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Vitamin D and Cancer

Rebecca Dover, Felicia Brooks, Elizabeth
Malik, John Hornung, Rebecca Willis,
Morganne Phraner
 Vitamin D is acquired primarily and most effectively through
exposure to the sun by means of the skin.
 It is believed that Vitamin D may inhibit tumor development
and growth and reduce mortality for certain cancers in the
human body.
 Many dermatologists believe sun exposure should be
minimized in order to prevent skin damage and cancer, but
research has also shown that vitamin D synthesized from
ultraviolet radiation actually has photoprotective effects for
the skin.
 Even if there is a risk of skin cancer from exposure to UV
radiation, though, is it not worth the risk in order to decrease
internal cancer mortality by synthesizing sufficient vitamin D?
 Article #1: Solar ultraviolet-B exposure and cancer
incidence and mortality in the United States, 1993-2002
– High quality and resolution data sets were used to determine
cancer incidence and mortality in the US and to show how many
cancers regressed in exposure to UV-B radiation.
– Over three million cancer incidents between 1998 and 2002 and
three million cases between 1993 and 2002 in the United States
were shown to regress with daily satellite-measured solar UV-B
levels. Numerous cofounders were adjusted for.
– Relative risks of reduced solar UV-B exposure were calculated
for 32 different cancer locations.
 Results:
– Ten sites in the human body showed a
decreased incidence and mortality of
cancer with exposure to UV-B radiation
 Bladder, colon, Hodgkin lymphoma, myeloma,
other biliary, prostate, rectum, stomach,
uterus, and vulva
 Weaker evidence of this same inverse
relationship was apparent in breast, kidney,
leukemia, non-Hodgkin lymphoma, pancreas,
and small intestine.
 This article attempted to overcome some of the limitations of
previous studies of this type by using both incidence and
mortality data, large sample sizes, county-level geographic
resolution, high-resolution solar exposure data, and
adjustment for numerous confounders.
 Confounders included age, poverty, income, smoking,
exercise, alcohol, outdoor occupation, urban/rural, and air
 Findings of this article back up the common idea that
optimal vitamin D synthesis from UV-B exposure
decreases certain internal cancer incidence in the
human body.

 Maintaining adequate vitamin D levels is also
important in slowing tumor progression.

 The findings were consistent with similar published
articles at this time, and even found new information
on positive effects of UV-B for leukemia, small
intestine, and vulva.
 Even though there are possible benefits of
prevention of internal and other cancers through sun
exposure, there is also great response and
consequence of affecting the skin in a negative and
detrimental manner.

 UV radiation is a carcinogen responsible for most of the
1.3 million skin cancer cases in the U.S. each year.
 Inthe best case scenario, UV rays will simply
compromise skin appearance and elasticity.
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 One study in the University of Florida was conducted with
hairless mice and other animal models demonstrating this
relation of skin damage repeatedly occurring since the 1920s
(particularly in squamous cells).

 Other studies conducted in the 1980s were of 100 healthy
human volunteers and multiple narrow-band UV light sources.
This study determined the relative efficacy of different
wavelengths of light in producing sunburn and suntan as well
as epidermal DNA damage.

 Discovered that the action spectra for all these responses
were strikingly similar with a peak of ~290-300nm.
 Another group of researchers determined the action spectra
for vitamin D synthesis in the skin in the same manner and
sample size and found it to be extremely similar to that of the
DNA damage with a peak of ~300nm.

 Therefore, the virtual identity of these multiple action spectra
implies that DNA damage is responsible for sun exposure and
that vitamin D synthesis cannot occur in the absence of DNA

 For that reason, because UV action spectra for DNA damage,
skin cancer, and vitamin D synthesis are all identical,
alternative methods for acquiring vitamin D should be
 In vivo and in vitro research study:
-Vitamin D is synthesized by the same
ultraviolet radiation that causes skin "mutagenic
DNA damage such as cyclobutane pyrimidine
dimers (CPD) and immunosuppression, both of
which play a role in skin carcinogenesis”

-This study showed that 1,25(OH)2D3 had
photoprotective properties in skin
 How?

-In vitro study- 69 human neonatal foreskins
-In vivo study- live, albino, hairless mice


-Irradiance for human skin samples: 203mj/mn² UVB and
1168mj/cm² UVA
-Irradiance for mouse skin samples: 3.98KJ/m² UVB and
63.8KJ/m² UVA
-for sunburn, CPD damage and immunosuppression

Results with application of 1,25(OH)2D3, or analog JN
-Cell Death
-CPD damage
-Immunosuppression in mice

-Photoprotective effect of 1,25(OH)2D3
-Prevention of skin cancer.
 Supplementation:

-Best way to ensure you meet the AI
-Works regardless of variables
-Daily supplements can completely compensate for
lack of vitamin D synthesized in the skin
-Toxicity is rare
 Diet:
-Vitamin D rich foods complement supplementation
-Natural sources include liver, beef, eggs, dairy products, and some
saltwater fish
-Fortified foods include milk, orange juice, and cereal
 Sunscreen:
-Avoiding the sun, is the best way to protect skin cancer. Since
many people love the outdoors, sunscreen is option number two.
-Sun protection factor or SPF is a measure of how well sunscreen
stops UVB
-1/SPF photons continuously transmitted
Ex: If bottle indicates SPF 15 about 1/15 or 7% photons transmitted
-Most sunscreen users do not apply enough
Food IUs per Percen
serving* t DV**

Cod liver oil, 1 tablespoon 1,360 340
Salmon, cooked, 3.5 ounces 360 90
Mackerel, cooked, 3.5 ounces 345 90
Tuna fish, canned in oil, 3 ounces 200 50
Sardines, canned in oil, drained, 1.75 250 70
Milk, nonfat, reduced fat, and whole, 98 25
vitamin D-fortified, 1 cup
Margarine, fortified, 1 tablespoon 60 15
Ready-to-eat cereal, fortified with 10% of 40 10
the DV for vitamin D, 0.75-1 cup (more
heavily fortified cereals might provide
more of the DV)
Egg, 1 whole (vitamin D is found in yolk) 20 6
Liver, beef, cooked, 3.5 ounces 15 4
Cheese, Swiss, 1 ounce 12 4
 Current research has been done only with
UV-B, UV-A, and UV-R exposure

 Supplementation Risks
 The anticancer properties have been
attributed primarily to calcitriol

 Research shows Vitamin D acquired by the
sun inhibits tumor development and growth
and reduce mortality for certain cancers

 Vitamin D circulating in blood benefits
 Studies accounted for variables

-Long-term vs. Short-term exposure
-Socioeconomic status
-Physical Activity
-Geographic Locations
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CON: Skin Phototypes
 Set of determinants that determine effects of UV
radiation on human skin

 Reflects extent of sunburning vs. subsequent
tanning after an initial moderate sun exposure after
a long period of little or no exposure

 Affect acute and chronic risks of UV exposure and
rate of Vitamin D synthesis
CON: Skin Phototypes
 Phototype I or II
– Burn readily and tan minimally if at all
– Achieve max Vitamin D synthesis quickly
– With long exposure suffer substantial DNA damage
 Phototype III
– Burn less and tan more easily than Phototypes I and II
– Similar rates of Vitamin D synthesis and DNA damage
– Tanning response dominates with repeat exposures
 Phototype VI
– High melanin protects skin from initial DNA damage
– Do not sunburn but synthesize little Vitamin D
– Tan darkly with repeat exposure
– Minimal photoaging and skin cancer risk
CON: Other Variables
 Skin Color
 Latitude
 Altitude
 Time of Day and Year
 Environmental Factors
 Elderly
 Homebound/Institutionalized
 Work Schedule
 Body Fat
 Common Medications
CON: Tanning and the Media

 Glamorous Image

 Target Groups

 Most responsive groups at lowest risk for Vitamin D

 Tanning beds often touted as a safe alternative
Final Words
 Boscoe, Francis P. and Maria J. Schymura. Solar ultraviolet-B exposure and
cancer incidence and mortality in the United States, 1993-2002. BMC Cancer
2006, 6:264. 10 Nov 2006.
 Dixon, K.M., S.S. Deo, A.W. Norman, J.E. Bishop, G.M. Halliday, V.E. Reeve,
R.S. Mason. In vivo relevance for photoprotection by the vitamin D rapid
response pathway. Journal of Steroid Biochemistry & Molecular Biology 103
(2007) 451-456.
 Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism.
4th ed. Belmont, California. Thomson Wadsworth: 2005: 343-352.
 Sizer F, Whitney E. Nutrition Concepts and Controversies. 9th ed. Belmont,
California: Thomson Wadsworth; 2003: 213, 218-220, 245, 457-458, 494.
 Gilchrest, BA. Sun exposure and vitamin D sufficienty. American Journal of
Clinical Nutrtion. 2008; 88: 570S-577S.
 The sunshine D-lemma. Harvard Health Letter. 2008; 6-7.
 Brown J. Nutrition Through the Life Cycle. 3rd ed. Belmont, California:
Thomson Wadsworth; 2008: 16, 163, 286, 470-471.