article] [PubMed]
81. Calvo MS, Whiting SJ, Barton CN. Vitamin D fortification in the United States and Canada: current status and data needs. Am J Clin Nutr. 2004;80:1710–1716. [PubMed]
82. Institute of Medicine of The National Academies, authors. Dietary Reference Intakes for Vitamin D and Calcium 2009.
83. Institute of Medicine of The National Academies, authors. Vitamin D and Calcium-A Systematic Review of Health Outcomes 2009.
84. Grant WB. How strong is the evidence that solar ultraviolet B and vitamin D reduce the risk of cancer? An examination using Hill’s criteria for causality. Dermato-Endocrinology. 2009;1:14–21. [PMC free article] [PubMed]
85. Grant WB. A critical review of Vitamin D and cancer: A report of the IARC Working Group on vitamin D. Dermato-Endocrinology. 2009;1:25–33. [PMC free article] [PubMed]
86. van der Mei IA, Ponsonby AL, Engelsen O, Pasco JA, McGrath JJ, Eyles DW, et al. The high prevalence of vitamin D insufficiency across Australian populations is only partly explained by season and latitude. Environ Health Perspect. 2007;115:1132–1139. [PMC free article] [PubMed]
87. Glass D, Lens M, Swaminathan R, Spector TD, Bataille V. Pigmentation and vitamin D metabolism in Caucasians: low vitamin D serum levels in fair skin types in the UK. PLoS One. 2009;4:6477. [PMC free article] [PubMed]
88. Gillie O. Sunlight Robbery: Health benefits of sunlight are denied by current public health policy in the UK. Reports HRFO. 2004. ed. London.
89. Hiom S. Public awareness regarding UV risks and vitamin D-the challenges for UK skin cancer prevention campaigns. Prog Biophys Mol Biol. 2006;92:161–166. [PubMed]
90. Sinclair C. Risks and benefits of sun exposure: implications for public health practice based on the Australian experience. Prog Biophys Mol Biol. 2006;92:173–178. [PubMed]
91. Norval M, Wulf HC. Does chronic sunscreen use reduce vitamin D production to insufficient levels? Br J Dermatol. 2009. In press. [PubMed]
92. Gorham ED, Mohr SB, Garland CF, Chaplin G, Garland FC. Do sunscreens increase risk of melanoma in populations residing at higher latitudes? Ann Epidemiol. 2007;17:956–963. [PubMed]
93. Hypponen E, Power C. Hypovitaminosis D in British adults at age 45 y: nationwide cohort study of dietary and lifestyle predictors. Am J Clin Nutr. 2007;85:860–868. [PubMed]
94. Albert MR, Ostheimer KG. The evolution of current medical and popular attitudes toward ultraviolet light exposure: part 2. J Am Acad Dermatol. 2003;48:909–918. [PubMed]
95. Albert MR, Ostheimer KG. The evolution of current medical and popular attitudes toward ultraviolet light exposure: part 3. J Am Acad Dermatol. 2003;49:1096–1106. [PubMed]
96. Reichrath J. The challenge resulting from positive and negative effects of sunlight: how much solar UV exposure is appropriate to balance between risks of vitamin D deficiency and skin cancer? Prog Biophys Mol Biol. 2006;92:9–16. [PubMed]
97. Weinstock MA, Moses AM. Skin cancer meets vitamin D: the way forward for dermatology and public health. J Am Acad Dermatol. 2009;61:720–724. [PubMed]

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