Wednesday, February 28, 2007

Arthur Schlesinger dies at 89   posted by Razib @ 2/28/2007 09:24:00 PM
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Arthur Schlesinger dies at 89.

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Tuesday, February 27, 2007

A note on the Common Disease-Common Variant debate   posted by p-ter @ 2/27/2007 05:19:00 PM
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One of the more heated debates in human medical genetics in the last decade or so has been centered around the Common Disease-Common Variant (CDCV) hypothesis. As the name implies, the hypothesis posits that genetic susceptibility to common diseases like hypertension and diabetes is largely due to alleles which have moderate frequency in the population. The competing hypothesis, also cleverly named, is the Common Disease-Rare Variant (CDRV) hypothesis, which suggests that multiple rare variants underlie susceptibility to such diseases. As different techniques must be used to find common versus rare alleles, this debate would seem to have major implications for the field. Indeed, the major proponents of the CDCV hypothesis were the movers and shakers beind the HapMap, a resource for the design of large-scale association studies (which are effective at finding common variants, much less so for rare variants).

However, CDCV versus CDRV is an utterly false dichotomy, as I'll explain below. This point has slipped past many of the human geneticists who actually do the work of mapping disease genes, and I feel the problem is this: essentially, geneticists are looking for a gene or the gene, so they naturally want to know whether to take an approach that will be the best for finding common variants or one for finding rare variants. However, common diseases do not follow simple Mendelian patterns-- there are multiple genes that influence these traits, and the frequencies of these alleles has a distribution. A decent null hypothesis, then, is to assume that the the frequencies of alleles underlying a complex phenotype is essentially the same as the overall distribution of allele frequencies in the population-- that is, many rare variants and some common variants.

This argument would seem to favor the CDRV hypothesis. Not so. The key concept for explaining why is one borrowed from epidemiology called the population attributable risk--essentially, the number of cases in a population that can be attributed to a given risk factor. An example: imgaine smoking cigarettes gives you a 5% chance of developing lung cancer, while working in an asbestos factory gives you a 70% chance. You might argue that working in an asbestos factory is a more important risk factor than cigarette smoking, and you would be correct--on an individual level. On a population level, though, you have to take into account the fact that millions more people smoke than work in asbestos factories. If everyone stopped smoking tomorrow, the number of lung cancer cases would drop precipitously. But if all asbestos factory workers quit tomorrow, the effect on the population level of lung cancer would be minimal. So you can see where I'm going with this: common susceptibility alleles contribute disproportinately to the population attributable risk for a disease. In type II diabetes, for example, a single variant with a rather small effect but a moderate frequency accounts for 21% of all cases[cite].

So am I then arguing in favor of the CDCV hypotheis? Of course not-- rare variants, aside from being predictive for disease in some individuals, also give important insight into the biology of the disease. But it is possible right now, using genome-wide SNP arrays and databases like the HapMap, to search the entire genome for common variants that contribute to disease. This is an essential step--finding the alleles that contribute disproportionately to the population-level risk for a disease. Eventually, the cost of sequencing will drop to a point where rare variants can also be assayed on a genome-wide, high-throughput scale, but that's not the case yet. Once it is, expect the CDRV hypothesis to be trumpted as right all along.

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CHRM2 and Intelligence   posted by Fly @ 2/27/2007 09:35:00 AM
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CHRM2 Gene Variants Associated with Intelligence

"Some of the participants in the study also took the Wechsler Adult
Intelligence Scale-Revised, a traditional IQ test. In all, members of 200
families, including more than 2,150 individuals, took the Wechsler test, and those results were matched to differences in individuals' DNA.

By comparing individual differences embedded in DNA, the team zeroed in on CHRM2, the neuronal receptor gene on chromosome 7. The CHRM2 gene activates multitude of signaling pathways in the brain involved in learning, memory and other higher brain functions. The research team doesn't yet understand how the gene exerts its effects on intelligence."
...
Dick's team is not the first to notice a link between intelligence and the CHRM2 gene. In 2003, a group in Minnesota looked at a single marker in the gene and noted that the variation was related to an increase in IQ. A more recent Dutch study looked at three regions of DNA along the gene and also noticed influences on intelligence. In this new study, however, researchers tested multiple genetic markers throughout the gene.

"If we look at a single marker, a DNA variation might influence IQ scores between two and four points, depending on which variant a person carries," Dick explains. "We did that all up and down the gene and found that the variations had cumulative effects, so that if one person had all of the 'good' variations and another all of the 'bad' variations, the difference in IQ might be 15 to 20 points. Unfortunately, the numbers of people at those extremes were so small that the finding isn't statistically significant, but the point is we saw fairly substantial differences in our sample when we combined information across multiple regions of the gene."

Dick says the next step is to look at the gene and its numerous variants to learn what is going on biologically that might affect cognitive performance. Presently, she says it's too early to predict how small changes in the gene might be influencing communication in the brain to affect intelligence, and she says it's nearly certain CHRM2 is not the only gene involved.

Prior GNXP references to CHRM2:

Thompson and Gray: Neuroscience, genes, and IQ

More red meat

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New blog posts   posted by rosko @ 2/27/2007 01:52:00 AM
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As a make-up for having hardly any time to post during the Week of Science, I have just added a set of four posts of pure science to my blog in rapid succession. On is on something that was already mentioned here, but the others are unrelated to anything on GNXP, so if you want to check them out, you can read them.

Monday, February 26, 2007

Recent Human Evolution in the house   posted by Razib @ 2/26/2007 10:17:00 PM
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Early man 'couldn't stomach milk'
Working with scientists from Mainz University in Germany, the UCL team looked for the gene that produces the lactase enzyme in Neolithic skeletons dating between 5480BC and 5000BC.

These are believed to be from some of the earliest farming communities in Europe.

The lactase gene was absent from the DNA extracted from these skeletons, suggesting that these early Europeans would not be tolerant to milk.


The paper will be Absence of the Lactase-Persistence associated allele in early Neolithic Europeans in PNAS. First LCT, then OCA2, and god knows what else? There is a limit in terms of what you can do with archeoDNA, but if the action went down in the last 10,000 years then it isn't such a sweat.

One thing, the summary in Science is weird. Check it:
The culture-historical hypothesis is that, shortly after the domestication of livestock, a few lucky farmers with a genetic anomaly hit white gold: nourishment via milk. Then, according to this theory, natural selection took over and these lactase-persistent folks proceeded to populate much of Europe with their milk-guzzling offspring. A competing hypothesis argues that ancient Europeans domesticated milk-bearing livestock because lactase persistence was already quite common in certain populations.


Quite common? The area of the genome around LCT was hit by a hammer blow of selection less than 10,000 years ago, that's why researchers use it to check if their methods for detecting selection are working. The fact that independent events of lactase persistence exist among other populations via alternative genetic architectures seems to indicate clearly the power of gene-culture coevolution. What's up with Science doing a "look at both sides" framework when the evidence is so lopsided? I suppose selection could have been induced by a causative factor aside from milk, but I think we're verging into Humean skepticism at this point, denying the ability to discern causality at all....

Carl Zimmer has much more....

Related: Lactose tolerance by a different stroke. Lactose tolerance/intolerance. Are multiple lactose tolerance mutations surprising? Genes & culture & milk. Lactose tolerance, is it "dominant"? Milk digestion, it does a body good.

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Sunday, February 25, 2007

Academic Blogs directory   posted by Razib @ 2/25/2007 09:28:00 PM
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I noticed a post at Crooked Timber about something called The Academic Blog Portal. It's a wiki. Both Gene Expressions are listed in the biology section. It is interesting to compare the representation of different disciplines, there are, for example, more linguistics and philosophy blogs than biology blogs, but also, more history blogs. Not all fields are represented to their proportion in academia, for example, only 4 engineering blogs.

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Typical GNXP reader?   posted by Razib @ 2/25/2007 07:28:00 PM
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Ultrabrown points me to an interesting site which profiles the demographics of a blog. Check out gnxp...there are obviously some issues, but good for a laugh.

Related: Previous polls of readers.

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The tactics of deceit   posted by Razib @ 2/25/2007 04:56:00 PM
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Over at The Edge the philosopher Daniel Dennett and evolutionary geneticist H. Allen Orr just had an exchange over Richard Dawkins' The God Delusion. I am not particularly interested in the details of this debate, rather, on the front page this selection from Dennett's letter caught my attention:
When I explained then in a private letter to you what I had meant, you conceded to me in your private response that you had not seen my point in the light I intended, and that my claim was not in fact the blunder you had said it was....

What could Dennett mean? I immediately thought back to this:

I did indeed misspeak (p. 126), but the result was ambiguity, not error. The issue is complicated: it depends on whether you're measuring the (average) speed of departure from a starting point in genetic space, or the speed of attainment of some particular evolutionary product. I meant the former. [Dennett]

Now I've been in the population genetics business for some time and, frankly, I have no idea what Dennett is talking about. And-I can find no polite way of putting this-it's hard to escape the conclusion that Dennett has no idea what he's talking about, either. Even the most charitable interpretation I can come up with is just plain wrong. [Orr's response]

Dennett's phrasing was awkward and peculiar to say the least. Orr is an evolutionary geneticist who "was awarded the Dobzhansky Prize by the Society for the Study of Evolution and the Young Investigator Prize by the American Society of Naturalists." In regards to a technical understanding of evolution Dennett was way out of his league. And only an analytic philosopher could confuse population genetic theory with such lexical opacity. That being said, I did not believe that Orr did not understand what Dennett was trying to say, unpolished though he was. This is how I unpacked it:

1) Because most mutations are deleterious, selection is generally a force for constraint, maintaining the ancestral state.

2) In contrast, random genetic drift operates upon evolutionarily neutral variation, so it exhibits (approximately) equal effect on mutants and ancestral alleles over the long term.

3) These insights lead to the contention of Kimura et. al. that most evolutionary change is driven by the substitution of neutral mutations, with random genetic drift a major engine. Even though the vast majority of neutral mutations go extinct, a small number perpetually substitute themselves over ancestral variants at a constant rate (i.e., the rate of substitution is proportional to the rate of mutation).

4) But, when there is a positively selected mutant, natural selection operates far faster in regards to fixing the variant than random genetic drift and stochastic processes might in the typical population size.

It is more complicated than that...but my point is that though Dennett wasn't exactly clear, I think a reasonable observer could understand what he was getting at, or at least the somewhat confusing waters into which he had ventured. Orr did not acknowledge this. As I said, Orr is a world renowned evolutionary geneticist (as he implies in his response), so I was skeptical that he was as clueless as he'd let on.

So, when I read Dennett's full letter, I was not surprised. Here is what he says:
You leveled very serious charges of error and incomprehension in that review, and when I challenged them, you responded with a haughty dismissal of my objections (in an exchange in the Boston Review). Quoting an example, dealing with the speed of evolution: "Now I've been in the population genetics business for some time and, frankly, I have no idea what Dennett is talking about. And-I can find no polite way of putting this-it's hard to escape the conclusion that Dennett has no idea what he's talking about either."

Dennett is bringing up exactly what I remembered in The Boston Review! This was 10 years ago, but Dennett obviously still resents Orr mocking him. In private correspondence Dennett states that Orr admitted that he wasn't really wrong, and Orr's response to this new salvo from Dennett does not contradict that characterization.

I writing about this for one primary reason: I thought, at the time, that H. Allen Orr was striking a low blow dishonestly when he could have stood on firm ground, though with a weaker impact. I've thought about this exchange on & off for several years now, and have considered blogging it, because I think it is perhaps a reflection of H. Allen Orr's character. Most of the readers of The Boston Review don't spend their free time reading The Genetical Theory of Natural Selection or Motoo Kimura's papers, they wouldn't be able to parse from Dennett's somewhat confused phrasing what he was trying to get at. In other words, assuming that Dennett wasn't a moron they couldn't really map his verbal exposition onto a range of evolutionary models, because it isn't exactly as if a broadly educated person is familiar with the great Neutralist vs. Selectionist debate of the 1970s. They were relying on H. Allen Orr's expertise. I just can't believe that H. Allen Orr didn't understand what Dennett was trying to say, or, that he couldn't have seen what he was getting at if he hadn't prejudged Dennett and his ideas as a whole. If I had been him I would have pointed out that Dennett's graceless exposition of the relationship between neutral and selective forces in evolution should be a clue that the man doesn't have the technical competency to engage in such an ambitious meta-project as the one he laid out in Darwin's Dangerous Idea. Instead, Orr is implying that Dennett simply doesn't know what he's talking about, and making him out to be the fool. This is rhetorically far more powerful, and I am sure it persuaded most readers of The Boston Review, who are not going to be conversant in the details of evolutionary genetics and trust H. Allen Orr. After all, who are you going to listen to on this topic? A philosopher or an evolutionary geneticist?

To my mind Orr did a disservice to science and intellectual discourse. He went for the knockout, calling an intellectual ignorant is basically undermining their worth. Saying that they are a bit confused lacks a similar punch. But the readers of The Boston Review, or the lay audience in general, is not looking for a legal case where you are an advocate for your position at all costs, because science and intellectual discourse is more than one battle, it is a long war against our moral and personal failings, against pride, against ego, against self-interest and self-aggrandizement. Most of the battles are lost, but slowly the war grinds on and the trenches keep moving inch by inch. Ph.D. scientists make considerably less in income than their intellectual inferiors in law or medicine. But the field in which they operate is one of great prestige, of civilizational significance. Presumably they wish to engage in the adventure of the ages, at the cost of financial status. Scientists are human, as the politics which suffuses any university department would confirm, but, like monks meditating upon the nature of God, abjuring themselves of worldly pleasures and satisfactions, scientists have to err on the side of truth as they see it, and not a short term rhetorical victory. For what shall it profit a man, if he shall gain the whole world, and lose his own soul?

Addendum: Readers can follow the links and judge for themselves if Dennett wasn't clear in his intent, even if he was being muddled about it. Perhaps Orr didn't understand what Dennett was trying to say. But if Orr could comprehend the opaque prose in The Genetical Theory, I can't see why he couldn't parse what Dennett was trying to get at. And just to be clear, though I point a finger at Orr on this occasion, rest assured that I understand that we are all guilty of this particular sin, and that includes myself. I simply want to emphasize Orr's transgression here because I think it is important for us to remember that no matter the satisfaction that victory in one battle gives us, we are not fighting without a long term purpose, and dishonorable victories are fundamentally Pyrrhic.

Addendum II: Also, I understand that in practice science between the bounds of accepted & rejected consensus is quite the bloodsport, and an adversarial & amoral dynamic is common. Though this injects quite a bit of "noise" into the system, I trust over the long haul that the scientific culture will beat expectation in modeling reality. That being said, the issue I am pointing to here is slight of hand by gatekeepers. Orr writes reviews books as an evolutionary geneticist, with all the expertise that that entails. His behavior in this case was repulsive to me because he sacrificed the chance to elucidate the nature of evolutionary change to a broad audience so that he could mock (in, I suspect, a dishonest manner) someone and so win a point in an exchange of letters. I will refrain from an evolutionary psychological analysis of how this was truly "rational" from Orr's individual perspective....

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Origami   posted by p-ter @ 2/25/2007 07:56:00 AM
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ALDaily points to this excellent article on the world's top origami artists. This guy has a hell of a bio:
Lang kept folding while earning a master's in electrical engineering at Stanford and a Ph.D. in applied physics at Caltech. As he worked on his dissertation-"Semiconductor Lasers: New Geometries and Spectral Properties"-he designed an origami hermit crab, a mouse in a mousetrap, an ant, a skunk, and more than fifty other pieces. They were dense and crisp and precise but also full of character: his mouse conveys something fundamentally mouse-ish, his ant has an essential ant-ness. His insects were especially beautiful. While in Germany for postdoctoral work, he and Diane were taken with Black Forest cuckoo clocks; the carved casings, pinecone-shaped weights, pendulums, and pop-out birds wouldn't seem to be a natural for origami, but Lang thought otherwise. He started a job at NASA's Jet Propulsion Laboratory, in Pasadena, in 1988, shortly after he had finished folding a life-sized cuckoo clock. It had taken him three months to design, and six hours to fold, and it made Lang a sensation in the origami world.

ADDENDUM: Andrew Gelman posts a picture of an origami tarantula, along with the corresponding fold pattern required to make it.

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Saturday, February 24, 2007

A very recent speciation time of human-chimp   posted by lol @ 2/24/2007 03:32:00 PM
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Hobolth A, Christensen OF, Mailund T, Schierup MH (2007) Genomic Relationships and Speciation Times of Human, Chimpanzee, and Gorilla Inferred from a Coalescent Hidden Markov Model. PLoS Genet 3(2): e7

They estimate 4.1 million years ago. It's open access so no excerpts needed.


Human cloning "inevitable"   posted by p-ter @ 2/24/2007 12:26:00 PM
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According to the editors of Nature.
[W]hat has been universally deemed as unacceptable is the pursuit of human reproductive cloning - or the production of what some have called a delayed identical twin. Here, the two issues that have dominated the discussion have been dignity and safety. There is a consensus that dignity is not undermined if a human offspring is valued in its own right and not merely as a means to an end. But there is no consensus that we will eventually know enough about cloning for the risks of creating human clones to be so small as to be ethically acceptable.

The debate may seem to have been pre-empted by prompt prohibition. But as the science of epigenetics and of development inevitably progresses, those for whom cloning is the only means to bypass sterility or genetic disease, say, will increasingly demand its use. Unless there is some unknown fundamental biological obstacle, and given wholly positive ethical motivations, human reproductive cloning is an eventual certainty.

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Friday, February 23, 2007

Epigenetics: the hippest field on the block   posted by p-ter @ 2/23/2007 07:15:00 PM
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The current issue of Cell is dedicated to the rapidly changing field of epigenetics, loosely defined at the ensemble of chromatin and DNA modifications that structure the genome and control gene expression. The only review I've worked my way through yet is this one: Timescales of Genetic and Epigenetic Inheritance.
According to classical evolutionary theory, phenotypic variation originates from random mutations that are independent of selective pressure. However, recent findings suggest that organisms have evolved mechanisms to influence the timing or genomic location of heritable variability. Hypervariable contingency loci and epigenetic switches increase the variability of specific phenotypes; error-prone DNA replicases produce bursts of variability in times of stress. Interestingly, these mechanisms seem to tune the variability of a given phenotype to match the variability of the acting selective pressure. Although these observations do not undermine Darwin's theory, they suggest that selection and variability are less independent than once thought.
The authors limit themselves largely to bacteria and yeast, but they document a great deal of evidence that parameters like the mutation rate change in response to external stimuli, perhaps in almost a "directed" fashion. Some work in primates has shown a correlation between the amount of mutation raining down on a population and the amount of beneficial mutations that arise. Could "directed" mutagenesis be an explanation for this?

The main points from the paper are summarized in the figure below; essentially, epigenetic inheritance is a way for a population to respond to environmental changes that occur on time scales shorter than those needed for genetic evolution.

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Explaining (some) Global Inequality: Genes, Culture, or Luck?   posted by Herrick @ 2/23/2007 11:48:00 AM
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Economists Wacziarg (Stanford) and Spolaore (Tufts) are using Cavalli-Sforza's genetic distance data. They find that countries that are genetically different from the rest of humanity tend to be poorer, even after controlling for lots of popular variables (like geography and colonial experience, two recent favorites). Their explanation: It's easier to get ideas from people who are similar--a contrast with much of the trade literature, where it's easier to get gains from trade from people who are dissimilar.

As Google Scholar shows, W&S have drawn some attention. Along related lines, Bill Easterly and his coauthors remind us that the countries that were more innovative in 1000 BC tend to be richer today--so not much is new under the sun.

Of course, W&S remind us that it's essentially impossible to disentangle genetic versus cultural stories when looking at nation-level data--and they note that their genetic measures are based on neutral markers, so it's "different," not "worse."

By contrast, one way to interpret Easterly's result is mere path persistence: A multiple-equilibrium story where you get it right once through sheer luck, and afterwards you're likely to stay lucky forever. Difficult to disprove--maybe it's a fair coin, and the West and East Asia just flipped Heads...

Genes, culture, luck: All three stories deserve some attention over the next few years. Two big problems: Measuring culture and luck. Genetic differences, those we'll be able to measure, with greater precision every year. But that's almost as much a curse as a blessing, since it'd be extremely valuable to be able to disentangle these hypotheses.

Thursday, February 22, 2007

William Wilberforce   posted by Razib @ 2/22/2007 10:26:00 PM
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This week's In Our Time is about William Wilberforce. Unfortunately, many on this side of the pond don't recognize the name. They should.


MicroRNA editing   posted by Fly @ 2/22/2007 01:45:00 PM
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Eurekalert:

"What we found was that, in certain cases, edited versions of these microRNAs are being produced that differ from the unedited versions by only a single nucleotide change," says Kazuko Nishikura, Ph.D., a professor in the Gene Expression and Regulation Program at Wistar and senior author on the study.

"These edited microRNAs are not encoded in the DNA, which means that at least two versions can being produced by one gene. This was not anticipated - it was something really new.

Looking more closely, we realized that the substitution we'd identified occurred in a particularly critical region of the molecule, the first 7 or 8 nucleotides - out of a total of only 19 or 21 - that define the molecule's target specificity. This suggested that the change might well redirect these edited microRNAs to silence entirely different sets of genes from the unedited versions."

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Social Irrationality?   posted by John Emerson @ 2/22/2007 09:44:00 AM
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Race IQ and SES   posted by lol @ 2/22/2007 12:31:00 AM
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Jensen (1998) makes a point that is worth repeating:
The pernicious notion that IQ discriminates mainly along racial lines, however, is utterly false.

Jensen presents what should be a predictable pattern for a highly heritable trait:
Source % of Variance Average IQ Difference
Between races (within social classes)
14 30 12
Between social classes (within races)
8 6
Interaction of race and social class
8
Between families (within race and social class)
26 65 9
Within families (siblings)
39 11
Measurement error
5 4
Total
100 17

This can be demonstrated most clearly in terms of a statistical method known as the analysis of variance. Table 11.1 shows this kind of analysis for IQ data obtained from equal-sized random samples of black and white children in California schools. Their parents' social class (based on education and occupation) was rated on a ten-point scale. In the first column in Table 11.1 the total variance of the entire data set is of course 100 percent and the percentage of total variance attributable to each of the sources6 is then listed in the first column. We see that only 30 percent of the total variance is associated with differences between race and social class, whereas 65 percent of the true-score variance is completely unrelated to IQ differences between the races and social classes, and exists entirely within each racial and social class group. The single largest source of IQ variance in the whole population exists within families, that is, between full siblings reared together in the same family. The second largest source of variance exists between families of the same race and the same social class. The last column of Table 11.1 shows what happens when each of the variances in the first column is transformed into the average IQ difference among members of the given classification. For example, the average difference between blacks and whites of the same social class is 12 IQ points. The average difference between full siblings (reared together) is 11 IQ points. Measurement error (i.e., the average difference between the same person tested on two occasions) is 4 IQ points. (By comparison, the average difference between persons picked at random from the total population is 17 IQ points.) Persons of different social class but of the same race differ, on average, only 6 points, more or less, depending on how far apart they are on the scale of socioeconomic status (SES). What is termed the interaction of race and social class (8 percent of the variance) results from the unequal IQ differences between blacks and whites across the Spectrum of SES, as shown in Figure 11.2. This interaction is a general finding in other studies as well. Typically, IQ in the black population is not as differentiated by SES as in the white population, and the size of the mean W-B difference increases with the level of SES.

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Wednesday, February 21, 2007

The Economist   posted by Razib @ 2/21/2007 11:20:00 PM
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Just a question...do you think it is worth $100 a year to subscribe to The Economist? I was a subscriber several years back and let it lapse mostly because I found that I wasn't checking in every week.

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Eric Alterman, a nationalist socialist   posted by Razib @ 2/21/2007 09:18:00 PM
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A few weeks ago I watched Bloggingheads.TV which I found really amusing. Eric Alterman was in a discussion with someone named Bill Scher. I don't know anything about Scher aside from the fact that he makes Jonah Goldberg seem really intellectual and a deep thinker (see their diavlog). But I was struck by the following exchange over foreign policy:
Alterman: "People in these countries don't want us, they hate us, they hate everything about us, they hate the idea of democracy, it's inconsistent with their vision of Islamic republics, which is what they clearly want. So you just like glossing over that, but I think that's fundamental. I think the promotion of democracy in the Arab world creates anti-American terrorists."

Scher: "Well, I mean, democracy in the broader sense, what kind of government do those people want. It doesn't have to be Jeffersonian-"

Alterman: "I don't want them to have the kind of government that they want. OK. I don't want Jordan and Pakistan and Saudi Arabia to have the kind of government that they want, because they will want to kill me with it!


I generally cheered for Alterman here. Whether you are an interventionist or not, the whole rhetoric about democracy and its universal appeal on both the Left and Right has gotten out of control. Whether there is a universal yearning for democratic freedom or not, its acceptance as a background assumption in the public discourse has become nearly religious. When someone like Alterman challenges it, you see a "deer in headlights" tendency. There are few counter arguments because people assume any contrary position is either absurd or immoral. These sort of dreamy tendencies are fine when you aren't an imperial power that has to make real-politik decisions (e.g., Iceland?), but at this point bad decisions informed by fallacious assumptions can cost a lot, at home and abroad.

To make the world as you wish it to be, you must first comprehend how it truly is.

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Tuesday, February 20, 2007

Religion & Politics & Derb   posted by Razib @ 2/20/2007 11:35:00 PM
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Check out Derb's latest column for NRO.

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Admin, etc.   posted by Razib @ 2/20/2007 10:29:00 PM
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I've received a half dozen complaints about the slowness of the site due to the technorati widget, so I've removed it for now. I see an improvement in load time. Yay or nay?

Also, to the right you should see an RSS feed logo from feedburner. I've always had a feed, with a small link provided, but I figured that regular readers should really be encouraged to use this. Of course, the RSS won't tell you which comment threads are hopping, but in terms of maximizing time utilization I think it's a good move. You can always bookmark the Haloscan thread of interest (speaking of which, anyone know a better offsite comment service? I don't like onsite comments because they are liable to take a site down because of repeated hits).

Finally, for those of you down with RSS, I highly recommend adding a few Google News queries to your feeds. For instance, I have genetics & evolution always updating in Google Reader (which has some downsides, but I like the total integration with my google home page). You can see the RSS links to the bottom left. The PLOS network also has an excellent set of feeds (page down) so you don't need to keep checking on their site for new articles (other journals have the