Did you know DNA can increase your risk of getting sunburnt?

Genetic variants determine if you will go bright red or develop a nice even tan

Tanning – it has gone in and out of fashion through history. Victorian women refused to venture outside without a sun bonnet, a parasol and a shawl. Pale skin was a sign of nobility and refinement until the early 20th century. Then in the 1920s, the fashion designer Coco Chanel and an American-born French entertainer Josephine Baker, single handedly altered the mindset of Parisians on sun-kissed skin. Society went from using whitening powders to sunbathing. Tanned skin became trendy and fashionable. It didn’t hurt that in 1903, Niels Finsen won the Nobel Prize for his “light therapy” to cure rickets, a bone disease caused by vitamin D deficiency.

Today we are well aware of the benefits of sunlight, and bronzed skin is still highly sought after in North America. But not all of us can return from a vacation to Cuba, Bahamas or Hawaii with the perfect tan. Our tanning ability is inherited, and genetics has a lot to do with how our skin will react to being in the sun.

We tan because of melanin, a pigment found in our bodies that gives colour to our eyes, hair and skin. Tanning is a natural defence mechanism against sunlight, since melanin protects us from the ultraviolet (UV) radiation that can damage our DNA. It minimizes the negative effects from the sun, and protects against sunburns.

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How our skin develops its tan, as well as how long we keep our tan, depends on the type of UV rays. Sunlight consists of ~96% UVA rays and 4% UVB rays. UVA darkens pre-existing melanin, which is then redistributed to give us glowing skin. However, there’s no increase in the total amount of melanin. This means that cosmetic tanning that uses just UVA, (e.g. tanning beds), won’t necessarily protect you from getting sunburns. UVB increases the production of melanin. The tan we get from UVA is transient and fades quite quickly, compared to the bronzing by UVB, which can last weeks or even months.

Melanocytes, the skin cells that make melanin, produce two different types of melanin. Pheomelanin is red or yellow in colour, and eumelanin is brown or black. Eumelanin is great at absorbing UV rays, while pheomelenin is much less efficient at blocking these rays. The melanocortin 1 receptor, found on the surface of melanocytes, is a protein that helps control the type of melanin we make.

Genetic variants of MC1R (the gene encoding the melanocortin 1 receptor) are linked to a poor tanning response. People who inherit variants, such as rs1805007, rs1805008 and rs1805009, can’t properly initiate the switch between pheomelanin to eumelanin. These same variants are also associated with pale skin, red hair and a greatly enhanced risk of skin cancer.

ASIP is another gene linked to this melanin switch. It encodes a protein which antagonizes the melanocortin 1 receptor, reverting the melanocytes back to pheomelanin production. The rs1015362 and rs4911414 variants of ASIP show a strong association with sun sensitivity, and enhanced risk of skin cancer.

Tyrosinase, a protein encoded by the TYR gene, also influences our skin’s ability to tan. It catalyzes the first step necessary to produce melanin. The rs1126809 and rs1393350 variants of this gene are linked to a person’s tanning ability.

Variation in the IRF4 gene affects our tanning ability in a more indirect way. IRF4 controls the levels of several other genes involved in melanin production. The rs12203592 variant of IRF4 is linked to reduced skin pigmentation.

The choice to tan comes with its own risks. Exposing ourselves to the sun ages our skin prematurely, and increases the risk of skin cancers. Moderation is key to both optimizing melanin production and acquiring vitamin D. We have access to a wide array of sun protection products that can fit the need of even the pickiest among us. Make the smart choice, especially if you are genetically predisposed to burn in the sun.

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