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 P_i
• 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