Paolo Giacomoni, PhD, Insight Analysis Consulting07.01.19
The illumination of a building at night depends on a large number of parameters. In the dark, houses can be seen with beautiful illuminated windows, sometimes with beautiful colors. The presence of light in the windows depends of course, on the master electrical switch being turned “on.” The intensity and the color of the lights in the windows will depend on the bulbs, the shades, the wallpapers, the individual switches in the rooms and so on.
An Internal Switch
In an analogous way, the presence of pigmentation in human skin depends on a master switch too. When it is “off,” we have the albino phenotype, and when it is “on,” we have a variety of colors that are under the control of more than an estimated 150 genes.
As a matter of fact, skin pigmentation is the consequence of the transfer of black bodies called melanosomes from the melanocytes in the epidermis to the surrounding keratinocytes. Melanocytes are cells with a characteristic star-like form. Each one has a number of “arms” called dendrites. The process of pigmentation requires the participation of specialized enzymes able to make the connection between a dendrite and a keratinocyte. These help the transfer of melanosomes. Melanosomes are vesicles containing other enzymes that are able to oxidize tyrosine to produce melanin.
Melanosomes are assembled first as pre-melanosomes in a peculiar cell compartment called the Golgi apparatus and then, they engulf the tyrosinases, the enzymes able to make melanin.
Pigmentation is under the control of countless specialized genes. The process requires genes committed to the synthesis and the assemblage of the proteins that form the walls of the pre-melanosomes, the synthesis of the different tyrosinases, the chaperoning of tyrosinases to the pre-melanosome, and the transfer of the melanosomes to the keratinocytes. In healthy individuals, this process leads to constitutive pigmentation, the pigmentation that determines hair color and skin color in people, irrespective of solar radiation.
Tan
When healthy skin is exposed to ultraviolet radiation, in the days following the exposure, it acquires a color that can vary according to the photo-type and the ethnicity of the individual. This skin coloring, which may span from golden-brown to dark lemon brown, is called facultative pigmentation, or a “tan” in lay terms. This is true for a majority of skins. Albinos (people with the master switch turned “off”) do not tan.
Other people, albeit non-albino, get such weak tans that when they are asked about the behavior of their skin under solar radiation, they may say that they always burn and never tan. Among Caucasians (people with “white” skin), one may also find people who acquire a brown color and always tan without burning. Many Mongolian Asians (people with “yellow” skin) acquire a dark lemon-yellow color when exposed to UV radiation.
Africans, African-Americans, Native Australians, Papua Asians, and other people with “black” skin can burn when exposed to UV, but it may be more difficult to evaluate by visual inspection the onset of facultative pigmentation or of sunburn.
Protection by Pigmentation
Tanning is a consequence of the production of melanin by the melanocytes in the epidermis triggered by exposure to UV. Melanin is transferred to keratinocytes and then agglutinated around the nucleus of the keratinocytes to form supra-nuclear structures. For a long time, scientists believed that a pigmentation, be it constitutive or facultative (a tan), was a protective reaction for the skin. We now know that this is not the case.
There are many scientific papers which show that the protection offered by a tan in Caucasian or Mongolian Asian skin is only equivalent to the protection offered by a sunscreen with SPF 3 or 4. That is basically no protection. Kaidbey and coworkers came to the conclusion that black skin attenuates five times as much UVR as white skin.1 Furthermore, Cripps assessed that the protection factor afforded by a Wisconsin summer tan (~45 degrees latitude North) in skin types II, III, and IV provide protection factors varying between merely 2.1 and 2.45.2
A paper from the Karolinska Institutet In Sweden entitled “Protective Effect of Tanning on Cutaneous DNA Damage in Situ,”3 demonstrates that there is no real difference in the generation of photoproducts in tanned or non-tanned skin. Photoproduct is the scientific name for UV-generated DNA damage. A Japanese paper, “Supra-nuclear Melanin Caps Reduce UV-induced DNA Photoproducts in Human Epidermis,”4 shows clearly that, under UV irradiation equivalent to several hours of solar exposure in Long Island (or Barcelona or Naples) in July, the number of photoproducts induced under a tan is only four times less than under a non-tanned skin. That is approximately equivalent to using a sunscreen with SPF 4, thus revealing that even in Mongolian Asian skin, a tan offers little protection against UV radiation.
What is the bottom line? Protect your skin at all costs, a tan won't defend your skin from harm.
References
Paolo Giacomoni, PhD
Insight Analysis Consulting
paologiac@gmail.com
516-769-6904
Paolo Giacomoni acts as an independent consultant to the skin care industry. He served as executive director of research at Estée Lauder and was head of the department of biology with L’Oréal. He has built a record of achievements through research on DNA damage and metabolic impairment induced by UV radiation as well as on the positive effects of vitamins and antioxidants. He has authored more than 100 peer-reviewed publications and has more than 20 patents.
An Internal Switch
In an analogous way, the presence of pigmentation in human skin depends on a master switch too. When it is “off,” we have the albino phenotype, and when it is “on,” we have a variety of colors that are under the control of more than an estimated 150 genes.
As a matter of fact, skin pigmentation is the consequence of the transfer of black bodies called melanosomes from the melanocytes in the epidermis to the surrounding keratinocytes. Melanocytes are cells with a characteristic star-like form. Each one has a number of “arms” called dendrites. The process of pigmentation requires the participation of specialized enzymes able to make the connection between a dendrite and a keratinocyte. These help the transfer of melanosomes. Melanosomes are vesicles containing other enzymes that are able to oxidize tyrosine to produce melanin.
Melanosomes are assembled first as pre-melanosomes in a peculiar cell compartment called the Golgi apparatus and then, they engulf the tyrosinases, the enzymes able to make melanin.
Pigmentation is under the control of countless specialized genes. The process requires genes committed to the synthesis and the assemblage of the proteins that form the walls of the pre-melanosomes, the synthesis of the different tyrosinases, the chaperoning of tyrosinases to the pre-melanosome, and the transfer of the melanosomes to the keratinocytes. In healthy individuals, this process leads to constitutive pigmentation, the pigmentation that determines hair color and skin color in people, irrespective of solar radiation.
Tan
When healthy skin is exposed to ultraviolet radiation, in the days following the exposure, it acquires a color that can vary according to the photo-type and the ethnicity of the individual. This skin coloring, which may span from golden-brown to dark lemon brown, is called facultative pigmentation, or a “tan” in lay terms. This is true for a majority of skins. Albinos (people with the master switch turned “off”) do not tan.
Other people, albeit non-albino, get such weak tans that when they are asked about the behavior of their skin under solar radiation, they may say that they always burn and never tan. Among Caucasians (people with “white” skin), one may also find people who acquire a brown color and always tan without burning. Many Mongolian Asians (people with “yellow” skin) acquire a dark lemon-yellow color when exposed to UV radiation.
Africans, African-Americans, Native Australians, Papua Asians, and other people with “black” skin can burn when exposed to UV, but it may be more difficult to evaluate by visual inspection the onset of facultative pigmentation or of sunburn.
Protection by Pigmentation
Tanning is a consequence of the production of melanin by the melanocytes in the epidermis triggered by exposure to UV. Melanin is transferred to keratinocytes and then agglutinated around the nucleus of the keratinocytes to form supra-nuclear structures. For a long time, scientists believed that a pigmentation, be it constitutive or facultative (a tan), was a protective reaction for the skin. We now know that this is not the case.
There are many scientific papers which show that the protection offered by a tan in Caucasian or Mongolian Asian skin is only equivalent to the protection offered by a sunscreen with SPF 3 or 4. That is basically no protection. Kaidbey and coworkers came to the conclusion that black skin attenuates five times as much UVR as white skin.1 Furthermore, Cripps assessed that the protection factor afforded by a Wisconsin summer tan (~45 degrees latitude North) in skin types II, III, and IV provide protection factors varying between merely 2.1 and 2.45.2
A paper from the Karolinska Institutet In Sweden entitled “Protective Effect of Tanning on Cutaneous DNA Damage in Situ,”3 demonstrates that there is no real difference in the generation of photoproducts in tanned or non-tanned skin. Photoproduct is the scientific name for UV-generated DNA damage. A Japanese paper, “Supra-nuclear Melanin Caps Reduce UV-induced DNA Photoproducts in Human Epidermis,”4 shows clearly that, under UV irradiation equivalent to several hours of solar exposure in Long Island (or Barcelona or Naples) in July, the number of photoproducts induced under a tan is only four times less than under a non-tanned skin. That is approximately equivalent to using a sunscreen with SPF 4, thus revealing that even in Mongolian Asian skin, a tan offers little protection against UV radiation.
What is the bottom line? Protect your skin at all costs, a tan won't defend your skin from harm.
References
- Kaidbey et al (1979) Potoprotection by melanin - a comparison of black and Caucasian skin. J Am Acad Dermatol 1: 249-260
- Cripps (1981) Natural and artificial photoprotection. J. Invest. Dermatol. 77: 154-157
- Bykov et al (2001) Protective effect of tanning on cutaneous DNA damage in situ Dermatology 202: 22-26
- Kobayashi et al (1998) Supra-nuclear melanin caps reduce UV-induced DNA photoproducts in human epidermis J. Invest. Dermatol. 110: 806-810
Paolo Giacomoni, PhD
Insight Analysis Consulting
paologiac@gmail.com
516-769-6904
Paolo Giacomoni acts as an independent consultant to the skin care industry. He served as executive director of research at Estée Lauder and was head of the department of biology with L’Oréal. He has built a record of achievements through research on DNA damage and metabolic impairment induced by UV radiation as well as on the positive effects of vitamins and antioxidants. He has authored more than 100 peer-reviewed publications and has more than 20 patents.
