Why red Indians aren’t white?
I was talking with a friend about Native American skin color. From the Canadian north down to Chile it seems that though there is variation these populations exhibit some sort of brownish shade. There are no black-skinned Amazonians, nor are there pink-skinned peoples on the Canadian Arctic. So what gives?
First, it seems likely that Native Americans have been “native” to the New World for only around the past 10,000 years.1 A physical anthropologist once told me that the body proportions of the natives of the Amazon are still quite “Siberian,” that is, they exhibit adaptations to cold weather after all these generations. And of course time is not the only parameter, Native American populations seem to have gone through a genetic bottleneck; they likely brought over very little standing genetic variation. So you have a relatively short period of time for selection to operate upon over a very limited range of trait value.2
But this isn’t persuasive to me for skin color, at least in the totality. We seem to know the genes at work now. We know that they can be selected very fast, and we know that there have been convergent dynamics across the World Island. 10,000 years is plenty of time. So perhaps the second parameter, extant genetic variation, is at work? That is, the Siberian migrants didn’t bring all the genes for selection to shift them toward new adaptive optimums. For dark skin the data suggest that there is a rough consensus sequence, a constrained set of alleles across skin color genes, which produces our species’ dark “Wild Type.” This suite of genes probably arose when we lost our fur and became strongly pigmented to counter the negative affects of radiation, and it seems like there hasn’t been any reinvention of the wheel here. Melanesian populations which are quite distant from Africans on most genes exhibit the same consensus sequences for skin color loci, by and large. I think that it is likely that the brown-skinned Siberians did lose some alleles at particular loci (that is, they were fixed for loss of function variants), so that for true blackness to reemerge there needs to be new mutations which gain the function back. And as you likely know, gain of function is far less likely than loss of function.
But that only explains why Native Americans don’t get very dark. As I imply above, loss of function isn’t all that hard. That’s why albinos can be found in most human societies, they’re an extreme mutant, but the same principle seems to be operative on many of the skin lightening genes. So why didn’t Native Americans get pink? I think the fact that Siberians and Inuit are relatively brown suggests that extreme depigmentation is not always entailed by life at high latitudes. As many workers have suggested groups like the Inuit consume marine animals who are heavily loaded with Vitamin D, the lack of which is one of the presumed selective pressures driving depigmentation. That being said, most Native American tribes did not live next to the sea. And yet the recent selection events for genes such as SLC24A5 and OCA2 strongly implies that European have become very depigmented very late in prehistory, perhaps almost into historical periods!
Why? I have proposed (following many others, such as L. L. Cavalli-Sforza) that the switch to agriculture resulted in a shift in diet and nutritional intake which entailed greater endogenous Vitamin D production by necessity. But there’s a problem with this model: forms of agriculture existed in the New World as well, and spread up (eventually) into what became the eastern United States. Granted, the latitude of much of this region is about where the Middle East is, but even then it seems that the natives were relatively swarthy. I discount the notion that agriculture was too recent when SLC24A5 might have had selection coefficents on the order of 0.10. Perhaps the people of the New World, at least in North America, kept a more diverse diet, supplementing their agriculture with hunting and fishing to a far greater degree than in the Old World? Additionally, one might suppose that maize was nutritionally superior staple to wheat, barley, millet or rice (I have read that this is so). Ultimately these sorts of questions need to be addressed by a survey of the archaeological literature, as well as assessing the nutritional differences. I’ll get to that at some point.
But there’s one last thing I thought of: disease. I can’t really explain with SLC24A5 goes so far south in India. You see frequencies as high as 25% in Tamil Nadu. Vitamin D deficiency? Certainly nutritional stress is a major issue, but, one thing is for sure, South Asia is subject to a lot of disease in comparison to any other densely populated part of the world. Of the Old World civilizational hearths India was certainly the one weighed down by the greatest endemic pathogen load, in large part because it was so far south and so wet. So perhaps it was disease.
Which brings us to Native Americans. Despite the recent uproar over syphilis, the New World was relatively pathogen free for humans. Granted, with greater population densities disease would have been a major issue among the agriculture populations of the New World, but there were structural reasons why they would have been less prone to epidemic outbreaks than Old World civilizations. The relative lack of domestic animals, the non-existence of closely related species (think of ape strains of viruses), the smaller and more fragmented population networks, and of course the fact that the original migrants probably only brought a small subset of the diseases of the Old World originally. Empirically we know that the Native Americans died like flies when the Eurasians showed up. Their civilization simply didn’t prepare them for Old World plagues. What I’m proposing here is that disease was a major driver of skin color evolution over the last 10,000 years. Or, at least, the same loci which control and modulate melanin production are critical in immune defenses.
I need to do a lot more digging for this to be anything more than a guess. But the disease angle seemed to be the last best hope in explaining why the New World was different. If they were subject to the same nutritional stress, why didn’t they go down the same path as Eurasians? The reason may be that the path was being forged by the threat of disease (Vitamin D deficiency increases susceptibility to infectious agents), which was a less important parameter in the New World. Implausible as it may sound, it seems the most plausible of the various explanations to me.
Note: If you are really curious about the topic, check out the many posts on skin color on this GNXP and the other.
1 – Even if Clovis First is debunked, it seems more and more likely that there are problems with genetic studies which claim that the earliest migrations date to 20-40 thousand years BP.
2 – All things being equal the rate of adaptive evolution is proportional to the extant genetic variation. If there is no genetic variation evolution has no raw material to work with.
Labels: Genetics, Pigmentation
In the post below on eyes, I parenthetically floated the idea that light skin may have acted as an amplifier of disease resistance. Just a special case of what others have proposed for plumage color in birds, etc.
Think of acne (although it’s true for any disease that shows and leaves visible signs). Take two Africans, one without and one with a lot of acne — the diff is perceptible, but not that much. Now give them both white skin — their disease resistance phenotypes are amplified.
If resistance to infectious disease is being selected for sexually — probably true — then lighter skin will be selected for as well. It increases the fitness even more for the light and clear-skinned person, as well as that of the chooser (who now doesn’t mate with a loser / catch parasites from them).
The relation isn’t monotonic obviously: Indians are darker than Swedes (may be under tighter functional constraint near the equator). But there could be something there.
To test this, you’d have to see if light skin harmed fitness for the pock-marked, but increased it for the spot-free. Another prediction is that variance in fitness will increase when skin lightens, since it’s easier for selection to see the variance in the target phenotype if there’s an amplifier. Now, how you really test that, idk.
Another odd thought — a fair chunk of the recent selection may be of this type, an index (honest signal of quality) and one or more amplifiers of it. Skin and eye color, and disease resistance are probably the canonical examples of recent selection.
This may also be another reason why selection sped up after agriculture. There are more mutations, and some of them could be for amplifiers, which will hasten the weeding out process for an index.
i’m actually thinking something like plague (you know, points of truncation selection). you’re thinking of selection via mate choice.
here is my logic laid out
* vitamin D levels are proportional to immune resistance
* increased population density results in the need for increased immune resistance because of more disease
* increased population density is due to agriculture. agriculture also results in a decrease of vitamin D from exogenous sources because of a switch to pure cereal (hunting, fishing & gathering might have had more vitamin D).
* so you have a situation where vitamin D levels are likely decreasing when there a greater necessity that they stay high to resist the new diseases which are sweeping over vulnerable populations.
* the only quick way to remedy this situation is depigmentation to radically increase the endogenous vitamin D production (e.g., 6 times more vit D produced by a “light skinned” vs. “dark skinned” person).
our models are not exclusive. questions:
* i need more data about how light skin is a better signal of disease. i have read that dark skin scars more easily, so someone weakened by illness but who recovers may show more evidence of past infection if they are dark. any dermatologists in the house? (acne is, to my understanding, a modern illness of lifestyle)
* the initial phases of selection are, to my mind, likely to have been what you saw with the ‘great dying’ in the new world. sexual selection is irrelevant when you have something like half the population dying in a wave of infection. think repeated bouts of truncation selection.
* ok, we need medical people to chime in on how many diseases are going to differ in terms of the amplifying affect. e.g., respiratory illnesses aren’t going to matter because no one is looking at the insides of the lung.
one prediction i wonder: does this mean that selection will be stronger in lowland areas? i am to understand that many pathogens don’t do as well at increased elevations.
a fair chunk of the recent selection may be of this type, an index (honest signal of quality) and one or more amplifiers of it.
this would go well with ideas that reproductive skew increased after agriculture. but in any case, re: ‘honest signal of quality,’ those have to have costs usually. expensive. amplifiers are a little different here insofar as they aren’t expensive at high latitudes. the constraint (in your model) is removed, and that is the key. this speaks to a difference in the models: i am proposing that skin color has a very close connection to resistance to disease in connection with particular demographic and ecological parameters, you are proposing that it increases the power of selection to weed out those who are susceptible to disease. the two an be combined of course. the nutrient deprivation combined with more disease would work for both models.
Let’s assume (not unreasonably) that the first modern humans to come Out of Africa were very dark-skinned. When they migrated into areas with weaker sunlight there was strong pressure for depigmentation to enable Vitamin D production. Let’s suppose the depigmentation process in northern Eurasia took some 10,000 years. Then some of those relatively depigmented Eurasians migrated into the Americas. Does it follow that they would become ‘repigmented’ in another 10,000 years? Not at all. It doesn’t even follow that they would ever become repigmented. The selection pressures (if any) for pigmentation are not simply the reverse of those for depigmentation. And we have no idea how long it took for modern humans in Africa to become strongly pigmented in the first place, so there is no basis for the assumption that the process has been slower in the Americas than in Africa.
so there is no basis for the assumption that the process has been slower in the Americas than in Africa.
…well, i didn’t say anything about the speed of pigmentation. but you’re right there, we have a good that depigmentation can happen fast, but not so much the reverse. though since UV radiation has a major affect miscarriage rates one presumes that selective pressure is strong so that if extant variation existed it would be powerful (i believe the jablonski paper reports that natives in the amazon are actually surprising averse to lots of exposure to the sun).
follow up on skin color as amplifier: does it follow that one would prefer someone who has never been infected? granted, those people might be resistant, but with smallpox those who survived would have high fitness in the event of future plagues. so there might be benefit of being able to signal that you were sick, and survived. the inference though is pretty ridiculous that preference for pock-marked chicks could have evolved.
sexual selection leads to to much tangled verbal speculation. i gotta check some formal models…back in a few days ;-)
not just latitude: altitude. mountains have less pathogens? right? i believe peruvians are darker (more UV?)…ethiopians lighter. i think tibetans are darker than chinese.
shout out to ethnographers: preference for light skin more pronounced during plague times? (think black plague)
Smallpox would seem a likelier, ongoing plague.
I’m particularly pleased by your suggestion to look at altitude variation.
Given heavy post-Columbian selection because of disease, would one expect their skins to have lightened appreciably?
Unless polymorphism at skin-color loci were low, pre-contact, I’d expect a lot of effect.
Indeed, given the unusual mortality from things like measles and smallpox, I’d expect North- and South-American, and Pacific-island indigenous populations to have inherited a lot of contact-disease, genetic fallout.
What problems with genetic components are in sharply increased frequency in, say, Amerinds, Na-Dene, or Polynesians?
Alcoholism pops to mind.
Given heavypost-Columbian selection because of disease, would one expect their skins to have lightened appreciably?
Unless polymorphism at skin-color loci were low, pre-contact, I’d expect a lot of effect.
1) right, if die off was around 90% that’s truncation selection.
2) most native groups have small amounts of european ancestry now. so the european alleles should have spread….
It seems likely to me that the selection pressure of skin cancer is not as strong as the pressure of vitamin D deficiency. Also, the timing and location of the spread into the Americas means that the people who arrived wore clothing probably to a greater extent than those who spread to India, Australia, and Micronesia, besides being less distant genetically from African ancestors.
Do we know anything about the skin cancer rates of Native Americans? Could there be another protective mechanism at work?
It seems likely to me that the selection pressure of skin cancer is not as strong as the pressure of vitamin D deficiency.
it isn’t cancer that selects against light skin, it’s the destruction of folate and resultant increase in fetal deformities. anything that hits reproduction is obviously evolutionarily powerful.
Ah, OK, I get what you’re saying now.
1) A signal doesn’t have to be a handicap — i.e. costly — in order to increase in frequency. If it’s an honest indicator of quality because it’s unfakeable (what most now call an “index,” previously called a “performance handicap” by some), that is sufficient too.
This is what’s behind all “good genes” arguments: if you don’t have the genes, you can’t express the phenotype. So having clear skin (or plumage) is an honest signal of disease resistance, if due to good genes. Other examples might include depth of roaring and body size.
2) An amplifier is neither a handicap (it’s not costly), nor an index (it’s not unfakeable). It just helps selection see variance in phenotype. Oren Hasson’s website has some free PDFs on their evolution.
3) High altitude is associated with a lower frequency of wingedness in insects, and likely of any migratory phenotype for disease vectors (not just insects). But this doesn’t bear on things like pneumonia — unless we could show that high altitude correlated with a tendency to stay put in humans too, rather than expose themselves to a bunch of other people nearby.
Well, one crude measure you could do is look for a correlation between altitude and Extraversion. Surely works for latitude (and I could probably even find a ref for that), but I don’t know if anyone would think to look at altitude.
So having clear skin (or plumage) is an honest signal of disease resistance, if due to good genes. Other examples might include depth of roaring and body size.
right, but there are lots of confounds here. after all, we know that body size has been shrinking with agriculture, not increasing. so extending your logic, might not there be selection for body size to show that you’re fit enough to be able to afford the cost? ah, but as you said…no cost here. the key here is exactly how much return-on-investment skin color changes produce re: clarity. my own impression (subjective) is that r.o.i. from very dark to middle brown is high, but far less than from middle brown to very light. that is, pimples so up pretty clearly on brown-skinned people (i’ve never had acne issues, but my brother has, and i tormented him about it). it seems likely that 10-20 K BP europeans were already light brown, like inuit.
but i’ll check the references.
p.s. if there is no cost though even marginal returns for sexual selection might be powerful. also, it seems that even with vit D driving resistance a sexual selection model could work secondarily, that is, those with preferences for light skin would do well and the traits would couple in a runaway.
Yeah, I’m talking more about initial move toward lighter skin — clearly, something else happened that made Swedes much lighter than Indians.
20al%202000b%20-%20Amplifiers.pdf
One other thing — the amplifier idea doesn’t rely just on mate-choice. Males too could be very interested in whether or not another male showed vigorous health. It is good information to know if they want to challenge him, plot against him, enlist him as an ally, avoid catching whatever is going around, bla bla bla bla.
Here’s a pretty simple & short one for folks to start off with:
http://www.orenhasson.com/publications/Taylor%20et%
I’m in a bit of a hurry, but I had to throw this out there.
Recently there have been studies linking elevated lead concentrations and vitamin D deficiency in dark (meaning black) people. The highest increase appears in early childhood.
I’ve got to go, but the abstract is on pubmed.
More to come!!
One additional note on agricultural differences between old world and new: thanks to the oddly temperate climate of Europe (did you know that London is further north than Bismarck North Dakota?), you can grow barley there at near to 60 north latitude. I’m not familiar with pre-Columbian agriculture in the Americas, but I doubt that the inhabitants got a substantial chunk of their calories from agriculture anywhere above about 45 north, just based on what I know about the difference in climates. So it may still be possible to rescue the agricultural theory of pallor. But then my bias towards agricultural and dietary explanations probably rivals agnostic’s bias towards pathogens as an evolutionary force…
Come on Razib. You are searching for depigmentation mechanism in South Asia, where people are not so depigmented at all. More than that- the most depigmented element there has arrived from the North East, almost in ?historical times?.
If we check the maps- most of the blue eyes, blondest hair and lightest skin in the world is concentrated around the Baltic sea. Sorry, but this area can hardly be classified as ?disease ridden?.
And what is special about the Northern Europe- it is the only place on the globe, where you can live above 50°N and still grow crops. Any depigmentation mechanism that doesn?t take into account this circumstance will be always suspicious to me.
Sorry,the “most depigmented element there has arrived from the” North WEST, of course…
arvydas, please don’t talk to me as if i don’t know anything
1) the frequency of SLC24A5 is very high in south asia, and on the order of 80-90 to 25% NW to SE. it accounts for 1/3 of the variation in skin color in south asia. it is also under very selection in the populations we have samples for, from europe to south asia. in other words, it isn’t a function of admixture. so what’s your explanation for this? we know that SLC24A5 is recent, so connect the dots, will you?
2) neutral genomic studies imply that probably around 90% of south asian’s ancestry is derived from pleistocene stock. in other words, stuff like haplogroup J does exist, but at rather low frequencies. M17 in south asia is probably indigenous, and not exogenous as the earlier studies implied. even if derived SLC24A5 is exogenous in origin (likely), ancestral admixture probably can’t explain why it is at 25% frequency among the tamils of sri lanka.
3) as for northern europe, do you know about something called the plague??? yes, i would grant it is less disease ridden than south asia (or africa), but the argument is obvious that i’m comparing relative pathogen loads across both space and time. there are more diseases at 45 degrees north in north america than there were 2,000 years ago.
4) i’ve already made reference to frank sweet’s model for northeast europe. i do find it plausible. that being said, i’ve addressed problems with the genetic architecture in terms of how it has played out over time before, i’m not going to rehash all my arguments to satisfy you.
5) please don’t take a “know it all” tone with me. it’s really tiresome, and makes me want to abolish comments. after reading 50 papers on skin color in the past month i’m really past being lectured to, OK?
Sorry if I sounded like this :)
In fact, I am devoted reader of your blog and generally enjoy your reasoning very much.
Keep it going…
np. i was tired…perhaps i misread your intent.
“… the oddly temperate climate of Europe (did you know that London is further north than Bismarck North Dakota?), you can grow barley there at near to 60 north latitude.”And it ought to have been a lot easier when they started doing it in the climatic optimum (although it probably didn’t feel like that at the time) preceding the onset of the sub-Atlantic. Date derived fron carbonised hulled and naked barley stuffed away in the house wall as cavity filler, along with all the other hearth sweepings (BM-441) 1564+/-120 bc (Ness of Gruting, 60.6N/0.81667W) by which time life was beginning to get a bit grim for farmers up there.
The Norwegians who eventually took the Northern Isles over characterised the aborigines as “pygmies, who hid away in their underground dwellings at noonday, through fear of the sun.”
Obviously they were having a laugh. I’ve never got further than cautiously removing the old waxed jacket in the lee of a gable-end, even at midsummer when you’ve got daylight 24/7. In the winter people go mad.
there are more diseases at 45 degrees north in north america than there were 2,000 years ago
On the Pacific coast at 45 degrees north there are more diseases now than there were 200 years ago.
How quickly does selection for pigmentation take? From the archaeological papers that I’ve read agriculture (maize, squash and beans as a combination, nutritionally far superior to cereal diets) didn’t hit 45 degrees north (Atlantic coast) until about a thousand years before Columbus, with strains slowly inching north and slowly selecting for colder climates from their native southern Mexico and Central America in the previous two thousand years. They were just reaching their maximum (modern expectations of) quality as food at the time of contact. The agricultural economy along the New England coast was just starting to take off as Columbus reached the Caribbean, with the indigenous population numbers peaking at the time of contact with Europeans before plummeting.
On the Pacific coast at 45 to 55 degrees north there’s recently discovered evidence of massive aquaculture cultivation from precontact, which was much more recent. European disease predated contact, as it was spread from the initial Cortez expedition to Mexico then northward through the plains, and hitting the sedentary peoples of the Pacific coast in the late 18th C. Captain George Vancouver reported in his logs for 1792 of towns and villages along the mainland coast of what would be British Columbia and Vancouver Island that were nearly depopulated, the few survivors horribly scarred and the beaches littered with human rib cages and skulls. This would have been smallpox.
I’m assuming I’m reading the same event as told by Mulks, a Squamish historian whose mother was a child at the time of contact with the British, and whose great nephew, Dr. Louis Miranda, left over 10,000 pages of handwritten notes and stories in the Squamish language. There’s a point I’m assuming is the after effect of the Tambora eruption in 1815, (the year without a summer in English language records, Mary Shelley wrote _Frankenstein_ this year,) and then a second plague, probably measles hitting almost immediately after that.
The British government (really the Hudson Bay Company at the time) refused to sign treaties with native groups in the 19th C, because their best demographic data told them all natives in British Columbia would be dead by 1950. The actual low point was 1923, after which native populations have increased.
Hardly scientific, but extensive personal experience leads me to believe that lighter skinned members of these groups received their pigmentation change through interbreeding with peoples of European descent.