Ultraviolet light technology is a hot topic among dermatologists. After all, excessive exposure to ultraviolet (UV) light increases the risk of skin cancer. But does this also apply to exposure to mild UVB light? According to a recent study by dermatologists at Amsterdam UMC, this is not the case.

Ultraviolet light damages skin cells. Skin cells can repair this damage and adapt in such a way that they are better able to withstand ultraviolet light. Essentially, the mechanism is no different from the way intensive physical exercise damages muscle cells. That sounds serious, but the body is designed to cope with this and is perfectly capable of repairing the damage. If the damage is not too severe, and the body has sufficient time after each exercise session to repair muscle damage, muscles can become stronger through repeated exposure to intense exercise. In fact, the body is designed to move. Exercise is healthy.

The same applies to ultraviolet light. It is becoming increasingly clear that people are healthier when they spend time outdoors during the day and their skin is exposed to light, which partly consists of UV light. However, just as too much intense exercise can lead to injuries, chronic exposure to too much UV light can increase the risk of skin cancer. After millions of people discovered sunbathing in the second half of the last century, the figures have undeniably risen sharply.

This does not apply to medical applications in which dermatologists treat skin patients with a measured amount of UV light. For years, doctors have been treating patients with the skin disease vitiligo, for example, by exposing them to narrow-band ultraviolet B light (NB-UVB), but studies show that this is not associated with an increased risk of skin cancer. Less clear is the situation regarding combined treatment with ultraviolet A light and medications that make the skin more sensitive to ultraviolet light. This specific treatment may increase the risk of some forms of skin cancer.

The Dutch company Dermasun has developed user-friendly UVB technology that people can install at home, which emits a mild amount of UVB light. The intensity of that light is less than that of the NB-UVB applications used by dermatologists, but Dermasun nevertheless funded a number of studies into the safety of its own technology.

One of those studies appeared in MOJ Immunology in 2016. In that study, dermatologists at Amsterdam UMC found no damage to the skin cells of test subjects who sat in front of a Dermasun Helios for ten minutes every day for two months.

That is reassuring, but two months is not a long time. Moreover, the number of test subjects was limited. For that reason, Dermasun funded another study into the safety of using the Dermasun Helios. That study was also conducted by Amsterdam UMC.

In the study, the dermatologists examined skin tissue samples from a total of 68 test subjects, who were divided into three different groups.

One group consisted of patients with a skin disease who were treated three times a week with narrow-band UVB light in a hospital for a month or longer. The subjects in the second group had a Dermasun Helios at home and had been using it daily for at least a year and a half. A third group consisted of skin patients whose doctors treated part of their skin with UV light, and whose researchers studied a piece of skin tissue that had not been irradiated.

The researchers studied the skin cells of the subjects before and after the UVB treatments began. As was the case in the first study, this study also showed that daily use of Dermasun Helios was safe.

Among other things, the researchers looked at the activity of the p53 protein in the skin samples. This is a repair protein that repairs damage to DNA. Such damage occurs countless times every day. In the skin cells of the subjects who received regular treatment with narrow-band UVB light, the activity of p53 was increased, but not in the subjects in the Dermasun group. This means that the skin cells of the subjects in the Dermasun group were not damaged, but the skin cells of the subjects in the other group were.

The researchers also looked at gamma-H2AX, which is a different protein from p53. Gamma-H2AX becomes active when the DNA of cells is actually damaged. The protein tells repair proteins exactly which part of the DNA they need to repair. The more gamma-H2AX there is in cells, the more damaged they are. Scientists consider gamma-H2AX to be an indicator of cell damage. In this case, the researchers found no increase in either group.

Because the amount of p53 was increased in the regular treatment, some damage is likely to occur in those treatments. The absence of an increase in gamma-H2AX suggests that the cells are able to repair that damage. In contrast, exposure to Dermasun Helios apparently causes no damage at all.


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