Feedback EADV 2018

Conference summaries

UV protection

Ultraviolet Protection and Vitamin D

Presented by: Prof. Thomas Vogt
Dept. of Dermatology, Saarland University, Germany

Ultraviolet B (UVB) is a full skin carcinogen and an immunosuppressant.1 The immunosuppressive action is an important part of the deleterious actions of UVB, which can lead to genetic instability.1 The key regulator in DNA repair and apoptosis is p53.2 A mutation in this gene could wreak havoc and lead to an increase of skin cancer.2

UVB also induces vitamin D synthesis in the skin, which limits the ability for cancer formation.3

Vitamin D is essential for:3

  • Intestines as it increases absorption of Ca2+ and Pi
  • Bones as it increases bone mineralization
  • Immune cells as it induces differentiation
  • Tumor microenvironment as it induces differentiation, inhibits proliferation and angiogenesis.

Low serum levels of vitamin D have been associated with prostate and colorectal cancer,3 but also with an increased risk of melanoma along with an unfavorable prognosis.4 In addition, direct molecular signaling has been demonstrated between active vitamin D receptors and the p53 gene.5,6

The big dilemma is that an anti-carcinogenic hormone is produced by a full skin carcinogen.7 Additionally, the optimal synthesis for vitamin D production is at 300 nm ± 5 nm of UVB, the same wavelength that is the most likely for generating skin cancer.7

Sun protection is recommended for skin cancer prevention, yet little is known about the role of sun protection on vitamin D levels. Sun protective behaviors are an important part of limiting the likelihood of developing skin cancer, but have been associated with lower levels of vitamin D production in Caucasians.8 In fact, Caucasians who protect themselves from the sun by seeking shade or wearing long sleeves may have lower vitamin D levels and be at risk for vitamin D deficiency.8

Vitamin D production increases exponentially when thinner sunscreen layers than recommended are applied [<2 mg cm(-2)].9 When the amount of sunscreen and sun protection factor advised by the World Health Organization are used, vitamin D production may be abolished.9 Re-evaluation of sun-protection strategies could be warranted.

Adequate vitamin D status of >50 nmol/L is present in less than 50% of the world population.10

This can be caused by multiple factors that are shown in the Table.

Preventative strategies, such as increasing fish consumption, fortification of foods, use of vitamin D supplements, and advice for moderate sunlight exposure, are warranted.10

While vitamin D supplements can be given, the sun is a better and healthier way to obtain levels of vitamin D. Full body narrowband ultraviolet B radiation three times per week is more effective in treating vitamin D deficiency than prescription of a daily oral intake of 1600 IU (40 μg) vitamin D.11 A systematic review and meta-analysis indicate that partial BSA exposure (for example: 10% of the skin) with moderate UV doses [for example: 1 standard erythema dose (SED)] is effective in generating or maintaining a healthy vitamin D status.12

Key messages

  • UVB is a full skin carcinogen and an immunosuppressant.
  • UVB exposed skin is the main source of vitamin D.
  • Sunscreens used in the recommended amounts do suppress vitamin D production.
  • In real life, sunscreens are not a significant cause of vitamin D deficiency, while other reasons are more relevant.
  • As considerable genetic damage does occur during longer exposures, sunscreens plus sun avoidance strategies should be encouraged and long exposures must be discouraged.
  • Oral supplementation in cases of vitamin D deficiency (<20 ng/ml) or insufficiency (<30 ng/ml) can be recommended.


REFERENCES

Present disclosure: The presenter did not provide any disclosure information.

Written by: Debbie Anderson, PhD

Reviewed by: Victor Desmond Mandel, MD



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