High IQ doesn’t have _evolutionry_ advantages in modern societies. It lowers your reproductive fitness, on average.

I think male preferences are not the reason that women with high IQs have fewer-than-average children.

The negative IQ-fertility correlation is very widespread nowadays, but it wasn’t in the past. I would guess that higher IQ, all else equal, was a plus in almost every society, but the balance of advantages and costs was not the same everywhere.
I think that transition to more complex money economies created a niche with higher reproductive rewards for IQ in a number of societies during premodern times, and in some cases, this niche persisted long enough to have measurable effects. But that trend certainly ended by the beginning of the 20th century.

fMRI + biofeedback. Should work.

Gregory Cochran

Risch doesn’t make a lot of sense. One of the key arguments is that high frequencies of _multiple_ mutations of the same gene or worse yet multiple mutations in each of a number of metabolically related genes, is incredibly unlikely. But that has happened: there are three overly common Tay-Sachs mutations among the Ashkenazi, two overly commom Gaucher mutations, three Niemann-Pick mutations of roughly equal frequency, two elevated mucolipidosis type IV mutations. Tay-Sachs, Gaucher, and Niemann-Pick all invovle sphingolipd degradation, and the sphingolipids that pile up in mutant homozygotes (and are presumably mildly elevated in heterozygotes) are nerve growth factors.

Boas calculated that the probability of the Gaucher mutation distribution alone is less than 1 in 500: Risch doesn’t address this at all.

I have no idea what his point is in comparing geographic distributions of lysosomal- and non-lysosomal mutations, considering that many or most of the non-lysosomal mutations have _also_ been made common by selection. CF has, almost certainly. There’s evidence that strong selection is occuring at the BRCA1 locus (again two mutations). Slatkin has said that there must have been selection elevating the factor XI clotting disorder mutations ( again two different mutations). The connextin-26 deafness mutation has clearly been favored by natural selction in many populations, probably as a disease defense.

I have been arguing with Derbyshire in Steve Sailer’s discussion group for four years, off and on. I don’t value his thought. As for MacDonald’s stuff on Judaism, I think that there was for sure an interesting evolutionary event there, but I can’t make any sense of most of what he says about it. Since Kevin has graciously aided me in some data gathering, I can only say that I don’t mean that in a _bad_ way.
If you want a nice solid neoDarwinian look at the Ashkenazi Jews, one with nice quantitative arguments, you won’t have to wait long. One is in preparation.

Peoples can easily change on historical time scales. Just rememeber that the narrow-sense heritability of practically every behavioral/cognitive trait you could shake a stick at is substantial, tens of percent. If the pattern of society causes certain traits to be rewarded (in terms of increased reproductive success) for a few hundred years, you’ll see noticeable change. A one-standard-deviation change is perfectly possible.

Hardly anybody seem to realize this.
I wonder why.

Look, _nobody_ thinks about this. I’m not just talking about people who want to celebrate their ancestors’ real or imagined achievements.

If you really want to understand long-range historical trends, assuming that that is even possible, you’re going to have to take selection over historical time into account. Or so it seems to me.

Of course.

I think you’re missing the point. There is an old-fashioned view, probably held by only a few people today, that every male citizen _should_ be willing to fight. The corollary is that anyone who won’t is without honor, contemptible – and especially unfit to command those who _are_ so willing, unfit to even _advocate_ war. The absolute risk involved isn’t the point, really; that can change radically when you least expect it, anyhow.
In this sense, ‘chickenhawk’ applies to people who avoided military service. The typical warblogger or opinion writer has not faced this and is merely militarily inexperienced, a different thing. Usually also ignorant of military history and technology – born that way, I expect.

I talked to Paul Ewald about SARS a couple of days ago. Evolution tends to favor milder strains of respiratory bugs, but it takes time. A new virulent strain may spread a long way before moderating.
The simnplst guide is history: what has happened, can happen. So you want to look at the 1918 flu epidemic, the English Sweat epidemics, etc.

Not many people have made the effort to learn the things one would have to understand in order to make a reasonable judgement on the merits of this war. More exactly, few know those subjects well enough to make critical judgements: well enough to sort informational wheat from chaff, which is a particular problem in this case.

Sometimes I used to enjoy the visitors from other timelines, back on h-bd. Remember the one from the line where Alexander the Great died in battle? But after a while it palled, because for some strange reason, they were all unusually stupid.
Evidently the same is true here. Maybe the transition fries their brains – probably some quantum mechanical effect.

Poe’s comments re the civil war are irretrievably stupid. It might help if you knew anything about the relative size and power of the Russian and British fleets in those days- it’s like comparing a lion with a dachshund. A dumb dachshund like mine. The Russian fleet could no more have deterred, or influenced in any way, British intentions towards the US than the man in the moon.

The British wouldn’t have lost a single warship. Contrariwise, the Germans would have lost tens of thousands dead if they’d invaded Switzerland in 1940.

Only a really stupid person would think the two situations very similar.

Maybe I shouldn’t use the word ‘stupid’. Somehow it doesn’t seem strong enough.

Of course genetic differences explain the pronounced ethnic differences in vulnerability to infectious disease. This is one of the fundamental facts of history.
For some infectious diseases, we know a lot about the genetic mechanisms causing ethnically varying resistance – particularlly malaria – for others we know the ethnic differecnes in vulnerability but know less about the mechanisms.

There is reason to believe that HLA heterozygosity increases fitness. This kind of diversifying selection is why the gene geneology for the HLA alleles goes back tens of millions of years. Slatkin’a analysis (and my casual look at the gene frequencies) suggest that there just wasn’t any such selection among Amerindians.

Or, you could read some history. When the 1918 flu hit British Samoa, it killed over a quarter of the population. In Europe it killed no more than 1%. There is plenty of documentation of higher mortality (and sometimes qualitatively different symptomology) in previously isolated populations (Amerindians, Polynesians, Australian Aborigines) when exposed to stuff like smallpox, measles, tuberculosis, leprosy, influenza, etc.
Don’t they teach this in school?

This article is useful: in my current manuscript I said this: . “The key cultural precondition, in our view, was a pattern of social organization that required literacy, strongly discouraged intermarriage, and that could propagate itself over long periods of time with little change. Literacy (which does not itself require high intelligence) was probably important in the shift from a nation to an urban occupational caste, acting as an entree to many urban professions. “

Anyhow, think it through: education was economically irrational for Jewish farmers, so it was arguably the the _smart_ ones that converted.
But there were lots of other economic reasons to convert: under Islam, the dhimmi-tax. A rational farmer would raise pigs too.

If conversion acted as the main selective force boosting IQ, the Sephardic Jews would have high IQ scores. They don’t. Scratch conversion.

There are fundamental demographic facts that need to be kept in mind. The first, and most confusing, is that as far as we know, just about every city in premodern times was a population sink. People had to keep moving in from the farms all the time just to keep population level. So one question is why the Jews didn’t dwindle away: the answer is that although true on average, this was not true of every population subgroup. Another fundanmental fact of medieval demography is that people who made more money had more_kids, than average, unlike today. If enough urban Jews made enough money, their population could grow or be stable (perhaps niche-limited). Within that group, there was strong selection for the traits that on average made you make more money – i.e. success in various urban occupations. This was not true of non-Jewish groups with similar occupati0ons, since theyexperience lots of farmer’s daughter gene flow, diluting any selection. . The Jews, endogamous as they come, did not.

The exact mix of urban occupations in a given population is crucial. If most are tanners, as in Byzantium, I see no strong selection for IQ. If ~85% are moneylenders or tax-farmers or toll-farmers or estate managers, as in the early days of the Ashkenazi in Poland (and back in Germany, most had been moneylenders) – now we’re talking.

The estimated ages of the Ashkenazi neurological mutations are almost all 1200 yeare or less. This is a hint.

Add to the list: BRCA1, BRCA2 (breast cancer risk genes), torsion dystonia, Factor XI deficiency (clotting disorder), non-classic CAH, familial Mediterranean fever, familial hyperinsulinism, familial hypercholesterolemi, glycogen storage disease VII, pentosuria, maple syrup urine disease, and mucolipidosis type IV.

If memory serves, every one of these mutations is autosomal. As for your point about paternal and maternal ancestries, read the paper more closely. The evidence for local founding mothers is strong in some groups but not for the Ashkenazi.

3/4ths of the Ashkenazi conenxin-26 deafness mutations are a common Middle Eastern mutation, one of the two factor XI mutations is shared with Asian jews, familial mediterranean fever is also found in Sephardic/Asian Jews and some other middle easterners.

Reasonable people estimate that around 80% of Ashkenazi ancestry is Middle Eastern and I have no trouble with that.

Admixture references:

Proc. Natl. Acad. Sci. USA, Vol. 97, Issue 12, 6769-6774, June 6, 2000
Jewish and Middle Eastern non-Jewish populations share a common pool of Y-chromosome biallelic haplotypes
M. F. Hammer et al

They get 23% +/- 7% from Y-chromosome data – less than 0.5% a generation.

back in 1982 Motulsky estimated 12.5% based on 18 classical genetic markers.
8. Motulsky, A. G. (1980) in Population Structure and Disorders, eds. Eriksson, A. W., Forsius, H. R., Nezanlinna, H. R., Workman, P. L. & Norio, R. K. (Academic, New York), pp. 353-365.

The right approach is use a bunch of microsatellites, but as far as I know this has not yet been done.

In terms of selection for IQ, I doubt if ancestry matters much: rather the social niche and low gene flow during the period of selection.

As for Risch: in general he must be wrong. Does he think that _drift_ increased Ashkenazi intelligence? You can’t drunkards-walk your way to high IQ.

You’re wrong. Just about every Jewish IQ study shows visuospatial skills equal or lower to general European scores, and if you were really tuned in, you’d know this already. It fits the occupational/professional patterns. Moreover, it fits my selective model – they were financiers, not engineers or architects or bowmen. ‘g’ is one principal component of intelloigence, but visuospatial is another principal component, statistically independent.

If you select for ‘g’ you get less of other things: this is inevitable.

If you want high viz skills, I’d look at the Mongols.

The time depth of separation between sub-Saharan Africans and anybody else is much, much greater than the time depth of separation between Europeans and Middle Eastern populations. So the fact that AShkenazi SNPS are a lot closer to European than to African tells you nothing about the extent to which Ashkenazi ancestry is European or Middle Eastern.
Again, the mtDNA study (Thomas et al, AJHG, 2002) clearly shows that many Jewish populations had very few female ancestors. In some populations, like the Bene Israel from India or The Falasha, the mtDNA is clearly local.

But in the case of the Ashkenazi, mtDNA gene diversity is not particularly low (0.973 versus 0.988 among Germans). Thomas says “The pattern in Ashkenazic Jews is of particular interest. Despite the common opinion that this population has undergone a strong founder event, it has a modal haplotype with a frequency similar to that of its host population (9.0% vs. 6.9%), providing little evidence of a strong founder event on the female side.” Nor can they tell _where_ Ashkenazi mtDNA comes from. Could be European, could be Middle Eastern.
On the topic of whether the Ashkenazi went through a bottleneck: neither Y-chromosome or mtDNA evidence suggests that. A bottleneck should decrease heterozygosity: I ran 88 loci out of Ken Kidd’s database, and the Ashkenazi show no decrease at all; just the same as Russians or Druze. . The Finns show a decrease, Samaritans do – not the Ashkenazi.

Ignoring the first poster as much as possible, the ACTN3 gene is interesting. I was talking with these Australians about it earlier in the year.

There are two common alleles of this fast-twitch muscle protein, one works and the other doesn’t. Both have worldwide distribution and presumably are at least as old as the move out of Africa – tens of thousands of years minimum.
Originally ythis Australian group thought it was a case of relaxed seelction, but the pattern is all wrong. With relaxed selection, as with some of the olfactory geens, you get lots of different inactivating mutations, not just one common and ancient one. And for the most part any relaxation of selection has been recent – people weren’t flipping channels and eating Doritos 50,000 years ago.
So the two alleles must be in some sort of balance. The Aussies think that the working form helps you sprint, and they have good evidence for that. They have weaker evidence that the null mutation somehow helps endurance.

There are basically two ways this can work. Either heterozygoites have a higher fitness than either homozygotem, or there is frequency-dependent selection in which each allele becomes advantageous when rare. In the second case, there exist social niches of some kind for both fast and not-fast people.

Being a cultural thing, it’s fairly easy for homosexual men to get get bored with it and turn heterosexual, or to change with just a wee bit of
encouragement, say aversion therapy using electric shock.

Yup.

to Jason M: you’re crazy. Naturally, I could go on and on at great length about how and why, but why would I want to argue with a crazy person? Parenthetically, I have read deeply in the kind of nonsensical literature you cite, and there are times that I think I’ll _never_ be clean again.

to jim: I suspect that what is happening is similar to narcolepsy, in which a particular brain function is trashed while leaving everything else substantially intact. Narcolepsy happens when the neuron subpopulation making a particular neurotransmitter, orexin, disappears. This happens almost only in people with a particular HLA type, so one suspects an autoimmune reaction. A viral trigger is reasonable and possible.

As for where this is going – I don’t believe it’d be hard to find out the cause, since we have a good experimental animal, sheep. 5-10% of male sheep in some herds are totally uninterested in females: you can tie a female in heat to the fence in front of them and they don’t do a thing. Males they hump. As far as I know, the only two mammals with a few-percent of males with this kind of preferential homosexual behavior are humans and sheep. The two species have often been seen together, and I doubt if this is entirely a coincidence. I’d bet money that the cause is the same, and that we contracted it from sheep. That’s thought to be the case for a lot of infectious agents – acquired from domesticated animals.

Gee, so now we have to look for the gay sheep gene! Actually we already did: the condition doesn’t show noticeable heritability. They do show funny endocrinologivcal patterns in the amygdala ( we get to dissect homosexual sheeo), but I’m sure you need to think more about neurotransmitters than they have so far. And about some infective agent, because of course that’s what it is.

Well, though, one should be fair. Maybe sheep homosexuality is a variant genetic strategy – maybe the gay sheep show increased creativity. Maybe they help raise their nephews and nieces., even though no male sheep do zip for their kids, like most mammals.

Maybe this sheep behavior was recently socially constructed! I could take this and run with it – but it would be wrong.

As I said, probably not hard to solve, may even happen by accident, but almost completely unfundable. This is banned science: anyone who proved such a thing or even worked on it would likely never get any federal money ever again. Blanchard asked about HLA correlations – they wouldn’t release the info. This is something man was not meant to know. I have even had one biologist who secretly came to a similar conclusion (Alan Grafen, who wishes I wouldn’t mention his name) suggest if proven it should perhaps be kept secret forever. What a chickenshit.

On the other hand a lot of the smarter evolutionary biologists think it has a pretty good chance of being correct. Bill Hamilton thought so. Trivers thinks it is much more likely than any other model he has heard of (of course he _is_ crazy) . Mike Bailey thinks it is the only evolutionarily plausible model that has ever been proposed.

You have to think like an evolutionary biologist to realize how utterly _implausible_ preferential homosexuality is, if at all common.
It makes just as much sense as a compulsion to poke yourself in the eye with a sharp stick. From an intelligent evo-psych point of view, it simply should not exist. Such a personality type should not even be possible.
We’re just used to it. Populations without any homosexuality react with incredulity when they hear about ir for the first time.
Compare it with this: in some parts of Africa, young men start showing blood in the urine. The locals call it male menstruation, consider it a rite of passage, make a big thing out of it, consider it normal. It’s enfolded in their silly culture. But it’s just a disease; they put the boys out working in the rice fields around that age, they contract schisotomiasis of the type that colonizes the bladder, and they get blood in the urine.
Things that have always been around don’t seem to need causes: they can’t seem anomalous. Same thing with beta-thalassemia – it was first recognized by a physician in _Detroit_ of all places. . In Sicily and Sardinia, it was common and therefore didn’t need a cause – just was.

If by 15% higher in the deaf community, they mean that homosexuality is 1.15 time more common among the deaf, then they are saying nothing at all, since the error bars on the prevalence of homosexuality in even the best surveys utterly swamp that.

If on the other hand it means that, say 17% of the deaf are homosexual, I’m interested. That would be time to wonder about rubella.

As for why a virus might have this effect on men and not women – well, I hate to reveal this secret, but men and women are not the same same. Nor are their brains. There are many easy-imagine-ways in which this might happen.

As for the idea that the hit causing homosexuality must be prenatal: although I cosnider it possible, I defy anyone to tell me why this must be the case. Note that when one of a pair of identical twins is homosexual, ~80% of the time his twin is not. Their genes are identical and their prebirth experiences very similar – there are more unshared experiences after birth than before. And narcoleptic MZ twins are also usually discordant, about 70% of the time.

I’m not exactly a journalist.

As for Thomas Gold and abiotic hydrocarbons: I don’t buy it. And money was spent – the Swedes spent tens of millions drilling the Siljian Ring, and came up empty.

Read _War before Civilization_. Better yet, look at the Y-chromosome distribution in western New Guinea. Lots of mtDNA diversity, very limited Y-chromosome diversity. One simple explanation.

to David B: quite wrong. The evidence is strong for a dysgenic trend.
This has probably happened before, in Classical times. Sylphium contributed.

What’s the narrow-sense heritability of g?

Keller is full of shit and has been for many years.
Geologists reject Occam’s razor. And I am not kidding.

It should be obvious to anyone that gradual mass extinctions are inherently unlikely. First realize that natural selection can operate far more rapidly than we see in the fossil record. Traits in higher organisms can evolve at several percent per century in nature – which means that that it can easily keep up with what a geologist would consider a ‘gradual’ change.
Look, a frog can evolve much greater tolerance of acidification in 40 years. Insects evolve faster than that. In order for something to cause a mass extinction, it must build up more rapidly than organisms can adapt to it. The simplest way in which this can happen is if the rise time is short compared to the time required for evolutionary response. This is not true of any change that a geologist woud call gradual, but it sure is true of an asteroid strike.

The kind of scenario you suggest could never produce anything like the K-T extinction. Look, there are plenty of ways in which you can wipe out a fair number of species – competition can do it. Look at what happened to the South Ameican mammalisn fauna after the isthmus of Panama formed; toast.
But we don’t use the phase ‘mass extinction’ casually – the K-T extinction is something dramatically different; not one large land animal survived anywhere in the world. A big fraction of _plant_ species disappeared – that’s not easy. The best guess is that only mammals survivng anywhere in the world were burrowing insectivores.
Keller is an expert at misclassifying the nannoplankton when it serves her screwy purpose. There is no question that most of the forams disappeared. I’m not sure what paleontological information one would be expected to get from Chixculub samples anyhow – you want to look at uninterrupted deposits, undisturbed strata, and a 180-kilometer diameter impact crater might not quite fit the bill. Impacts can turn strata upside down as the edges peel back – that has been seen in the Barringer crater in Arizona.
If you turn up the intensity enough, a gradual geological process could cause a mass extinction. But it has to be more intense, the effect has to be far stronger, things must go past where _anything_ can adapt. And it’s harder to find a
refuge, since that refuge has to last hundrds of thousands or millions of years. THere could have been short-term refuges that allowed _some_ higher life to survive an asteroid mpact. For example, living underground could shield small mammals during the hours after the impact in which re-entering debris raised the entire surface of the Earth to a few hundred degrees.
I think a forest buried in one of the landslides caused by the asteroid-caused earthquakes, a millionfold stronger than any we have ever seen, could have been a good refuge for insects and burrowing insectivores. Lakes in karst country could have shielded some freshwater fauna from the temperatures and from the acid rain.

Surely Norwegian fsrmersw circa 1850 were incredibly crime-ridden, because they sure were poor.

That’s sarcasm.

I don’t have to put much effort into explaining Jewish criminal activity in the first half of the 20th century, because there wasn’t much. Those tenements in the Lower East Side had really low crime rates. I recall reading of a project in which some students looked at old New York crime records for that area – they were amazed that you seldom saw an offense more serious than running a vegetable cart without a permit.
It’s perfectly possible to have poor city-dwellers with low crime rates. At one time, there was a census district in San Francisco that was the poorest in the state, had the highest incidence of TB and the lowest crime rate. Chinatown.
The idea that poverty causes crime is stupid – and at this point, boring.

On a more interesting note, that Levite chromosomal study shows what can happen from drift. I don’t that drift was very important in the Ashkenazi population as a whole (and I have the numbers to prove it) but the Levites were only about 4% of their population, and the effectvie population size for a Y chromsome is four times smaller than that of an autosomal chromsome – so the effective N for the levite y chromsome was 1/100th of the _effective_ Jewish population size, which was itself probably no more than a third of the Ashkenazi population at any given point in time.

“you’d have to tinker with a huge number of them [genes], perhaps hundreds or thousands.”

Nope.

Gregory Cochran

“You’d have to get tens of thousands of people to have sex only with one another for centuries. Good luck.”

It’s been done. Is everybody a straight man?

My only problem is that I don’t believe that points 1,2 and 3 have much to do with why AIDS is such a big problem in much of Africa.

I think that ultimate cause is malaria and bananas.

to bbartlog: Right. If the constraints ease, if you get some elbow room in the trade space, there’s often nothing blocking major improvement in a quantitative trait.
And in some cases there will be strong single-gene effects. Teosinte -> maizze seems to have been caused, in the main, by changes in just a few genes of strong effect.

I rememeber the case. It was one of the funniest murders ever. If memory serves, some guys had ripped off Eddie Nash (Abdel Nasrallah), a drug suplier, restaurenteur and club owner, and Holms was periphrally involved. Nash and his bodyguard got some info on this out of Holmes and killed the thieves.
The LAPD never thought Holmes did the deed, but they thought he had information – so they chaged him with the murder. “Murder with a blunt instrument” was the charge.
I rolled on the floor laughing. Holmes refuesed to talk – they held him for a long time, but finally gave up and released him. Nash bribed a juror and got off scot-free.

Hungary. Turkey. Sometimes it happens, sometimes it doesn’t.

Applying a high level of abstraction, seeing the world through a lens of theory, doesn’t do you any good unless you test the theory and find it to be valid. Of course, in political science, nobody does this. It is merely a way of going more elaborately wrong: someone who sticks to what has worked in the past will do better. Someone who had a valid predictive theory of history would do better yet, but no such thing exists.
Often people who take this approach are called idealists, and the word is used approvingly. In practice, it just means that their predictions, which of course their plans are based on, are unlikely to come true.

History is not physics: you do better by knowing a lot of facts than by applying a few simple principles.

I said it because that’s what I think. Look, man, if a new version of a gene controlling myelination can go from one individual 6500 years ago to over 50% today – and it has, neuregulin – and if there are _many_ genes undergoing such sweeps, which there are – there are likely going to be real differences in human inclinations and capabilities over time. Biology keeps culture on a leash. It may be a short leash.

Those numbers are mostly wrong, David. The idea that 80% of kids didn’t make it to reproductive age is especially wrong.

I suppose I should have an opinion on this. I do, too: on some biological questions, physicists have an advantage. It’s a secret.

There’s more to it than that. Tribes often have _extremely_ limited HLA variation, contain only a small subset of the variation that you see in a wider set of Amerindians. Whereas in the old world, even little tiny groups with very low gene flow have lots of different HLA alleles. [Cavalli-Sforza 1994] You’d think that they’d lose those rare alleles by drift, but they don’t – has to be frequency-dependent selection, the same force that has kept alleles around for tens of millions of years. But in the Americas, it appears that those frequency-dependent forces simply did not exist. [Slatkin and Muirhead, 2000]
So, two things going on, which may or may not modify your conclusions. First, a bottleneck, probably: afterwards, a world in which HLA simply does not matter.

Gene frequency of the standard connexin-26 mutation (35delG) in southern Europe is roughly 1.5%, frequency among Ashkenazi Jews (3/4 a Middle Eastern mutation, 1/4 35delG) is about 2.5 %.
“maladaptive” is way too weak a work. Profound congenital deafness, in the old days, was a fate worse than death.
As for the idea that lethal and effectively lethal mutations like CF and connexin-26 deafness could reach such high frequencies in large mixed populations – not so.
Check the numbers. They’re both mostly a single allele: you won’t see that from continuing mutation.

RPM: no. for a lethal recessive, the equilibrium gene frequency is the square root of the mutation rate. Since the gene frequency is over 2% in Europeans, that would imply a mutation rate of 4 x 10-4, which is implausibly high. In addition, it’s a hell of a lot rarer in non-Europeans. On top of that, a single allele, delta-F508, account for the majority of mutations in most European populations.
It’s selection. For that matter, selection is the cause of a lot of less-common genetic diseases, such as hemochromatosis.
Typically, lethal recessives have slight negative effects in heterozygotes as well, which would further reduce the equilibrium gene frequency: judging from Drosophola, the typical recessive lethal lowers heterozygote fitness by 2%.
You might also note that if the normal gene frequency for a recesive lethal was 2%, then the chance of _not_ having _some_ lethal genetic condition (assuming 25000 genes) would be about 1 in 20,000. We’d all be dead.

Correction: hemochromatosis is fairly common. But it’s impact on reproductive fitnewss is fairly small. I tend to think in terms of the individual fitness decrease multiplied by the frequency of the condition.

Still want one of those T-shirts, razib?

John Derbysire has on occasion called me a friend: the feeling is not mutual.

Linkage disqeuilibrium and allele statistics such as Tajima’s D are in many cases a better way of determining selection than a mechanistic test: they don’t require that you recreate past selective environments. Other approaches, such as a probability analysis of the way in which common mutations cluster in particular metabolic paths can also tell you a lot – you can apply this to many red-cell polymorphisms thought to have been selected as defenses against malaria Although nobody has yet, except for my first-cut analysis. Ken Weiss may not not be sure that alpha-thalassemia is a defense against malaria, but I am. Evidently he’d rather not know. Go figure.
The review disagrees exception to a lot of things that are simple facts. For example it takes exception to Wade’s statement that “the alleles involved in differentiating the human population are likely to be of
the selected kind not the neutral kind. ”
That statement happens to be true. As we check them out, the alleles differentiating races and ethnic groups _do_ mostly appear to be the products of recent selection. That is the case: check out the recent literature. Recent because they postdate the separation of the racial groups (and are therefore not universal), selected because what else coud have raised them to high frequency so fast?

In maize, some pairs of strains nick and some don’t.
Could well be the same for humans.

From all reports, the upper classes in Classical times had few kids, while the opposite was the case for Europe in 1700.
Economics?

I once dreamed about rescuing a damsel in distress: she was immured in a castle wall, so I had to demolish it open quickly, before she suffocated. As I prepared to set off the bomb, I asked myself ‘adiabatic or isothermal’?
Adiabatic, I thought, and blew open the wall.

Probably no more than three standard deviations.

Well,we can explain how picking up _favorable_ alleles is likely even when overall levels of mixing are quite low (and thus you don’t see much non-African neutral stuff).
That’s not something I’ve seen before: Coon, Stringer, etc all seem not to have drunken deeply at the spring of population genetics.

It’s the first big-media mention of the Neanderthal-boost idea.

Builds upon, but not originally inspired by. Thoughts about that 2s effect were worked out in 2001: germ of the idea, in 1998, maybe earlier. Save your email.

I have to talk to this guy.

If there was such a transfer of populations, it could be significant. Genes are not ink.

Why not hate them both?

But it’s logically necessary. All of the key psychological traits have high enough heritability to change rapidly. You can’t get out of this.

Nonsense. There is of course significant correlation between IQ and brain volume in the normal range: you think that we have a lot of microcephalic university students in the MRI studies? Anyhow there has to be: if function was independent of volume, we’d all have brains the size of an apple: metabolically cheaper and far lower birth risk.
And frankly, everything else colugo said was just as clueless. Every result in behavioral genetics shows that the effects of between-family differences on IQ – the kind of environmetal effects everyone reaches for – are weak.
As for the idea that all human populations have extremely similar distributions of cognitive and personality traits: all those traits are heritable enough that’d you’d expect to see differences emerge rapidly given different environents with different selective pressures – and people have been exposed to extremely different social and ecological environments for time enough to see plenty of divergence. And that’s what the results of psychometrics show.
No point in arguing with me about it – go argue with
Fisher and Falconer.

The shape of skulls in England has changed significantly the period in question. The height of the forehead had increased by about 20%. 
 
But “there is no biological or genetic story going on here. ”

I’d guess that thriftiness has not much to do with it, more adaptation to a carbohydrate-rich diet. That’s a huge, for-sure change – something like a factor of three. Should not be that hard to check.

Murray is wrong, of course. Non-Ashkenazi Jews do not have high IQ scores today: see Lynn and David. Nor is there the slightest sign that that Jews were sharper than average in Classical times: not one single paragraph in preserved classical literature suggests that anyone had that impression. Nor did the Byzantines.  
 
Murray has not made a close study of the available history, he has ignored available psychometric results, and is oblivious to the genetic data – even though I told him about all those things. The mutations that look like IQ boosters – for example the sphingolipid mutations – are pretty much confined to the Ashkenazi.  
 
Genetic isolation is a precondition for this kind of selection and I can imagine that it happened in some Jewish group other than the Ashkenazi. The Iberian Jews, if anyone. The same is true for them having mostly urban occupations – it’s a precondition. But that shift hadn’t happened at all by Classical times – it began hundreds of years later and was only more-or-less complete by 800 AD. And only among the Ashkenazi was there a shift to (almost entirely) white-collar jobs. And the effects of any such selection among non-Ashkenazi Jews clearly no longer exist: look at the psychometrics and the occupation/educational pattern in Israel.  
 
Since the average IQ in England is probably higher than that of non-Ashkenazi Jews, will Murray next become a British Israelite?

On the other hand, I guess he did a reasonable job of reporting our work.  
 
One other point: the mutations that look like boosters are mostly new (~1000 years old) as well as being confined to the Ashkenazim.

Yes, it would be naughty.

Probably PZ Myers doesn’t know anything about quantitative or population genetics. I hear they’re old hat.

There were people. animal breeders, who were at least vaguely aware of the perils of inbreeding hundreds of years earlier. Maybe far earlier than that. Darwin may well have known of this.

We need lots of redheads to check this out properly. I was thinking of putting an ad in the Times – using a ruse, of course, to avoid putting other researchers onto the scent.

You know my methods.

In the dogs, muscle spasms, if memory serves. In the cattle, calving difficulties.

I thought their results were implausible. The idea that an avalanche of European and African pathogens would select for Amerindian alleles makes no sense.

to that last anonymous: if someone’s detailed predictions come true, that means that he understands the situation.

Mine did. I understand. You, on the other hand, are just another God-damned fool.

I don’t think nukes are for sale for that kind of money: it could get the seller in trouble, by which I mean extremely dead.
If they were for sale for 100 million, I can think of a number of countries that would have already bought them. Hasn’t happened.

Today I’m not so sure about Wolfowitz’s motives: I now suspect he’s a different kind of fool than I thought back then. An Arab girlfriend may have had something to do with it.

Invading Iraq looks to have a long-term unfavorable outcome for most of the people who supported it: unfavorable to their causes, with any luck unfavorable to them personally. Were they smart?
I would say that they made wrong decisions – wrong considering the causes they wished to advance – in many cases because they weren’t smart, in large part because they were profoundly ignorant of history, and most of all, because they were susceptible to the madness of crowds.

I can see that we’re going to have to beat a lot of nonsense out of you this fall.

At one point, they were attacking Mike for his associates. In particular, _me_.  
Now _that’s_ McCarthyism !

I’m sure I could straighten out Dyson in five minutes.

The invasion of Kuwait didn’t shock _me_ – I predicted it. I
talked about it for two weeks before it happened, annoying everyone at work.
I guess that just shows what a national security idiot I am.

And of course both the Duelfer report and the GAO agree with me on the money Saddam had available for weapons programs.

“Take out the advanced sciences, law and medicine and most of the rest (95% or more of the classload) is filler.” 
 
You exaggerate – you’ve forgotten engineering. It’s more like 80% filler.

With cholera, you either die in a short time or recover fully. The same, most of the time, for smallpox, yellow fever, typhus, typhoid, and a host of childhood infections.  
There are chronic diseases that reduce work output – many involve parasitic worms: ascariasis, schistosomiasis, hookworm, filariasis, dracunculiasis, onchocerciasis, loa loa.  
Also falciparumj malaria, but it often kills as well.

A big fraction of the alleles with large differences in regional frequency are the product of recent sweeps: you’ll see a lot of the most useful alleles on Frudakis’ list in the Wang/Moyzis or  
Voight/Pritchard papers. Probably most of them.

” Am I wrong in my reasoning here? Really, could someone tell me why the existence of differing genetic profiles among human populations means an automatic causational factor in psychological makeup?” 
 
Wrong. Rapid response to different selective regimes, which selected for traits both above and below the neck.

Concerning those four Ashkenazi mtDNA types, which together account for about 40% of Ashkenazi lineages: three are probably from the Middle East, but the largest, which accounts for about 20% of Ashkenazi lineages, has sister lineages only in the western Mediterranean – in Italy, north Africa, and the Iberian peninsula, if memory serves. No sister lineages from the Middle East – so it’s not from the Middle East.  
 
As for the other 60%, I can’t tell. But I’d guess that a lot are European, since if you look at autosomal genes, the Ash look about 40% European, as we said in our paper.  
 
As for Goldstein: in the cases I’ve looked at, he’s competent and honest.

How neat, a human genetics reference from 1980. 
Motulsky didn’t have ~150 autosomal gene frequencies to work with: we did. Today you could do better yet, using SNPs.  
 
” Considering the Circum-Mediterranean distribution of K1a1b1 lineages and the essentially exclusively Jewish distribution of K1a1b1a, a Middle Eastern origin for the common ancestor is entirely plausible” 
 
Except that all the evidence you’ve got suggests it originated somewhere else. I’d guess Roman – from the geographic distribution and from history.

Romans settled in North Africa a lot more than Carthaginians settled in Italy.

Mine had to be kept secret.

People talk about ‘modern human behavior’ as if it were a boolean variable rather than a quantitative trait.
Likely they’re wrong.

It turns out that we’re an atypical species.

Neither.

Tell me more about my social class. I gots to know!

As for that hypothetical 35-year old Marine captain –
how long can he tread water?

No, from analysis of autosomal genes.

2 centrifuges, actually.

You could have a promising future at the CIA, oh evil one. Wretchard as well.

E. O. Wilson was never much of a theoretician, and it takes unusual situations for group selection to occur. It’s usually a weak force compared to individual-level selection.

D. S. Wilson has never made any sense to me, while Howard Bloom is an idiot.

It’s more likely an increasing degree of adaptation to a high-carbohydrate diet. There are other factors worth considering: wimp neurological adaptations that decrease interpersonal violence, 
maybe differential resistance to undiscovered or poorly understood pathogens involved in chronic diseases. Selection for increased IQ could also increase lifespan summat.

There’s a claim that fighters aces were unusually likely to have blue eyes – supposedly 80% did. I’d like to see the documentation.