Thursday, 2 July 2009

Why are Europeans white?

Why are Europeans so pale-skinned? The most popular explanation is the vitamin-D hypothesis. Originally developed by Murray (1934) and Loomis (1967), it has been most recently presented by Chaplin and Jablonski (2009). It can be summarized as follows:

1. To absorb calcium and phosphorus from food passing through the gut, humans need vitamin D. This vitamin is either produced in the skin through the action of UV-B light or obtained from certain food sources, notably fatty fish.

2. Humans are often vitamin-D deficient, even in tropical regions where UV-B exposure is intense and continual. This deficiency has led to high frequencies of rickets in many populations, particularly western Europeans and North Americans during the great rickets epidemic from c. 1600 to the mid-20th century. This epidemic occurred in areas where human skin was already producing sub-optimal levels of vitamin D because of the naturally weak sunlight at northern latitudes. These levels then fell even further wherever the Industrial Revolution had reduced sun exposure through air pollution, tall buildings, and indoor factory life.

3. If ancestral humans were often sub-optimal for vitamin D, natural selection should have favored lighter skin color, as a way to produce more of this vitamin by allowing more UV-B into the skin. Such selection, however, would have been counterbalanced in the tropical zone by selection for darker skin, to prevent sunburn and skin cancer.

4. This equilibrium would have ceased once ancestral humans had left the tropical zone. On the one hand, selection for darker skin would have relaxed, there being less sunburn and skin cancer. On the other, selection for lighter skin would have increased, there being less UV-B for vitamin-D production.

Ancestral humans thus began to lighten in skin color once they had entered Europe’s northern latitudes. This selection pressure eventually drove European skin color almost to the limit of depigmentation.

Were ancestral Europeans deficient for vitamin D?

There are several problems with the vitamin-D hypothesis. First, if lack of this vitamin created the selection pressure that led to white European skin, why are Europeans genetically polymorphic in their ability to maintain blood levels of vitamin D? At least two alleles reduce the effectiveness of the vitamin-D binding protein, and their homozygotes account for 9% and 18% of French Canadians (Sinotte et al., 2009). If lack of this vitamin had been so chronic, natural selection would have surely weeded out these alleles. And why does European skin limit vitamin-D production after only 20 minutes of UV-B exposure? (Holick, 1995). Why is such a limiting mechanism necessary?

There is also little evidence that ancestral Europeans suffered from vitamin-D deficiency. Before the 17th century, we have only sporadic evidence of rickets in skeletal remains and even these cases may be false positives, as Wells (1975) notes:

It is likely that these low frequencies of rickets should be even lower because some of the authors quoted above have based their diagnoses on such features as plagiocrany (asymmetry of the skull), which may occur merely from cradling habits and other causes (Wells, 1967a) or on irregularities of the teeth, which probably result from many adverse factors in foetal life as well as in infancy.

On this point, Chaplin and Jablonski (2009) affirm: “Despite taphonomic biases, it [rickets] has been recognized in early archeological and Neolithic materials at the rate of 1-2.7% (a reasonably high selective value).” In fact, Wells (1975) reports no cases from Paleolithic Europe and only sporadic cases from Neolithic Europe. The range of 1-2.7% seems to apply to “a gradual, albeit slow, increase of the disease during the European Middle Ages” (Wells, 1975). Wells (1975) cites a series of Hungarian remains that indicate an increase in frequency from 0.7 to 2.5% between the 10th and 13th centuries. As Wells notes, even this low incidence is probably inflated by false positives.

Why is skin white only among Europeans?

The vitamin-D hypothesis raises a second problem. Why is white skin an outlier among the skin tones of indigenous human populations north of 45° N? Skin is much darker among people who are native to these latitudes in Asia and North America and who receive similar levels of UV-B at ground level. Murray (1934) attributes their darker skin to a diet rich in vitamin D:

One of the chief difficulties up to now in accounting for the origin of the white or unpigmented race has been the existence of the darkly pigmented Eskimo in these same dark sunless Arctic regions which we have been discussing as the probable original habitat of the white race. The unravelling of the causes of rickets has fully explained this anomaly. 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. Cod liver oil, as has been stated, is fully as efficient as sunlight in preventing rickets. Now the daily diet of the Eskimo calculated in antirachitic units of cod liver oil equals several times the minimum amount of cod liver oil needed to prevent rickets. 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.

This argument fails to explain why skin is equally dark among inland natives of northern Asia and North America who consume little fatty fish and yet show no signs of rickets. One might also point out that fatty fish has long been a major food source for the coastal inhabitants of northwestern Europe. According to carbon isotope analysis of 7,000-6,000 year old human remains from Denmark, the diet must have been 70-95% of marine origin (Tauber, 1981). Yet Danes are very pale-skinned.

Some have suggested that sufficient vitamin D could have been obtained from the meat of land animals, if eaten in sufficient quantities (Sweet, 2002). This has led to a revised version of the vitamin-D hypothesis: ancestral Europeans lightened in color when they made the transition from hunting and gathering to agriculture 8,000 to 5,000 years ago, and not when they first arrived some 35,000 years ago.

Do we know when Europeans became white? This change has been roughly dated at two gene loci. At SLC45A2 (AIM1), Soejima et al. (2005) have come up with a date of ~ 11,000 BP. At SLC24A5, Norton and Hammer (2007) suggest a date somewhere between 12,000 and 3,000 BP. These are rough estimates but it looks like Europeans did not turn white until long after their arrival in Europe. As a Science journalist commented: “the implication is that our European ancestors were brown-skinned for tens of thousands of years” (Gibbons, 2007). Thus, the original version of the vitamin-D hypothesis no longer seems plausible.

Of course, the revised vitamin-D hypothesis is still plausible, i.e., Europeans became pale-skinned after giving up hunting and gathering for agriculture. But this scenario does raise problems. For one thing, it would mean that many Europeans turned white at the threshold of history. In the case of Norway, agriculture did not arrive until 2400 BC and fatty fish, rich in vitamin D, have always been a mainstay of the diet (Prescott, 1996).


Chaplin, G., & Jablonski, N.G. (2009). Vitamin D and the evolution of human depigmentation, American Journal of Physical Anthropology, early view

Gibbons, A. (2007). American Association Of Physical Anthropologists Meeting: European Skin Turned Pale Only Recently, Gene Suggests. Science 20 April 2007:Vol. 316. no. 5823, p. 364 DOI: 10.1126/science.316.5823.364a

Holick, M.F. (1995). Noncalcemic actions of 1,25-dihydroxyvitamin D3 and clinical applications, Bone, 17, 107S-111S.

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.

Prescott, C. (1996). Was there really a Neolithic in Norway? Antiquity, 70, 77-87.

Robins, A.H. (2009). The evolution of light skin color: role of vitamin D disputed, American Journal of Physical Anthropology, early view.

Sinotte, M., Diorio, C., Bérubé, S., Pollak, M., & Brisson, J. (2009). Genetic polymorphisms of the vitamin D binding protein and plasma concentrations of 25-hydroxyvitamin D in premenopausal women, American Journal of Clinical Nutrition, 89, 634-640.

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.

Tauber, H. (1981). 13C evidence for dietary habits of prehistoric man in Denmark, Nature, 292, 332-333.

Wells, C. (1975). Prehistoric and historical changes in nutritional diseases and associated conditions, Progress in Food and Nutrition Science, 1(11), 729-779.


Tod said...

"It has been suggested by those who have little knowledge of human nutrition and little expertise in the field of vitamin D that everyone can obtain enough of their vitamin D requirement from their diet and that any unprotected sun exposure should be avoided (5). However, most experts agree that 1,000 IU of vitamin D3 is required if there is no exposure to sunlight (1–3, 6,7). It has been assumed that fish, especially oily fish such as salmon, mackerel and blue fish are excellent sources of vitamin D3. However, our analysis of the vitamin D content in a variety of fish species that were thought to contain an adequate amount of vitamin D did not have an amount of vitamin D that is listed in food charts. There needs to be a reevaluation of the vitamin D content in foods that have been traditionally recommended as good sources of naturally occurring vitamin D".

Lu Z, Chen TC, Zhang A, Persons KS, Kohn N, Berkowitz R, Martinello S, Holick MF. An evaluation of the vitamin D(3) content in fish: Is the vitamin D content adequate to satisfy the dietary requirement for vitamin D? J Steroid Biochem Mol Biol. 2007 Jan 29; [Epub ahead of print] doi:10.1016/j.jsbmb.2006.12.010

Tod said...

Don at Primal Wisdom pointed out

"A 3.5 ounce serving of wild (salmon contains 500-1000 IU of D and about 200 kcal [...] (35 ounces) would supply only 2000 kcal (two thirds the requirement of an active young male) and 5K to 10K of vitamin D. ".

Salmon are obviously not typical fish, not only are they - especially Sockeye - by far the best food source of vitamin D but they are only available in quantity during a salmon run. Eating other fish would supply far less. Over a year the Inuit were getting more of their vitamin D from the sun on their face then from fish I think.

Don's argument is similar to that of Linus Pauling who gave the water soluble vitamin C content of 110 raw natural plant foods in an amount giving 2500 Kcals of food energy. The average for 110 foods was 2300mg while peppers gave 14200 -16500mg, salmon would be the peppers. Even the lowest group of foods gave 600- 1200mg. It was known at the time that at a small dailly intake of vitamin C - up to about 150mg - the concentration in the blood is nearly proportional to the intake. 5mg per litre for an intake of 50 mg, 10mg for an intake of 50mg, 10mg per litre for an intake of 1000mg Above an intake of 150mg a day the concentration in the blood increases much less with increasing intake , reaching about 30mg per litre for an intake of 10 GRAMS a day.

Compare Vieth's data on D, the dose response is significant.
"Two studies showed that in response to a given set of ultraviolet light treatment sessions, the absolute rise in serum 25(OH)D concentration was inversely related to the basal 25(OH)D concentration. In the study by Mawer et al (34), the increase in 25(OH)D in subjects with initial 25(OH)D concentrations <25 nmol/L was double the increase seen in subjects with initial concentrations >50 nmol/L. Snell et al (27) showed that in subjects with initial 25(OH)D concentrations <10 nmol/L, ultraviolet treatments increased 25(OH)D by 30 nmol/L, but in those with initial 25(OH)D concentrations approaching 50 nmol/L, the increase was negligible."(Vieth 99)

Dr. Vieth's latest -
Vitamin D and cancer mini-symposium: the risk of additional vitamin D..
"The physiological buffer for vitamin D safety is the capacity of plasma vitamin D-binding protein to bind the total of circulating 25(OH)D, vitamin D, and 1,25-dihydroxyvitamin D [1,25(OH)2D]. Hypercalcemia occurs when the free concentration is inappropriately high because vitamin D and its other metabolites have displaced 1,25(OH)2D from vitamin D-binding protein. Evidence from clinical trials shows, with a wide margin of confidence, that a prolonged intake of 10,000 IU/d of vitamin D(3) poses no risk of adverse effects for adults, even if this is added to a rather high physiologic background level of vitamin D."

It never occurs to Dr. Vieth to wonder -

"why are Europeans genetically polymorphic in their ability to maintain blood levels of vitamin D? At least two alleles reduce the effectiveness of the vitamin-D binding protein, and their homozygotes account for 9% and 18% of French Canadians (Sinotte et al., 2009)"

This is very telling, especially as "Many studies have discussed the link between vitamin D binding protein phenotypes and susceptibility or resistance to osteoporosis, Graves' disease, Hashimoto's thyroiditis, diabetes, COPD, AIDS, multiple sclerosis, sarcoidosis and rheumatic fever."

Biological and clinical aspects of the vitamin D binding protein (Gc-globulin) and its polymorphism.

RG said...

Even if vitamineD is not the primary cause of depigmentation, the problem of europeans turning white at the dawn of history still remains.
I still don't understand how Peter's mechanism of sexual selection can turn white a huge number of brown-skinned europeans.

All our matrilineal ancestors (the Seven Daughters of Eve of the european clans, as described by Brian Sykes from their mitochondrial matrilineage ) are older than 12 000 years, except the clan of Jasmine.

From Sykes web site at
"The clan of Jasmine
(Persian for flower)
is the second largest of the seven European clans after Helena and is the only one to have its origins outside Europe. Jasmine and her descendants, who now make up 12% of Europeans, were among the first farmers and brought the agricultural revolution to Europe from the Middle East around 8,500 years ago."

Say this clan of farmers, in agreement with the vitamineD hypothesis, was carrying the mutations for white skin, how the mutations are going to spread to all the descendants of the other clans, who are widespread far away all over Europe ?

I accept the sexual selection for neotenic-fair traits as a likely mechanism, but that's not enough to me. I am convinced that a post-glacial male hunter would not choose a female only for her fair complexion IF there was not something else. Because for a male hunter, that's the kids that matters, not really the female. The light-skinned kids must have been better somehow at something, which I think would be hunting.
A male kid with fair skin must have been able to bring food better than his father. Otherwise I don't see enough selective pressure to spread these new genes all over Europe.

Tod said...

In 'Infectious Causation of Disease' Cochran et al say;-
"Alleles will be lost in proportion to the fitness costs that they impose, and will be generated only slowly by mutation; thus, only small fitness loads can be maintained solely by mutation. An allele that causes a severe genetic disease at a frequency that is too high to be maintained by mutation must generate fitness benefits to itself that compensate for the extra fitness costs it incurs. It is difficult to imagine how severe damage to biological machinery could somehow improve some other aspect of the basic functioning of the machinery sufficiently to compensate for the damage. It is easy, however, to envision how genetic damage to biological machinery can guard against even greater damage from a parasite."

One might suspect that the "alleles [that]reduce the effectiveness of the vitamin-D binding protein". Thereby increasing "susceptibility or resistance to osteoporosis, Graves' disease, Hashimoto's thyroiditis, diabetes, COPD, AIDS, multiple sclerosis, sarcoidosis and rheumatic fever" confer an advantage that outweighs these fitness costs. One way could be by somehow increasing resistance to a very common and devastating infection. There is one obvious candidate:-

"Mycobacterium tuberculosis kills more people than any other single pathogen, with an estimated one-third of the world's population being infected."

Genetic polymorphisms in vitamin D receptor, vitamin D-binding protein, Toll-like receptor 2, nitric oxide synthase 2, and interferon-γ genes and its association with susceptibility to tuberculosis .
"The correlation between serum level of vitamin D and risk for tuberculosis latent infection or disease development has been described in African immigrants living in Australia (3). Lower mean vitamin D levels were observed in latent infection compared with individuals with no M. tuberculosis infection and lower in tuberculosis patients. Higher vitamin D levels were associated with lower probability of any M. tuberculosis infection (4[...]
The active metabolite of vitamin D, 1,25(OH)2D3, suppresses growth of M. tuberculosis in vitro and this effect may be facilitated by TLR in vivo (10). Thus, there is an elegant system of control of innate immunity by 1,25(OH)2D3. The most reasonable explanation suggests that vitamin D stimulates the immune cells to resist M. tuberculosis infection by mediating protection against tuberculosis by `nonclassical' mechanisms.[...]
A role of DBP polymorphism in autoimmune diabetes mellitus and infectious disease in Polynesia and Japan (25) has been suggested. Until now, only one study evaluated the DBP phenotype in tuberculosis patients and no differences were seen among patients and the control group. In that study, a 33% frequency of Gc2 in tuberculosis patients was slightly but not significantly higher than in the control group (26%), and this elevation was at the expense of both Gc1F and Gc1S alleles (26). Further studies are necessary to understand the physiological role of VDBP and its phenotypes on susceptibility to tuberculosis and other diseases. [...]
Until now, only one study evaluated the DBP phenotype in tuberculosis patients and no differences were seen among patients and the control group. In that study, a 33% frequency of Gc2 in tuberculosis patients was slightly but not significantly higher than in the control group (26%), and this elevation was at the expense of both Gc1F and Gc1S alleles (26). Further studies are necessary to understand the physiological role of VDBP and its phenotypes on susceptibility to tuberculosis and other diseases. "

As far as I can make out the DBP polymorphisms that lower 25(OH)2D3 do not noticeably protect against Mycobacterium tuberculosis.

It seems that high vitamin D levels are something that is more damaging to fitness than an increased risk of myriad diseases, including TB

ItsTheWooo said...

Well, all creatures will turn pale / lose pigment when they are in environments deprived of sunlight. Consider cave dwelling animals; pretty much pale and blind (Obviously eurpeans wouldn't become blind because that would require a level of light deprivation as extreme as literal cave dwelling.)

Seeing as a cave dwelling animal evolves to become pale, and this change is directly related to lack of light, it's pretty much established that the pigmentless eyes, hair, and skin of many europeans is most likely related to ancestral light exposure that is much less than darker humans.

This need not involve vitamin d. At all.

Perhaps it isn't a question of why we are selecting for pigmentlessness... but maybe, instead, it is a phenomenon of relaxed selection pressure on darker complexions? Perhaps creatures / humans become increasingly more pale not because it is an advantage... but perhaps pigment no longer has any value when light is removed from the equation.

Sort of like the fact that we didn't evolve specifically to not have a tail... but maybe when we stopped climbing trees, a tail no longer became a huge selection pressure so that now all that remains is a little stub of sacrum.

With absence of pressure (heavy sunlight) to select for dark skin/eyes/hair, don't be surprised when you end up with creatures that don't put in the extra work to make pigment.

ItsTheWooo said...

As for the reason sunlight qualifies as a pressure to select for pigment producing cells in the hair/eyes/skin... I have evidence of that right on my arms (a sun burn).

Sun radiation can sorta cause burns, which can sorta lead to infections and death in a natural environment.

Having darker skin and thicker skin is a valuable when you're blasted with sun all day.

But, take sun out of the picture, meh, don't be surprised when your melanocytes get lazy.

Peter Frost said...


"Evidence from clinical trials shows, with a wide margin of confidence, that a prolonged intake of 10,000 IU/d of vitamin D(3) poses no risk of adverse effects for adults, even if this is added to a rather high physiologic background level of vitamin D."

I haven't read the article read, but I'm surprised by the above statement. The adverse effects of excessive vitamin D seem to be long-term and similar to the effects of aging. It would be difficult to establish such effects without a well controlled longitudinal study.

Thanks for the fish reference!


I don't adhere to the vitamin D hypothesis of European skin depigmentation. I think it is important, however, to examine what this hypothesis would predict. The original version predicts that Europeans began to lose skin pigmentation once they had arrived in Europe (c. 35,000 years ago). The new version predicts that this depigmentation occurred very late, almost at the threshold of human history (and even after in the case of Norway).

Once we have firm dates for the 'new' skin pigment alleles, both versions will probably be invalidated. As I've stated elsewhere, the European phenotype changed within a relatively narrow time window during the last ice age, apparently because of an increase in sexual selection of women.

Its the Woo,

The problem with your explanation (relaxation of selection for dark skin) is that it does not explain why other indigenous population at similar latitudes (northern Asia, North America) have remained much darker-skinned than Europeans. These other populations are exposed to the same amount of UV light at ground level.

RG said...

Peter, I understand globally your theory except for the geographic and demographic situation. 12000 years ago, Ireland was populated, same in Gaul, and by the time of Ceasar, Gaul population was estimated between 10and 20 millions. Such numbers suggests very old settlements in agreement with record paintings in caves, but if the human settlement is old, then it is made of brown skinned people. Now, the new gene flow for white skin come from the east, 3000 km from Ireland. How these genes are going to be tranfered so that all the brown skinned turned white by the time of ceasar? Where are all the brown skinned gone? (beside some rare isolates). I could understand this if the white skins were positively selected and the dark skins were whiped out by some sort of strong negative selection.

But please, describe with examples how do you see that happen. What is this temporal window that you are talking about ? could it be a period with constant cloud cover and less light all over Europe ?

Likewise, Itsthewoo, if you get a sunburn, and you can get a sunburn even in England, therefore there is light, therefore there is a need for melanine.

ItsTheWooo said...

Peter frost:
Here is a website containing a map showing the intensity of uv radiation on all regions of the earth:

Here is a website containing a map showing the intensity of skin color of native inhabitants on all regions of the earth:

The skin color map superimposes over the uv radiation map.

Sorry, but it's fairly obvious to me that we evolved skin color, thickness, hair color/texture traits primarily under pressure of sun radiation.

People who are pale are pale because they don't have to be dark. There is no need for dense hair, thick skin, very dark pigments when you're not located in central africa. Paleness did not evolve, it is darker skin which evolved (in response to heavy duty sun). Paleness is the default state, it is an absense of something. It serves no purpose.

RG - It's not black or white (LOL get it). It's not "either you need melanin or you don't"... it's a question of how much you need. People in central africa need a whole lot. People in southern europe need a little. People in northern europe/northern asia don't need that much and some are almost totally void of pigment.

And, there is the additional factor of "the tan". Even people with moderate/mild pigments can become situationally dark when the sun hits the skin. The tan is an adaptation to environments where the sun intensity was unpredictable.

People in england (well, most of them... some are too pale to tan) will develop a tan when late spring comes, reducing the likelihood of seasonal sun exposure/burns.

ItsTheWooo said...

RG - How do you believe skin color translates into hunting skill? Curious. Even if we assume skin color is just a marker for some other advantageous trait, what IS it?

Even more puzzling, why are we all dismissing the fact that every single animal is colored the way it is primarily because of it's environment/light exposure? Why would / should humans be any different? Why are we being so personal (white skinned people were better hunters, white women were more sexually desirable, etc). This is such obviously biased thinking.
Just look at a little cave fishie. It doesn't haveta deal with light, so it doesn't bother producing pigment. It also doesn't have eyes, because those are useless without light.

Euros are basically like the cave fish - why bother making pigment when you don't need to. Evolution is a reaction, not an action.

Also, I'm curious as to the whole "euros are white because of sexual selection of females" idea. Trying not to snicker too much, but does anyone bother asking why our ancestors found pale skin desirable in a female? Well pale skin is desirable today in a female because of our culture, because it ALREADY has become familiar to us... but assuming slightly lighter skin were this new mutation thinger, what would motivate people to seek it out?

Fads and fashion as a special case (culture/social motivation)... the things people find sexually attractive are things that indicate fitness to our primal brain, they are evolutionarily hard coded. What would be the motivation for males to select pale females? I suppose it is true that pale skin may indicate femininity (male hormones make the skin darker) so there may be a tendency for males to view paler skin as an indication of fertility (HYPOTHETICALLY speaking) ... but it seems obvious to me this is an inadequate explanation.

Given the good overlap between uv radiation/skin color density, given the cave fishies and such creatures... it seems a much better explanation is the simple one.

It is dark skin that evolved.
White skin is what you have when you don't need special skin that much because you aren't dealing with particularly extreme amounts of light. It's the default mode.

RG said...

"RG - How do you believe skin color translates into hunting skill? Curious. Even if we assume skin color is just a marker for some other advantageous trait, what IS it?"

It's a guess, I don't know what it is, but I am convinced that sexual selection for pale skins will not be enough to explain ice age european depigmentation. As you said, skin color could have been a marker associated with other traits, language, behavior, etc, anything that can bring more food on the table.

Europeans are no cavefish. Many of your points have been adressed in this blog before. I think the biggest blow to the vitamineD theory is the discovery that white skins genes appeared between 12000 and 3000 years ago, meaning that for almost 30 thousands years Europeans had a darker skin and were fine with that. These darker skin europeans got as much vitamineD with their putatively light-brown skin than white skin people can get at the same latitude. Why then, did natural selection suddenly depigmented them to the point where they could get sunburned, whith no advantage in vitamineD synthesis?

OK, you say it's darkness that evolved, but first, you have a small time frame, at most 12000 years, to de-pigment ice age europeans, and second, because of the point above, you have no selection pressure if you dimiss sexual selection.

If you could prove that light insulation was very low all over Europe, possibly because of a permanent cloud cover when the glaciers were melting, then maybe depigmentation is doable in a few thousands years. The main advantage of the "cavefish" theory is that this selection, and therefore depigmentation, would apply everywhere in Europe.

Sexual selection for pale skin is a serious boost to depigmentation, but, as opposed to your theory, it depends on a gene flow from "white skin donnors". In particular it has to explain the spreading of the genes to remotely distant brown-skinned populations from which european still descent.

Peter Frost said...


Twelve thousand years ago, the population of Europe was quite small. The estimates I've seen are in the tens of thousands. It was also a very mobile population, particularly on the plains of northern and southern Europe. It was in this region and within that time period (probably the second half of the ice age) that I see this phenotypic changes occuring.

Its the wooo,

The link you provided is a dead link. In any case, variaton in human skin color does not closely correlate with variation in UV at ground level. Please see the maps on my website:

If you wish to criticize the sexual selection hypothesis, you should probably first read up on it. It is discussed in my last article:

Frost, P. (2008). "Sexual selection and human geographic variation", Proceedings of the 2nd Annual Meeting of the NorthEastern Evolutionary Psychology Society, The Journal of Social, Evolutionary & Cultural Psychology 2 (supp.): 49-65,

RG said...

Peter, it is clear that the older are these "white" genes, the smaller is the european population and the easyer your theory can explain the whole story.
But these genes have to go all the way from the northen plains of europe trough montains and oceans, not just plains, to Ireland. And the population grows fast, millions by the time of Ceasar, all white: Gauls, Germans, Latins, Britons, Basques etc.
If the white genes appears so far as 10 000 years ago, as you seem to believe, there is few europeans to convert and your theory stands alone.
Have you though about a reproductive advantage for the fair skin mothers, like easyer or more abundant pregnancies ?

Steve Sailer said...

Why do I feel happier after I've been out in the sun?

How widespread is that feeling?

Do people of other races feel that way as much as white people do?

Tod said...

Steve Sailer said...
"Why do I feel happier after I've been out in the sun?"

Maybe because it's a break, those who work in the sun may feel differently about it.

Peter Frost said...


There seems to be a mental algorithm that diminishes aggressive impulses and stimulates feelings of care when people view lighter-colored skin (see my website for my writings on this subject). In traditional cultures, lighter-skinned women are preferred as mates, apparently because they are perceived as being more feminine. In non-traditional settings, this preference is less hegemonic because there is more emphasis on short-term, non-committing relationships.

I suspect that intense sexual selection rapidly changed the phenotype of the nomads who ranged across the steppe-tundra of northern and eastern Europe, probably around 15,000 to 10,000 BP. During and after that period, there was a more gradual change among European populations on the periphery of this zone, as a result of gene flow pushing outward. For a number of reasons, there has been a general trend since the last ice age of human populations expanding southward from the temperate/subarctic zone.


Nowadays, people say they feel happier after being in the sun, but this kind of reaction is relatively recent (post-1920s). During the late 1980s, I interviewed elderly farmers who had come of age before the 'sunshine movement' of the 1920s. They would often say that people didn't see the sun in the same way back then. People actually felt uncomfortable if they were in the sun too long, especially the midday sun (which was shunned as much as possible). There was a feeling that the sun's rays had a withering effect, making people older and weaker.

Yes, this is diametrically opposite to the prevailing view today. It's a bit like the view that ethnic diversity is 'vibrant' and that 'whitebread' society is inferior. We hear this view so often in our cultural environment that we end up believing it.

救援部 said...


倶楽部 said...


プロフ公開 said...


素人 said...


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Bris said...

RG said...

"Even if vitamineD is not the primary cause of depigmentation, the problem of europeans turning white at the dawn of history still remains.
I still don't understand how Peter's mechanism of sexual selection can turn white a huge number of brown-skinned europeans."

Genghis Khan has an estimated 150 million direct living descendants. He lived only 700 years ago.

Hunter-gatherer societies are polygamous and nearly all the children are fathered by a very small number of men. A single male could father dozens of children. If females strongly preferred males with less pigmentation then de-pigmented children would become a majority within a few generations.

Celeste said...

You are all forgetting that humans have been wandering around Europe and settleing different areas at different times, and that the environment itself (ice ages, inter-ice-ages, short bursts of higher temps etc) has been changing.
In order to answer the question 'why are the american indians still dark skinned?' you have to look at when they arrived in america. They've only been there 5-8000 years, not long enough to evolve major changes. Its also about what is necessary, there is more light in many parts of ameria than northern europe, especially northern europe during an ice age, the indians arrived in america relatively late and not during an ice age. The fact that europeans have such dramatic depigmentation shows how long they have been adapting to their environment.

The same goes for Asia, don't assume that northern Asia has been populated or even been accessible for very long, and remember that we are in an -inter-glacial period which only goes fore about 10,000 years, opening up a few opportunities for settlement but not long anough to evolve major changes.

Euopeans have been in Europe for much longer than 25,000 years. If native Australian aborginiees have been in Oz for 40,000 (now more like 70,000) and Oz is a long way away from Africa, then why wouldn't Europeans have wandered up to relatively close-by Europe in the North. It would have been exploited much earlier, and in waves, some unsuccesful, timed with ice ages and inter-glacial periods.

Its way more complicated than 'people from Tahiti look the same as people from NZ', you have to assess how long theyve been there and the slow ticking-clock that is evolutionary time.

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