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Looks as if my transmission needs work.  And dental crowns aren’t free.

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The Water-Crossers

Science Magazine

One interesting and puzzling question is when and how humans  developed the ability to make ocean crossings.  Although much of the Indonesian archipelago turns into a peninsula during the glacial peaks (Sundaland), it’s never possible to walk to Sahul (Australia/New Guinea). I don’t think it was ever quite possible to walk to the main Philippine islands, either. Palawan had a land connection with Borneo at times of extreme glaciation, but the last time that happened was something like four hundred thousand years ago, well before modern humans.

Homo erectus had a limited ability to cross these water barriers, as far as we can tell. They seem to have managed to get to Flores (judging from old tools and of course  hobbits) , which meant that they had to make two short sea crossings, Bali to Lombok and then Lombok to Flores. Apparently some kind of tool-maker reached Timor as well, and some other islands of Wallacea.  But none managed to get all the way to Sahul – if they had, they would have spread widely and left plenty of very old stone tools, which have not been found.

Modern humans were better at crossing water barriers: they made it to Sahul and the Philippines. The two colonizing populations were evidently related – you can see this in some of the remaining Philippine Negritos, like the Mamanwa, that also have that characteristic Denisovan admixture. These people went on to colonize the Solomon Islands about 40,000 years ago, but  didn’t go further: after the Solomons  you have to cross 200 miles of open ocean to go further, and that didn’t happen until the Polynesians arrived, relatively recently.

This is hard to square with the fact modern humans apparently couldn’t manage to settle Cyprus and some other Mediterranean islands ( judging by the late survival of their odd fauna, such as 3-foot elephants)  until just a few thousand years ago, but that’s what it looks like.

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It has long been known that inbreeding is bad for you. A new paper in Nature (Directional dominance on stature and cognition in diverse human populations) finally gives us a good quantitative estimate of just how bad it is. They find that the offspring of first cousins suffer an average reduction of  1.2 cm in height and 0.3 sd in g ( ~4.5 IQ points) .  They directly measured runs of homozygosity –  more accurate than estimating from genealogy, and better in other ways as well.  Children of first cousin marriages also suffer an elevated incidence of significant genetic disease, roughly 1.5-2 times the non-inbred risk.

That’s not all that far from my previous horseback guess.  The field was full of old and messy studies, so horseback guesses were the best you could do, until now.

The article mentions that Darwin recognized negative effects of inbreeding (a bit too late): they also say that he was among the first to do so, which is not true.  Al-Jahiz talked about it back in the Abbasid caliphate (around 800 AD) and assumed that everybody knew about it: “as the reader knows, the same is the case with horses, camels, asses and pigeons when they are inbred. ”  I suspect that people noticed this soon after farm animals were domesticated, thousands of years ago.

In some parts of the world, mainly the Middle East and North Africa, cousin marriage is very common, with tens of percent of the population practicing it.  Repeated marriages among close relatives can sometimes push the homozygosity up considerably higher than the first-cousin level, with even worse results.

Some retards (British papers) have been spinning this as saying that there are big benefits to mixed-race marriage.   Untrue: to avoid lots of ROH (runs of homozygosity), just marry someone who isn’t from the same isolated population as you. We’re talking outside the valley or across the river : intercontinental travel is not necessary.  Now there might be a degree of hybrid vigor in some distant crosses (currently unclear) – but likely not enough to compensate for someone coming from a group that has low trait values. Marry a Pygmy and your kids are going to be short.  Marry someone from a population whose average IQ  is below 90 (much of the world) and your kids will on average be less smart.

Naturally, enlightened opinion increasingly supports legalization of first-cousin marriage, due to its usual ignorance, perversity, and nihilism.

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National Merit

The National Merit Scholarship is a competition for recognition and scholarships. About 0.5%  of each class become semifinalists, and about 95% of those semifinalists become finalists.  The threshold score varies by state, adjusted so that half a percent of students in each state qualify – which means that the threshold scores varies somewhat by state.

Some finalists get a small scholarship from the organization itself ($2000 over four years)  but more scholarships, with more money, are available from some colleges, also to children of employees in some corporations, etc.  Free rides are possible.

The test is not quite a national IQ test with prizes, since the winning threshold varies by state – but it’s pretty close to one, probably closer than anything else.  The threshold is about 2.58 stds above average – which would be about 139 on an IQ test.

There are those who don’t like this test, probably mostly because they don’t like the overall results, some because they personally did poorly, but there are other reasons.  It is certainly the case that members of influential classes in this country are probably chosen more by test scores than they were once upon a time, while they seem to be crazier  and less competent than they were back in the day: you have to wonder.  Not that our political class is a mandarinate yet: you can find Senators with combined SAT scores of 800, Governors with an ACT score of 18.

One objection is that very few members of minority groups become finalists. Patrick Hayashi, a retired senior University of California official who had overseen admissions at UC Berkeley for ten years, asserted that not one of the hundreds of National Merit Scholars who came to the campus during those years was black or Hispanic. He estimated that “the percent of National Merit Scholars who are black, Hispanic, and American Indian is close to zero and that the absolute number of poor students from these groups is also close to zero”.

To Hayashi, this proves that there is something wrong with the test, but of course it is exactly what you should expect, since the fraction of a group with a significantly lower mean of some quantitative trait that exceeds a high threshold (in height, IQ, whatever) is very much smaller than in a group with a significantly higher mean, as I have pointed out before.  Consider black Americans. If their mean IQ is one std lower than whites, while the width of their distribution is lower (12 points instead of 15) – then for them the NMSPQRT threshold  is 4.475 standard deviations. Instead of 1 in 200, the fraction of winners is less than 1 in 200,000.

This is too simple: IQ can’t be exactly Gaussian, blacks in the US are not perfectly homogeneous, etc.  But it does show the trend: such high scores are much, much, much rarer in groups with low mean scores. It’s also the case that any black kid with such a high score would get a far better offer from Harvard.

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Make Room! Make Room!

There is a recent article in Phys Rev Letters (“Programed Death is Favored by Natural Selection in Spatial Systems”) arguing that aging is an adaptation – natural selection has favored mechanisms that get rid of useless old farts.  I can think of other people that have  argued for this – some pretty smart cookies (August Weismann, for example, although he later abandoned the idea) and at the other end of the spectrum utter loons like Martin Blaser.

If this were the case, it would be a good thing, because we could then hope to significantly extend the human lifespan just by interfering with key steps in the programmed aging mechanism.

We would be able to easily identify those key steps because of natural experiments – people born with mutations that screwed up their kill switch and therefore lived lots longer than normal – you know, like those inventions that get released by mistake (the gasoline pill, the 100 mpg carburetor, etc.) .  The problem is, I  have never heard of any such slow-aging genetic syndrome. I don’t think any exist in humans. Too bad.  And humans are the species to look at – not just because we hope to apply this to humans, but also because we know an enormous amount about human genetics.  Milo of Crotona couldn’t lift a current paper edition of OMIM .

On the other hand, there may well be cases in which something like this happens in other species, particularly in semelparous organisms – those that reproduce only once, like Pacific salmon. Normally those salmon go back to their original spawning grounds, breed and die. In dying, they create a nutrient-rich environment for their off spring, and for other offspring that are on average closely related.  You can see how programmed death might pay off in this case. A simple change does slow down senescence in those salmon: castration before they flame out triples their life span.

There might could be mutations that significantly extended lifespan but had consequences that were bad for fitness, at least in past environments –  but that isn’t too likely if mutational accumulation and antagonistic pleiotropy are the key drivers of senescence in humans. As I said, we’ve never seen any.

It is possible that old people were once useful (materially contributed to the fitness of near relatives), especially in preliterate days.  Back in the ice age climate could change rapidly (Dansgaard-Oeschger  cycles) – old farts may have remembered previous climates, and that might have been useful.  When Peter Panum studied the 1846 measles epidemic in the Faeroes, he found that quarantine could prevent contagion – but  the old farts that had lived through the 1781 epidemic already knew that. People who listened to them, about a quarter of the population, were shielded from the epidemic.

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Inverse weathervanes

I was thinking about something Razib Khan said – that sociology  is useful, because it has negative predictive value.  He’s probably right, but when you think about it, that’s odd. There are a lot more possible wrong theories than right ones  – which means that identifying the right theories is difficult.  Identifying anti-correct theories, exact negatives of the truth,  should be just as difficult. Perverse, too, of course, but who’s counting?

Considering that sociologists typically deny the very existence of some of the most important causal factors on human behavior (like genetics), you’d think their theories would make about as much sense as Galenic medicine or Freudian psychology – not even wrong.  Their theories should not make antisense – more like random nonsense.

Probably they manage this by denying experience.  Experience can show that a method works centuries before anyone has a correct theory of why it works.   There are things that your grandmother (and her grandmother) knew –  (the apple doesn’t fall  far from the tree, blood is thicker than water) –  and without those grannies,  sociologists wouldn’t know what to disbelieve.


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101 Eurasians

There is a new paper out in Nature, mostly about the spread of the Indo-Europeans.  They confirm that the Yamnaya ( from the Ukraine) were the main ancestors of the Corded Ware culture (northern Europe, from Germany far on east).  The Sintashta culture, (base of the Urals down to the Caspian, first with chariots, and ancestors of the Indo-Iranians), looks like a migration of Corded Ware to the east.

The Yamnaya were also the source of the Afansievo culture in the Altai, possible ancestors of the Tocharians.

The European lactose tolerance mutation is not common in the early Bronze Age, but it does exist, particularly in the Yamnaya, where the gene frequency is about 30% (in this study – zero in the Haak study) This suggests that the European mutation originated on the steppe (not Bavaria !) – which would explain why the same mutation is fairly common in northern India and Pakistan.  It’s not clear if it was common enough to have social and demographic significance back then – since it’s dominant, a gene frequency of 30% would mean that 51% of the Yamnaya were lactose tolerant. In other words, I said that I must be wrong about lactose tolerance mattering in the Indo-European expansion, but I am no longer sure about that.  But these samples are small – time to excavate more kurgans. Conceivably the frequency varied significantly by social class.  Anyhow, it had to have been spread by a massive invasion – it couldn’t have spread that fast as a Fisher wave.

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