Why Do Humans Have Different Skin Colors?
Skin color is the balance your ancestors struck between two vitamins that sunlight treats in opposite ways. Ultraviolet B builds vitamin D in your skin; longer ultraviolet destroys folate in the blood beneath it. Dark skin protects folate where the sun is relentless, pale skin preserves vitamin D where it is scarce, and latitude decides which loss you cannot afford.
Sunlight writes two messages into skin
Ultraviolet B lands on bare skin, reaches a cholesterol molecule in the epidermis, breaks it open, and leaves vitamin D3 — the only vitamin D the body can make. The longer wavelength, ultraviolet A, travels deeper, reaches the small vessels running under the surface, and destroys folate.
Branda and Eaton measured that in 1978. Human plasma exposed to simulated strong sunlight lost between 30 and 50 percent of its folate within one hour, and light-skinned patients treated with ultraviolet light had abnormally low serum folate. Two parts of one spectrum, two opposite jobs, and skin color is the dial between them.
| Wavelength | Where it lands | What it does | Where the pressure bites |
|---|---|---|---|
| UVB (short) | Cholesterol in the epidermis | Builds vitamin D3 | High latitude, winter, when the sun is too low |
| UVA (long) | Vessels under the skin surface | Destroys folate | Low latitude, all year, where ultraviolet is high every month |
Melanin does not switch ultraviolet off; it turns it down. Eumelanin absorbs across the ultraviolet, so the more of it sits above those vessels, the less light reaches the folate. That is why skin color tracks latitude rather than ancestry: populations sharing a latitude converge on similar skin through entirely different genes.
The sunscreen story fails on timing and on pattern
Ask almost anyone and you get a clean answer: dark skin is armor against the sun, ultraviolet damages DNA, DNA damage causes cancer, so dark skin evolved to prevent cancer. Every step of that is true except the last one.
Selection does not care what kills you. It cares what kills you before your children are born. In the United States the median age at melanoma diagnosis is 67, and fewer than four in a hundred new cases appear between 20 and 34, with 0.3 percent under 20. The damage accumulates over decades, and the deaths arrive after the children.
The geography is wrong as well. If ultraviolet were the driver, melanoma in dark-skinned people should appear where the sun hits hardest. It does not. In United States cancer registries the commonest melanoma in patients recorded as Black is acral melanoma: palms, soles, under the nails, at about 36 percent of their melanomas against roughly 1 percent in non-Hispanic white patients. Melanin blocks ultraviolet light; that part is real. Blocking skin cancer is not the job it was hired for.
Folate is what the equator defends
Near the equator ultraviolet is high in every month, so the binding constraint is folate. Folate is the raw material for DNA synthesis and cell division, which puts a shortage exactly where selection is watching: at conception and in the first weeks of pregnancy. Deficiency causes anemia, infertility, fetal loss and maternal death, and it causes neural tube defects, the failure of the spine or skull to close.
The effect is not subtle. In the Medical Research Council trial published in 1991, folic acid taken before and around conception cut the recurrence of neural tube defects by 72 percent, a relative risk of 0.28. A nutrient that can swing a pregnancy that hard is one selection will defend, and dark skin is how it defends it.
Vitamin D is what the north defends
Above roughly 42 degrees of latitude the winter sun sits too low for ultraviolet B to reach the ground in useful amounts. Webb, Kline and Holick showed that in Boston, at 42 degrees north, no vitamin D3 is made in skin from November through February, and that at 52 degrees north in Edmonton the gap covers most of the year.
Vitamin D lets the gut take up calcium, and calcium hardens bone. A child short of it develops rickets: soft bones that bend. A 1956 survey of African-American women, a cohort born before vitamin D was routinely added to milk, found that about 15 percent had significantly deformed pelvises from childhood rickets, and that vaginal delivery was impossible in about one case in ten of those complicated deliveries. That is a cost paid at the moment of birth, in the currency selection reads. Pale skin at high latitude is not a preference; it is a way of keeping the little ultraviolet that arrives.
The bones agree, and the genes arrived late
A man who died about 7,000 years ago in a cave at La Braña-Arintero, in northern Spain, makes the point from the other direction. His bones came out in 2006 and his DNA read clean: blue eyes, dark skin, at 42 degrees north, carrying the ancestral versions of the two strongest light-skin genes in modern Europeans. By every rule we repeat to children he should have been pale. He was not.
The genes for light skin are common in Europe now, but they were late arrivals. SLC24A5 was already fixed in the first farmers who moved into Europe from Anatolia, so much of its early spread was migration rather than mutation, and SLC45A2 carries the second strongest selection signal in a set of 230 ancient Eurasians. Lighter skin also evolved separately in Europe and East Asia, from different genes, on two continents: the same problem solved twice.
The exchange rate is now wrong
Skin color is not a shield and it is not a rank. It is an exchange rate between two vitamins, set by the average ultraviolet of the place your ancestors lived. Dark skin is a bet that folate is the scarce thing; light skin is a bet that ultraviolet B is. Both bets were correct where they were placed.
What changed is that people move faster than the setting can follow. A survey of British pediatricians found symptomatic vitamin D deficiency in children under five at 7.5 cases per 100,000 overall and 95 per 100,000 in children of Black African or African-Caribbean origin. Those children inherited a good adaptation to a different sun. Reverse the direction and the same mismatch appears as skin cancer in lightly pigmented people living under ultraviolet their ancestors never met: same mechanism, opposite sign, and largely a consequence of modern human migration.
Frequently asked questions
Why do humans have different skin colors?
Skin color is the balance point between two vitamins that sunlight treats in opposite ways. Short-wave ultraviolet builds vitamin D in the skin, and long-wave ultraviolet destroys folate in the blood just beneath it. Dark skin slows both reactions; pale skin lets more of each through, which pays where the winter sun is too weak to make vitamin D at all.
Did dark skin evolve to prevent skin cancer?
No. Melanin does block ultraviolet light, but skin cancer kills too late to matter much to selection: the median age at melanoma diagnosis in the United States is 67, and fewer than four in a hundred cases appear between 20 and 34. The pattern is wrong too, because the commonest melanoma in patients recorded as Black is acral melanoma on palms, soles and under the nails, which is not where the sun lands.
Why do people from the tropics get vitamin D deficiency in northern countries?
Because skin color is tuned to the sun their ancestors lived under, and the tuning takes thousands of years while migration takes decades. In a survey of British pediatricians, symptomatic vitamin D deficiency in children under five ran at 7.5 cases per 100,000 overall and 95 per 100,000 in children of Black African or African-Caribbean origin.
Sources
- Branda, R. F., & Eaton, J. W. (1978). Skin color and nutrient photolysis: an evolutionary hypothesis. Science 201(4356), 625-626. https://doi.org/10.1126/science.675247
- Webb, A. R., Kline, L., & Holick, M. F. (1988). Influence of season and latitude on the cutaneous synthesis of vitamin D3. Journal of Clinical Endocrinology & Metabolism 67(2), 373-378. https://doi.org/10.1210/jcem-67-2-373
- MRC Vitamin Study Research Group (1991). Prevention of neural tube defects: results of the Medical Research Council Vitamin Study. Lancet 338(8760), 131-137. https://doi.org/10.1016/0140-6736(91)90133-A
- Bradford, P. T., Goldstein, A. M., McMaster, M. L., et al. (2009). Acral lentiginous melanoma: incidence and survival patterns in the United States, 1986-2005. Archives of Dermatology 145(4), 427-434. https://doi.org/10.1001/archdermatol.2008.609
- Jablonski, N. G., & Chaplin, G. (2010). Human skin pigmentation as an adaptation to UV radiation. PNAS 107(Suppl 2), 8962-8968. https://doi.org/10.1073/pnas.0914628107
- Olalde, I., Allentoft, M. E., Schröder, F., et al. (2014). Derived immune and ancestral pigmentation alleles in a 7,000-year-old Mesolithic European. Nature 507, 225-228. https://doi.org/10.1038/nature12960
- Mathieson, I., Lazaridis, I., Rohland, N., et al. (2015). Genome-wide patterns of selection in 230 ancient Eurasians. Nature 528, 499-503. https://doi.org/10.1038/nature16152
- Jarrett, P., & Scragg, R. (2020). Evolution, prehistory and vitamin D. International Journal of Environmental Research and Public Health 17(2), 646. https://doi.org/10.3390/ijerph17020646
- Callaghan, A. L., Moy, R. J. D., Booth, I. W., et al. (2006). Incidence of symptomatic vitamin D deficiency. Archives of Disease in Childhood 91(7), 606-607. https://doi.org/10.1136/adc.2006.095075
- National Cancer Institute. SEER Cancer Stat Facts: Melanoma of the Skin. https://seer.cancer.gov/statfacts/html/melan.html
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