This is part 5 of a ten part series on the myths surrounding melanin. This myth claims skin Melanin levels are related to sunlight. Are skin melanin levels really because of sunlight?
Depends. If you look at the Fitzpatrick Scale it tells you everything you need to know.
There are six different skin types according to the Fitzpatrick Scale. Four of them burn after the first hour of sun exposure. If skin melanin levels were related to sunlight NO ONE WOULD BURN. That is, melanin levels would adjust with sunlight levels. There are people whose skin melanin remains constant all year round. There are people whose skin melanin level fluctuates according to the amount of sunlight or UV Radiation exposure. What’s the difference?
If melanin levels are related to sunlight, everyone in the same environment would have the same level of skin melanin. When someone from West Asia (Europe) goes to, Africa, the higher levels of sunlight would, eventually, change their skin melanin levels to match that of the rest of the population in Africa. We know that does not happen. Even in Africa, people living in the same environment have different skin melanin levels. There are people in the same family in Africa with different skin melanin levels.
Taking it a bit further we realize what some people call “tanning” is actually burning. One of the major risks for skin cancer is the tendency to burn due to UV radiation exposure, as indicated in the Fitzpatrick Scale above. The acting U.S. Surgeon General Boris Lushniak issued a “Call to Action to Prevent Skin Cancer” in 2014. He intended to address the misconceptions regarding tanning and burning, as well as, take action because he saw skin cancer as a major public health problem. In his words “tanned skin is damaged skin.” His call to action included “five strategic goals to support skin cancer prevention.”
The Melanoma Research Foundation says as many as 90 percent of melanomas, the most deadly form of skin cancer, are estimated to be the result of UV Radiation. Every hour of every day one person dies of melanoma and over 160,000 cases of melanoma were diagnosed in 2017 in the USA.
Melanin production in skin is based on a number of factors. In vertebrates α-Melanocyte Stimulating Hormone is produced by the pituitary gland. Also known as Alpha MSH or aMSH a synthetic form, Melanotan-II, produces higher levels of melanin in skin.
But that’s not all.
African albinos. Yes, there are albinos in Africa. If there can be people in Africa without melanin in their skin then UV radiation must not be the reason we produce melanin. When humans first rose as a species in Africa there was no Sahara Desert. Hundreds of thousands of years ago Africa was lush forest. How did albinos come to exist? In a dense forest UV radiation was absorbed mostly by the trees and plants. Yet people with high levels of skin melanin manifested anyway. Why are albinos born in an environment with high levels of UV radiation?
The answer could be simple genetics…or complex genetics. The genes TH, SLC24A5, SLC45A2, ASIP, TYR, and OCA2 all have an effect on melanin levels in skin, hair and eyes. The amount of sunlight does not change their effect. Our physical appearance is the result of these different genes producing our melanin levels in hair, skin and eyes. African albinos are literally proof of random chaos in the human gene pool.
The answer to whether cutaneous melanin levels and ultraviolet radiation levels are related came in the form of a simple chemical difference. Mrs. Paula Vaughn was 32 years old when she participated in a study conducted by the University of Oregon Medical School in 1966. She had psoriasis. The thickening and roughening of the skin which afflicts millions of people worldwide. It was something she hoped could be cured. As part of the study, she unknowingly became part of medical history. When Dr. Kenneth M. Halprin of the U.S.A. and Dr. Akira Ohkawara of Japan stumbled on the secret to why some people have more melanin in their skin they were looking for an answer to a totally different question.
The two dermatologists had no idea their research into psoriasis would credit them with an explanation that had been unanswered for decades prior. Mrs. Vaughn had been one of 12 patients in the study. They were looking for different enzymes in the skin of people with psoriasis and those without it. Of the twelve, Vaughn was the only African-American.
In her sample, which was obtained through using a surgical shaver to peel skin off the study subjects’ back, they found a difference. Glutathione reductase, an enzyme in skin, was not at measurable levels in Mrs. Vaughn’s skin. This difference caused the doctors to recall Dr. Stephen Rothman’s 1946 study Inhibitory Action of Human Epidermis on Melanin Formation.
Samples from the upper layer of both cadaver and fresh human skin were processed into an extract by Rothman. The result was combined with a solution containing the amino acid which starts melanogenesis, tyrosine, along with tyrosinase and a buffer. Rothman, Helen Krysa and Adelaide Smiljanic, found something was preventing the formation of melanin in their extracts. The more of the epidermal extract they added to test tubes, the less melanin was produced. They also found Iodoacetamide reversed the effect.
Halprin and Ohkawara wondered whether the substance preventing melanin from forming in Rothman’s study could be glutathione reductase. Reduced glutathione could not be converted from oxidized glutathione without the glutathione reductase enzyme. High levels of melanin occurs through melanogenesis. Glutathione reductase inhibits melanogenesis.
A follow up investigation by Halprin and Ohkawara using samples from 50 inmates of the Portland City Jail, who were paid $5 for volunteering their skin samples, substantiated their suspicions. Melanin challenged people had high levels of glutathione reductase and melanin people had low levels. One East Indian was found to have levels almost exactly in the middle of the subjects.
What is remarkable about the findings of Halprin and Ohkawara is they actually presented nothing novel. As early as 1941, Frank H. J. Figge identified the Effect of Glutathione on Tyrosinase and the Significance of the Dopa Reaction. As Figge noted, the process of melanogenesis was first revealed through the work of Swiss chemist Bruno Bloch in 1916. Bloch also first demonstrated it was impossible to find tyrosine in the dermis of vertebrates having slight (low) melanin levels. Rothman, et. al. explained why Bloch could not find tyrosine.
Rothman’s group knew Figge had identified Glutathione as having an effect on melanin production. He compared dopa and tyrosine in various mixtures to determine the effect of each. Cysteine and glutathione were found to only slightly oxidate dopa.
It took three hours of light absorption before tyrosine could begin melanin production in the presence of cysteine and glutathione. The other substances actually accelerated melanogenesis. Figge also did a comparison to the rate of melanogenesis of the substances used with glutathione added. The resulting inhibition of tyrosine oxidation into melanin, but only had a slight inhibiting effect on dopa.