Toggle Health Problems and D

Skin color may not be entirely related to amount of sunshine

A set of blog posts by Peter Frost, anthropologist

Vitamin D and Skin Color Part I October 2008

from http://evoandproud.blogspot.com/2008/10/skin-color-and-vitamin-d.html
Differences in human skin color are commonly explained as an adaptive response to solar UV radiation and latitude. The further away from the equator you are, the weaker will be solar UV and the less your skin will need melanin to prevent sunburn and skin cancer.

A variant of this explanation involves vitamin D, which the body needs to make strong bones and which the skin produces with the help of UV-B. The further away from the equator you are, the lighter your skin will be to let enough UV-B into its tissues for vitamin D production. Or so the explanation goes.

To test this hypothesis, Osborne et al. (2008) measured skin color and bone strength in a hundred white and Asian adolescent girls from Hawaii. Skin color was measured at the forehead and the inner arm. Bone strength was measured by section modulus (Z) and bone mineral content (BMC) at the proximal femur. A multiple regression was then performed to investigate the influences of skin color, physical activity, age, ethnicity, developmental age, calcium intake, and lean body mass on Z and BMC. Result: no significant relationship between skin color and bone strength.

Is there, in fact, any hard evidence that humans vary in skin color because they need to maintain the same level of vitamin D production in the face of varying levels of UV-B? Robins (1991, pp. 204-205) found the data to be unconvincing when he reviewed the literature. In particular, there seems to be little relationship between skin color and blood levels of 25-OHD—one of the main circulating metabolites of vitamin D:

The vulnerability of British Asians to rickets and osteomalacia has been ascribed in part to their darker skin colour, but this idea is not upheld by observations that British residents of West Indian (Afro-Caribbean) origin, who have deeper skin pigmentation than the Asians, very rarely manifest clinical rickets … Moreover, artificial irradiation of Asian, Caucasoid and Negroid subjects with UV-B produced similar increases in blood 25-OHD levels irrespective of skin pigmentation … A study under natural conditions in Birmingham, England, revealed comparable increases in 25-OHD levels after the summer sunshine from March to October in groups of Asians, West Indians and Caucasoids … This absence of a blunted 25-OHD response to sunlight in the dark-skinned West Indians at high northerly latitudes (England lies farther north than the entire United States of America except for Alaska) proves that skin colour is not a major contributor to vitamin D deficiency in northern climes.

The higher incidence of rickets in British Asians probably has less to do with their dark color than with their systematic avoidance of sunlight (to remain as light-skinned as possible).

Skin color and natural selection via solar UV

Solar UV seems to be a weak agent of natural selection, be it through sunburn, skin cancer, or vitamin D deficiency. Brace et al. (1999) studied skin color variation in Amerindians, who have inhabited their continents for 12,000-15,000 years, and in Australian Aborigines, who have inhabited theirs for some 50,000 years. Assuming that latitudinal skin-color variation in both groups tracks natural selection by solar UV, their calculations show that this selection would have taken over 100,000 years to create the skin-color difference between black Africans and northern Chinese and ~ 200,000 years to create the one between black Africans and northern Europeans (Brace et al., 1999). Yet modern humans began to spread out of Africa only about 50,000 years ago. Clearly, something other than solar UV has also influenced human variation in skin color ... and one may wonder whether lack of solar UV has played any role, via natural selection, in the extreme whitening of some human populations.

Indeed, people seem to do just fine with a light brown color from the Arctic Circle to the equator. Skeletal remains from pre-contact Amerindian sites show little evidence of rickets or other signs of vitamin D deficiency—even at latitudes where Amerindian skin is much darker than European skin (Robins, 1991, p. 206).

Why, then, are Europeans so fair-skinned when ground-level UV radiation is equally weak across Europe, northern Asia, and North America at all latitudes above 47º N? (Jablonski & Chaplin, 2000). Proponents of the vitamin D hypothesis will point to the Inuit and say that non-Europeans get enough vitamin D at high northerly latitudes from fatty fish. So they don’t need light skin. In actual fact, if we look at the indigenous peoples of northern Asia and North America above 47º N, most of them live far inland and get little vitamin D from their diet. For instance, although the Athapaskans of Canada and Alaska live as far north as the Inuit and are even somewhat darker-skinned, their diet consists largely of meat from land animals (caribou, deer, ptarmigan, etc.). The same may be said for the native peoples of Siberia.

Conversely, fish consumption is high among the coastal peoples of northwestern Europe. Skeletal remains of Danes living 6,000-7,000 years ago have the same carbon isotope profile as those of Greenland Inuit, whose diet is 70-95% of marine origin (Tauber, 1981). So why are Danes so light-skinned despite a diet that has long included fatty fish?

Skin color and sexual selection via male choice

Latitudinal variation in human skin color is largely an artefact of very dark skin in sub-Saharan agricultural peoples and very light skin in northern and eastern Europeans. Elsewhere, the correlation with latitude is much weaker. Indeed, human skin color seems to be more highly correlated with the incidence of polygyny than with latitude (Manning et al., 2004).

This second correlation is especially evident in sub-Saharan Africa, where high-polygyny agriculturalists are visibly darker than low-polygyny hunter-gatherers (i.e., Khoisans, pygmies) although both are equally indigenous. Year-round agriculture allows women to become primary food producers, thereby freeing men to take more wives. Thus, fewer women remain unmated and men are less able to translate their mate-choice criteria into actual mate choice. Such criteria include a preference, widely attested in the African ethnographic literature, for so-called 'red' or 'yellow' women — this being part of a general cross-cultural preference for lighter-skinned women (van den Berghe & Frost, 1986). Less mate choice means weaker sexual selection for light skin in women and, hence, less counterbalancing of natural selection for dark skin in either sex to protect against sunburn and skin cancer. Result: a net increase in selection for dark skin.

Just as weaker sexual selection may explain the unusually dark skin of sub-Saharan agricultural peoples, stronger sexual selection may explain the unusually light skin of northern and eastern Europeans, as well as other highly visible color traits.

Among early modern humans, sexual selection of women varied in intensity along a north-south axis. First, the incidence of polygyny decreased with distance from the equator. The longer the winter, the more it cost a man to provision a second wife and her children, since women could not gather food in winter. Second, the male death rate increased with distance from the equator. Because the land could not support as many game animals per unit of land area, hunting distance increased proportionately and hunters more often encountered mishaps (drowning, falls, cold exposure, etc.) or ran out of food, especially if other food sources were scarce.

Sexual selection of women was strongest where the ratio of unmated women to unmated men was highest. This would have been in the ‘continental Arctic’, a steppe-tundra environment where women depended the most on men for food and where hunting distances were the longest (i.e., long-distance hunting of highly mobile herds with no alternate food sources). Today, this environment is confined to the northern fringes of Eurasia and North America. As late as 10,000 years ago, it reached much further south. This was particularly so in Europe, where the Scandinavian icecap had pushed the continental Arctic down to the plains of northern and eastern Europe (Frost, 2006).

The same area now corresponds to a zone where skin is almost at the physiological limit of depigmentation and where hair and eye color have diversified into a broad palette of vivid hues. This ‘European exception’ constitutes a major deviation from geographic variation in hair, eye, and skin color (Cavalli-Sforza et al., 1994, pp. 266-267).


Brace, C.L., Henneberg, M., & Relethford, J.H. (1999). Skin color as an index of timing in human evolution. American Journal of Physical Anthropology, 108 (supp. 28), 95-96.
Cavalli-Sforza, L.L., Menozzi, P., & Piazza, A. (1994). The History and Geography of Human Genes. Princeton: Princeton University Press.
Frost, P. (2006). European hair and eye color - A case of frequency-dependent sexual selection? Evolution and Human Behavior, 27, 85-103
Jablonski, N.G. & G. Chaplin. (2000). The evolution of human skin coloration, Journal of Human Evolution, 39, 57-106.
Manning, J.T., Bundred, P.E., & Mather, F.M. (2004). Second to fourth digit ratio, sexual selection, and skin colour. Evolution and Human Behavior, 25, 38-50.
Osborne, D.L., C.M. Weaver, L.D. McCabe, G.M. McCabe, R. Novotony, C. Boushey, & D.A. Savaiano. (2008). Assessing the relationship between skin pigmentation and measures of bone strength in adolescent females living in Hawaii. American Journal of Physical Anthropology, 135(S46), 167.
Robins, A.H. (1991). Biological perspectives on human pigmentation. Cambridge Studies in Biological Anthropology, Cambridge: Cambridge University Press.
Tauber, H. (1981). 13C evidence for dietary habits of prehistoric man in Denmark. Nature, 292, 332-333.
van den Berghe, P.L., & Frost, P. (1986). Skin color preference, sexual dimorphism and sexual selection: A case of gene-culture co-evolution? Ethnic and Racial Studies, 9, 87-113.

Vitamin D and skin color. Part II Nov 2008

Is white skin an adaptation to the cereal diet that Europeans have been consuming for the past five to seven thousand years?

When early Europeans switched from hunting and gathering to cereal agriculture, the new diet may have provided less vitamin D (i.e., from fatty fish), which the body needs to metabolize calcium and create strong bones. There would thus have been stronger selection for endogenous production of vitamin D in the skin’s tissues. Since such production requires UV-B light and since melanin blocks UV, this selection may have favored a lighter skin color (Sweet, 2002). In addition, cereals seem to increase vitamin D requirements by decreasing calcium absorption and by shortening the half-life of the main blood metabolite of vitamin D (Pettifor, 1994; see Paleodiet).

Undoubtedly, lighter skin allows more UV-B into the skin. As Robins (1991, pp. 60-61) notes, black African skin transmits three to five times less UV than does European skin. But is this a serious constraint on vitamin D production? Apparently not. Blood metabolites of vitamin D show similar increases in Asian, Caucasoid, and Negroid subjects when their skin is either artificially irradiated with UV-B or exposed to natural sunlight from March to October in Birmingham, England (Brazerol et al., 1988; Ellis et al., 1977; Lo et al., 1986; Stamp, 1975; also see discussion in Robins, 1991, pp. 204-205).

The vitamin D hypothesis also implies that European skin turned white almost at the dawn of human history. Cereal agriculture did not reach northern Europe until some 5,000 years ago and, presumably, the whitening of northern European skin would not have been complete until well into the historical period. Is this a realistic assumption, given the depictions of white-skinned Europeans in early Egyptian art?


Brazerol, W.F., McPhee, A.J., Mimouni, F., Specker, B.L., & Tsang, R.C. (1988). Serial ultraviolet B exposure and serum 25 hydroxyvitamin D response in young adult American blacks and whites: no racial differences. Journal of the American College of Nutrition, 7, 111-118.
Ellis, G., Woodhead, J.S., & Cooke, W.T. (1977). Serum-25-hydroxyvitamin-D concentrations in adolescent boys. Lancet, 1, 825-828.
Lo, C.W., Paris, P.W., & Holick, M.F. (1986). Indian and Pakistani immigrants have the capacity as Caucasians to produce vitamin D in response to ultraviolet radiation. American Journal of Clinical Nutrition, 44, 683-685.
Pettifor, J.M. (1994). Privational rickets: a modern perspective. Journal of the Royal Society of Medicine, 87, 723-725.
Robins, A.H. (1991). Biological perspectives on human pigmentation. Cambridge Studies in Biological Anthropology, Cambridge: Cambridge University Press.
Stamp, T.C. (1975). Factors in human vitamin D nutrition and in the production and cure of classical rickets. Proceedings of the Nutrition Society, 34, 119-130.

African Americans and vitamin D July 9 2009

Vitamin D insufficiency is more prevalent among African Americans (blacks) than other Americans and, in North America, most young, healthy blacks do not achieve optimal 25-hydroxyvitamin D 25(OH)D concentrations at any time of year. This is primarily due to the fact that pigmentation reduces vitamin D production in the skin. Also, from about puberty and onward, median vitamin D intakes of American blacks are below recommended intakes in every age group, with or without the inclusion of vitamin D from supplements. (Harris, 2006)

It’s well known that African Americans have low levels of vitamin D in their blood. In fact, this seems to be generally true for humans of tropical origin. In a study from Hawaii, vitamin D status was assessed in healthy, visibly tanned young adults who averaged 22.4 hours per week of unprotected sun exposure. Yet 51% had levels below the current recommended minimum of 75 nmol/L (Binkley et al., 2007). In a study from south India, levels below 50 nmol/L were found in 44% of the men and 70% of the women. The subjects are described as “agricultural workers starting their day at 0800 and working outdoors until 1700 with their face, chest, back, legs, arms, and forearms exposed to sunlight” (Harinarayan et al., 2007). In a study from Saudi Arabia, levels below 25 nmol/L were found in respectively 35%, 45%, 53%, and 50% of normal male university students of Saudi, Jordanian, Egyptian, and other origins (Sedrani, 1984).

These low levels are usually blamed on the darker skin of tropical humans, i.e., melanin blocks the UV-B component of sunlight, which the skin needs to make vitamin D. Actually, dark skin is not a serious constraint on vitamin D production. While it is true that a single UV-B exposure of moderate intensity will produce less vitamin D in black skin than in white skin, this difference narrows with longer exposure times, since white skin cuts back vitamin D production after only 20 minutes in the sun (Holick, 1995). Even in England, where sunlight is relatively weak, Asian, West Indian, and European adolescents show similar increases in vitamin D levels during the spring and summer (Ellis et al., 1977).

Another possible reason why tropical humans make less vitamin D is that there is no need to build up a reserve for the winter, when this vitamin cannot be produced. In contrast, such a reserve is necessary in the temperate zone. This seasonal variation is shown by a study of Nebraskan men after a summer of landscaping, construction, farming, and recreation. Their mean vitamin D level was initially 122 nmol/L. By late winter, it had fallen to 74 nmol/L (Barger-Lux & Heaney, 2002). Tropical humans may thus produce less of this vitamin because their skin doesn’t have to ‘make hay while the sun shines.’ This adaptation would then persist in those groups, like African Americans, that now inhabit the temperate zone.

Whatever the reason for this lower rate of production, tropical humans seem to compensate by converting more vitamin D into its active form. Although a single UV-B exposure produces less vitamin D3 in black subjects than in whites, the difference narrows after liver hydroxylation to 25-OHD and disappears after kidney hydroxylation to 1,25-(OH)2D. The active form of vitamin D is thus kept at a constant level, regardless of skin color (Matsuoka et al., 1991, 1995).

Robins (2009) notes that nearly half of all African Americans are classified as vitamin-D deficient and yet show no signs of calcium deficiency, which would be a logical result of vitamin D deficiency. Indeed, they “have a lower prevalence of osteoporosis, a lower incidence of fractures and a higher bone mineral density than white Americans, who generally exhibit a much more favourable vitamin D status.” He also cites a survey of 232 black (East African) immigrant children in Melbourne, Australia, among whom 87% had levels below 50 nmol/L and 44% below 25 nmol/L. None had rickets—the usual sign of vitamin-D deficiency in children (McGillivray et al., 2007).

In short, low vitamin D levels seem to be normal for African Americans and nothing to worry about. Such contrary evidence, however, doesn’t deter the vitamin D worrywarts:

Despite their low 25(OH)D levels, blacks have lower rates of osteoporotic fractures. This may result in part from bone-protective adaptations that include an intestinal resistance to the actions of 1,25(OH)2D and a skeletal resistance to the actions of parathyroid hormone (PTH). However, these mechanisms may not fully mitigate the harmful skeletal effects of low 25(OH)D and elevated PTH in blacks, at least among older individuals. Furthermore, it is becoming increasingly apparent that vitamin D protects against other chronic conditions, including cardiovascular disease, diabetes, and some cancers, all of which are as prevalent or more prevalent among blacks than whites. Clinicians and educators should be encouraged to promote improved vitamin D status among blacks (and others) because of the low risk and low cost of vitamin D supplementation and its potentially broad health benefits. (Harris, 2006)

The National Institute of Health is now studying the benefits of giving African Americans mega-doses of vitamin D, in the hope of bringing their disease rates down to those of other Americans. "We're excited about the potential of vitamin D to reduce this health gap," says the study co-leader. "But it is important to get answers from clinical trials before recommending megadoses of this supplement." (see article)

Yes, it might be best to get a few answers first. Unfortunately, there are millions of people out there who are now taking mega-doses of vitamin D every day. The mass experiment has already begun and the results should be ready in a decade or so, particularly among African Americans.

But why wait? The same experiment was performed from the mid-1980s to 2009 on an African American. The results are now in …

Was MJ done in by the D men?

A local journalist recalled interviewing Michael Jackson three years ago and noted that this man, then in his mid-40s, had the withered look of someone much older—like a vieillard.

What was responsible? His repeated plastic surgeries? His starvation diet? His abuse of painkillers and tranquillizers? These are the usual suspects. In the shadows, however, lurks another suspect who will never be questioned.

Michael Jackson had probably been taking mega-doses of vitamin D. This regimen would have started when he began bleaching his skin in the mid-1980s to even out blotchy pigmentation due to vitiligo. Since this bleaching made his skin highly sensitive to UV light, his dermatologist told him to avoid the sun and use a parasol. At that point, his medical entourage would have recommended vitamin D supplements. How high a dose? We’ll probably never know, but there are certainly many doctors who recommend mega-doses for people who get no sun exposure.

Such a recommendation would have dovetailed nicely with Michael’s fondness for vitamins. A 2005 news release mentions vitamin therapy as part of his health program:
“He’s getting vitamin nutrients and supplements,” the source said.
This source would not elaborate on the type of supplements or the way in which they are being administered.

There is also an interview with his former producer Tarak Ben Ammar:
C'était un hypocondriaque et on savait jamais vraiment s'il était malade car il a été entouré de médecins charlatans qui vivaient de cette maladie, qui lui facturaient des milliers et des milliers de dollars de médicaments, de vitamines…
[He was a hypochondriac and one never really knew whether he was sick because he was surrounded by charlatan doctors who lived from this sickness, who billed him for thousands and thousands of dollars of medication, of vitamins …]

It’s known that Michael Jackson was receiving injections of the ‘Myers cocktail’ (a mix of vitamins and nutrients), but this mix doesn’t normally contain vitamin D. He was probably taking the vitamin in tablet form.

What effects can we expect from long-term use of vitamin D at high doses? Keep in mind that we are really talking about a hormone, not a vitamin. This hormone interacts with the chromosomes and will gradually shorten their telomeres if concentrations are either too low or too high. Tuohimaa (2009) argues that optimal levels may lie in the range of 40-60 nmol/L. This is well below the current recommended minimum of 75 nmol/L. Furthermore, compliance with this optimal range may matter even more for populations of tropical origin, like African Americans, since their bodies have not adapted to the wide seasonal variation of non-tropical humans.

If this optimal range is continually exceeded, the long-term effects may look like those of aging:

Recent studies using genetically modified mice, such as FGF23-/- and Klotho-/- mice that exhibit altered mineral homeostasis due to a high vitamin D activity showed features of premature aging that include retarded growth, osteoporosis, atherosclerosis, ectopic calcification, immunological deficiency, skin and general organ atrophy, hypogonadism and short lifespan.

… after the Second World War in Europe especially in Germany and DDR, children received extremely high oral doses of vitamin D and suffered hypercalcemia, early aging, cardiovascular complications and early death suggesting that hypervitaminosis D can accelerate aging. (Tuohimaa 2009)

Have we opened a Pandora’s box? Far from being a panacea, vitamin D could be an angel of death that will make millions of people old before their time.

Poor Michael. He looked to his doctors for eternal youth and they gave him premature old age.


Barger-Lux, J., & Heaney, R.P. (2002). Effects of above average summer sun exposure on serum 25-hydroxyvitamin D and calcium absorption, The Journal of Clinical Endocrinology & Metabolism, 87, 4952-4956.
Binkley N, Novotny R, Krueger D, et al. (2007). Low vitamin D status despite abundant sun exposure. Journal of Clinical Endocrinology & Metabolism, 92, 2130 –2135.
Ellis, G., Woodhead, J.S., & Cooke, W.T. (1977). Serum-25-hydroxyvitamin-D concentrations in adolescent boys, Lancet, 1, 825-828.
Harinarayan, C.V., Ramalakshmi, T., Prasad, U.V., Sudhakar, D., Srinivasarao, P.V.L.N., Sarma, K.V.S., & Kumar, E.G.T. (2007). High prevalence of low dietary calcium, high phytate consumption, and vitamin D deficiency in healthy south Indians, American Journal of Clinical Nutrition, 85, 1062-1067.
Harris, S.S. (2006). Vitamin D and African Americans, Journal of Nutrition, 136, 1126-1129.
Holick, M.F. (1995). Noncalcemic actions of 1,25-dihydroxyvitamin D3 and clinical applications, Bone, 17, 107S-111S.
Matsuoka, L.Y., Wortsman, J., Chen, T.C., & Holick, M.F. (1995). Compensation for the interracial variance in the cutaneous synthesis of vitamin D, Journal of Laboratory and Clinical Medicine, 126, 452-457.
Matsuoka, L.Y., Wortsman, J., Haddad, J.G., Kolm, P., & Hollis, B.W. (1991). Racial pigmentation and the cutaneous synthesis of vitamin D. Archives of Dermatology, 127, 536-538.
McGillivray, G., Skull, S.A., Davie, G., Kofoed, S., Frydenberg, L., Rice, J., Cooke, R., & Carapetis, J.R. (2007). High prevalence of asymptomatic vitamin-D and iron deficiency in East African immigrant children and adolescents living in a temperate climate. Archives of Disease in Childhood, 92, 1088-1093.
Robins, A.H. (2009). The evolution of light skin color: role of vitamin D disputed, American Journal of Physical Anthropology, early view.
Sedrani, S.H. (1984). Low 25-hydroxyvitamin D and normal serum calcium concentrations in Saudi Arabia: Riyadh region, Annals of Nutrition & Metabolism, 28, 181-185.
Tuohimaa, P. (2009). Vitamin D and aging, Journal of Steroid Biochemistry and Molecular Biology, 114, 78-84.

The vitamin-D hypothesis and ancestral Europeans July 2010

http://evoandproud.blogspot.com/2010/07/vitamin-d-hypothesis-and-ancestral.html - same author

Some writers argue that European skin became white to offset a decline in dietary vitamin D. Pre-agricultural diets, however, were rich in vitamin D only among coastal Europeans who consumed fatty fish.

The ‘vitamin D hypothesis’ is often invoked to explain differences in skin color among human populations (Loomis 1967; Murray 1934). As modern humans spread out of Africa, they entered northern regions, like Europe, where sunlight is weaker and less conducive to synthesis of vitamin D by the skin. Thus, to maintain the same level of vitamin-D synthesis, there was strong natural selection to depigment the skin and let the sun’s rays penetrate it more easily.

This might explain the whiteness of Europeans, but what about the darker skin of northern Asians and native North Americans? They too live at high latitudes. And they too receive much less sunlight than do tropical peoples.

The standard reply is that they get enough vitamin D from their diet, specifically fatty fish, so natural selection has not lightened their skin to the same degree:

The Eskimo though deeply pigmented and living in a dark habitat, nevertheless is notoriously free from rickets. This is due to his subsisting almost exclusively on a fish oil and meat diet. Because of his diet of antirachitic fats, it has been unnecessary for the Eskimo to evolve a white skin in the sunless frigid zone. He has not needed to have his skin bleached by countless centuries of evolution to admit more antirachitic sunlight. He probably has the same pigmented skin with which he arrived in the far north ages ago (Murray 1934).

Actually, this explanation holds true only for a minority of northern natives, i.e., the Inuit, the Aleuts, and some other coastal peoples. Fatty fish is absent from the diet of non-coastal peoples, i.e., most Algonkians, Athapaskans, and indigenous Siberians. Yet the latter are if anything darker-skinned than the Inuit.

Conversely, fatty fish has long been a staple of Scandinavians, who nonetheless are very white-skinned. And the word ‘long’ is no exaggeration: skeletal remains of Danes living 7,000-6,000 years ago have the same carbon isotope profile as those of Greenland Inuit, whose diet is 70-95% of marine origin (Tauber 1981).

But the vitamin-D hypothesis has another shortcoming: Europeans did not turn white until long after their ancestors came to Europe some 35,000 years ago. If we examine the various alleles that lighten European skin color, the time of origin seems to be relatively late. At the SLC45A2 (AIM1) gene, the date is ~ 11,000 BP (Soejima et al. 2005). At SLC24A5, the date falls between ~ 12,000 and 3,000 BP (Norton & Hammer 2007). As a Science journalist commented: “the implication is that our European ancestors were brown-skinned for tens of thousands of years” (Gibbons, 2007).

This has led to an updated version of the vitamin-D hypothesis. It has two postulates:

  • 1. Selection for white skin began long after modern humans entered Europe.
  • 2. The cause was not the weak sunlight of Europe’s high latitudes, but rather less intake of vitamin D from food sources. This happened when a diet of terrestrial game, fish, and wild plants gave way to one based on grains and livestock—in short, the advent of agriculture (Khan & Khan 2010; Sweet 2002).

If we pursue this line of reasoning, Europeans must have turned white almost at the dawn of history. We know that agriculture spread into southeastern Europe from the Middle East around 9,000 years ago. By 7500 BP it had reached a line stretching from the Netherlands through Central Europe and to the Black Sea. Thus, the extreme skin depigmentation of northern Europeans would have occurred over the last seven millennia or so. Actually, the time frame is even narrower, since white-skinned Europeans appear in ancient Egyptian art from the second millennium B.C.

So we’re left with around 3,000 years, at most. Is this pace of phenotypic change consistent with selection due to weak sunlight? Not according to current opinion. Brace et al. (1999) studied how skin color varies among Amerindians, who have inhabited North and South America for 12,000-15,000 years, and among Aborigines, who have inhabited Australia for some 50,000 years. If latitudinal variation in skin color tracks natural selection due to the intensity of sunlight, calculations show that this kind of selection would have taken over 100,000 years to create the skin-color difference between black Africans and northern Chinese and ~ 200,000 years to create the one between black Africans and northern Europeans.

But there’s another problem. How do we know that ancestral Europeans did ingest much less vitamin D when agriculture replaced hunting/fishing/gathering? This question is met only with affirmations, e.g. “Because of the lack of meat and fish in the diet of the new farmers, vitamin D intake would have been drastically reduced” (Khan & Khan 2010). No one seems to have actually quantified vitamin-D intake before and after the advent of agriculture.

To gain a rough idea, we can consult Loomis (1967) for a listing of vitamin-D content by food source:

Food source - Vitamin D content (I.U./gram)
Halibut liver oil – 2,000-4,000
Cod liver oil – 60-300
Milk – 0.1
Butter – 0.0-4.0
Cream – 0.5
Egg yolk – 1.5-5.0
Calf liver – 0.0
Olive oil – 0.0

Sweet (2002) provides a longer list:

Food source – Vitamin D content (I.U.)
Cod liver oil, 1 tbs – 1,360
Salmon, 3.5 oz. – 360
Mackerel, 3.5 oz. – 345
Herring, 3.5 oz. – 315
Sardines, 3.5 oz. – 270
Eel, 3.5 oz. – 200
Shrimp, 3.5 oz. – 150
Beef liver, 3.5 oz. – 30
Egg, 1 whole – 25
Beef, pork, chicken, 3.5 oz. – 20
Cheese, 1 oz. – 4
Unfortified milk – 0
Unfortified cereal - 0

Clearly, fatty fish has a lot of vitamin D. But the same cannot be said for terrestrial animals, like calves. Furthermore, the figures from the first list were initially published in 1938, when most cattle were kept outdoors and exposed to sunlight. These were also American cattle. They lived farther south than the game animals that ancestral Europeans once hunted and whose flesh probably had a lower vitamin-D content.

Thus, before agriculture, Europeans got substantial vitamin D from their diet only in coastal regions, like Scandinavia, where people ate fatty fish. Europeans who lived inland—the majority—did not have this dietary source. One might counter that the issue is not vitamin-D content per se but rather substances, like phytic acids in cereals, that deplete the body’s supply of calcium and phosphorus. The advent of agriculture would have artificially increased the body's need for vitamin D.

Perhaps. Ultimately, this debate will end only when we know the precise time frame when Europeans became white. We already know that this time frame considerably postdates the arrival of modern humans in Europe (c. 35,000 BP). If it significantly predates the arrival of agriculture (after 9,000 BP), the vitamin-D hypothesis will be out of the running, even in its updated form.

This puzzle will then be placed within a larger one. Why do Europeans possess such unusual color traits that involve not only the skin but also the hair and the eyes? How did they evolve so rapidly a white skin and a diverse palette of eye and hair colors? If humans were any other animal, such traits would be readily put down to sexual selection.


Brace, C.L., Henneberg, M., and Relethford, J.H. (1999). Skin color as an index of timing in human evolution. American Journal of Physical Anthropology, 108 (supp. 28), 95-96.
Gibbons, A. (2007). American Association Of Physical Anthropologists Meeting: European Skin Turned Pale Only Recently, Gene Suggests. Science 20 April 2007, 316. no. 5823, p. 364 DOI: 10.1126/science.316.5823.364a http://www.sciencemag.org/cgi/content/summary/316/5823/364a
Khan, R. and B.S.R. Khan. (2010). Diet, disease and pigment variation in humans, Medical Hypotheses, early view.
Loomis,W.F. (1967). Skin-pigment regulation of vitamin-D biosynthesis in Man, Science, 157, 501-506.
Murray, F.G. (1934). Pigmentation, sunlight, and nutritional disease. American Anthropologist, 36, 438-445.
Norton, H.L. & Hammer, M.F. (2007). Sequence variation in the pigmentation candidate gene SLC24A5 and evidence for independent evolution of light skin in European and East Asian populations. Program of the 77th Annual Meeting of the American Association of Physical Anthropologists, p. 179.
Soejima, M., Tachida, H., Ishida, T., Sano, A., & Koda, Y. (2005). Evidence for recent positive selection at the human AIM1 locus in a European population. Molecular Biology and Evolution, 23, 179-188.
Sweet, F.W. (2002). The paleo-etiology of human skin tone. http://backintyme.com/essays/?p=4 (visited on July 10, 2008).
Tauber, H. (1981). 13C evidence for dietary habits of prehistoric man in Denmark. Nature, 292, 332-333.

See also VitaminDWiki

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