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May 20, 2005


I'm on semi-vacation, but I want to give a quick blurb to Armand Leroi's Mutants. This is a really entertaining book, though if you aren't into developmental biology and epigenetics, you'll have to get used to weird uses of words like "abolished" (or "silenced," for some reason specific technical uses of these terms in molecular/developmental genetics always sounds pompous to me, I always imagine methyl groups going ssshhhh!!! in a school-marmish fashion). The pictures are pretty bizarro, and I've had multiple queries from strangers asking what the hell I'm reading. Also, there is stuff on midgets in here, so it's already a keeper in my book (though some of the midget stuff is Mengele related, so that was kind of a downer).

Jason Malloy adds: This might also be a good time to share a website I stumbled onto many weeks ago and never got around to posting:

'Race and Genomics'. It features new articles from a number of familiar people in the anti-race crowd specifically commenting on Leroi's March pro-race essay, A Family Tree in Every Gene in the New York Times. Probably of most interest is the response by Richard Lewontin. It's hard to know what arguments Leroi actually made that Lewontin could be fighting against when he writes things like this:

"For purposes of medical testing we do not want to know whether a person is “Hispanic” but rather whether that person’s family came from a Caribbean country such as Cuba, that had a large influx of West African slaves, or one in which there was a great deal of intermixture with native American tribes as in Chile and Mexico, or one in which there was only a negligible population of non-Europeans. Racial identification simply does not do the work needed. What we ought to ask on medical questionnaires is not racial identification, but ancestry. “Do you know of any ancestors who were (Ashkenazi Jews, or from West Africa, from certain regions of the Mediterranean, from Japan)?” Once again, racial categorization is a bad predictor of biology."

Heh. So note the following "ancestry" categories (just don't call em' "racial" categories!) Lewontin advocates as informative about human genetic difference:

1) Japanese (national group)

2) Ashkenazi Jews (ethno-religious group)

3) West African (broad geographical region)

4) Non-European (i.e. Amerindian - continental group)

If this is true, Lewontin has nothing else important to argue about - he admits that genetic diversity tracks patterns of historical social and geographic endogamy, and that these patterns can carry genetic and trait relevant information. "West African" is not just a social construct, because West Africans are not an ethnic group. West Africans in Haiti, Cuba, Ohio, Canada, and Senegal do not share a social identity, they do share genes and ancestry.

If Lewontin wants to argue that Japanese, West-African, and Amerindian "ancestry" is informative about genetic differences (with varying levels of resolution) then there isn't much of substance to argue about, though we can quibble about whether we want a trendy euphemism to describe this differentiation that exists below the species level. But let's not pretend that biology doesn't already have a word for this, or that it has rejected this word - because it does and it hasn't.

And it hardly needs saying that quantitative genetic traits like intelligence, personality, and all manners of behavior, can certainly differ distributionally by these genetically informative groupings as well, and almost certainly do to some extent. No argument that Lewontin could produce would make these facts go away (though he makes plenty of arguments that effectively muddy them), and I know that tears him up inside, but he doesn't need to take it out on messengers like Armand Leroi or Theodosius Dobzhansky.

Related: Human biodiversity hits The New York Times, THE NATURE OF NORMAL HUMAN VARIETY, Race Does Exist -- New York Times, Debunking Leroi, Responses to

Posted by razib at 01:04 PM | | TrackBack

French baby boom?

I noticed a news report this week that the population of France was predicted to rise from 60 million to 75 million by 2050. As I found this surprising, I tried to find out more.

For those who can read French, the fullest report seems to be here.

For the benefit of others, the key points are as follows.

The population of France is currently just over 60 million. The French authorities have previously forecast that it would rise to 64 million by 2050. But using new population data from local registration they now think this is an underestimate. A French Government Minister has talked of 75 million, but this is not an official estimate. Some demographers think it is too high, and 70 million is more plausible.

The rising trend is attributed to three main factors:

- the birth rate is higher than expected

- life expectancy is continuing to increase

- net immigration is continuing and is also higher than expected.

Some readers will suspect that immigration is the main factor, but this doesn’t seem to be the case. Net annual immigration is running at about 100,000, which if it continues for 45 years (and assuming the immigrants reproduce themselves) would only account for 4.5 million. Moreover, net immigration of 50,000 a year had already been allowed for in population forecasts, so the higher observed rate only accounts for about 2.25 million of the increase in the estimate. Incidentally, it is said that immigration from Britain is an important element in the increase. There has certainly been a stream of people moving from Britain to rural France, escaping high house prices, yobs, and the general deterioration of the physical and social environment. There is hardly a middle-class Englishman who doesn’t dream of boules, brie and baguettes in the sunshine. But most of the British migrants are retired or ‘downshifting’.

The most interesting factor is the increase in the birth rate. The ‘indice conjoncturel de fécondité’, which seems to be equivalent to the Total Fertility Rate, has increased from 1.78 in 1998 to 1.92 in 2004. Higher birth rates among immigrants only account for a small part of this. The main factor seems to be that women who have postponed childbearing into their 30s are now ‘bearing fruit’. I pointed out some time ago (here) that changing patterns of conception made TFRs unreliable.

There is some uncertainty how far the birth rate will increase. The ‘optimists’ think it will reach a TFR of 2.1, which is about sufficient for replacement, while others are more cautious. This is the reason for the differing forecasts.

One must remember that in France the birth rate has traditionally been a matter of national pride and concern. Governments have always been ‘pro-natalist’, against the background that since 1800 French population grew much more slowly than that of Britain and Germany. French commentators are now gleeful that if the rising French trend continues, while in Germany the birth rate stays low, the population of France will be bigger than that of Germany by 2050. This is premature, as trends cannot be reliably forecast that far ahead, and an improvement in the German economy could draw in large immigration from eastern Europe.

For comparison, the population of the UK is also just over 60 million and is officially forecast to rise to 65 million by 2050. But at current rates of net immigration to the UK this level would be reached by 2030. Much of the recent migration is from Eastern Europe, especially Poland, and is proving generally popular, as the migrants are polite, hard-working, and well-behaved. Let’s hope they don’t send their children to British schools and spoil all that!

As in France, the birth rate is also increasing in Britain. According to the Office for National Statistics, ‘if the provisional 2004 patterns of fertility were to remain unchanged, as represented by the total fertility rate (TFR), then an average of 1.79 children would be born per woman. This is the highest rate since 1992 (1.80) and continues the gradual increase from a low point in 2001 when the TFR was 1.63’.

I don’t personally welcome an increase in the population of England, which is already over-populated. France, on the other hand, is relatively lightly populated, and could easily accommodate an increase to 70 million or so.

Posted by David B at 06:40 AM | | TrackBack

May 19, 2005

"Intelligent Design" or Intelligent Decline?

Be sure to check out Robert McHenry's excellent article on "Intelligent Design" over at TechCentralStation.

Then there is the simple fact that the "theory" of ID is no theory at all, not in the sense that the word is used in science. It is not based on the best available evidence; it enables no predictions; and it is thus not testable. It is, at best, a paltry substitute myth that incorporates some of what actual science has learned or theorized but spurns not only scientific rigor but any intention to perform science. It is not, as claimed, a legitimate criticism of a scientific theory but a criticism of having such a theory at all. No less than the Creation Scientists, and no less than dear Bishop Wilberforce in 1860, though far less forthrightly, the proponents of ID wish to draw an arbitrary line and use the force of the state to declare that science shall not cross it.

. . .

The ID man is heir to a culture of knowledge-building that has evolved over millennia, and, for quite private reasons that have nothing to do with the rest of us, he declines the legacy. To be sure, he has every right, for himself, to decline whatever, and however far, he chooses. It only remains for the rest of us decline to decline with him. That would be intelligent.

I couldn't have said it better!

Posted by Arcane at 08:43 PM | | TrackBack

May 18, 2005

Borg Sperm

I got an email from Greg Cochran last night, with the full text of this article: There's Something Curious About Paternal Age Effects

There seems to be a good connection between paternal age and short-limbed dwarfism. A simillar pattern can be seen in Apert's syndrome. Both these disorders seem to be present in the population at higher levels than the mutation rate would indicate. The explanation? Selection for mutant spermatogonia.

It now seems likely that there are three main classes of gene mutations causing genetic disorders: (i) nucleotide substitutions scattered along the gene, usually with substantial sex and age effects; (ii) small insertions and deletions, mainly deletions, with no age effect and a slight maternal excess; and (iii) hot-spots occurring almost exclusively in males and rising steeply with age. Three genes--fibroblast growth factor receptor 3 (FGFR3, mutated in achondroplasia), FGFR2 (mutated in Apert's syndrome), and RET (mutated in multiple endocrine neoplasia)--are examples of the hot-spot class. In this class, genes carry mutations that are clustered at just one or two nucleotide sites.

Update from Razib: I have addressed ziel's #2 complaint (don't know about the first ;). See text below....

As early as 1912, Wilhelm Weinberg (1) reported that children with dominant achondroplasia (short-limbed dwarfism) born to normal parents were usually among the last-born children in the family. With astonishing insight, he suggested that this finding argued for a genetic mutation as the cause of sporadic achondroplasia. A deeper understanding had to await the work of Penrose, who in 1955 showed that the effect observed by Weinberg was due to paternal age, not maternal age or birth order (2). This, of course, implied a much greater mutation rate among males than females. Haldane demonstrated just such a disparity in mutation rates between male and female gametes in the X-linked disorder hemophilia (3). Since then, the sex-difference and paternal-age effect have been confirmed for several X-linked recessive and autosomal-dominant diseases (4, 5). Missing to date has been an analysis of mutations in spermatozoa, but new techniques have finally made this possible. The results are shocking. First, a recently published analysis of sperm from men of different ages reported only a slight increase in mutant sperm with paternal age, much less than would be predicted by the clinical data (6). Now, on page 643 of this issue, Goriely, Wilkie, and colleagues (7) report their analysis in men of different ages of sperm carrying the mutation that causes Apert's syndrome, another classic disease where the clinical data predict a large sex and paternal-age effect. They argue that the mutation rate for this disorder is low, and that the apparent high rate is because mutant spermatogonia are positively selected before the start of meiosis (the two cell divisions that give rise to sperm). Very unorthodox.

It now seems likely that there are three main classes of gene mutations causing genetic disorders: (i) nucleotide substitutions scattered along the gene, usually with substantial sex and age effects; (ii) small insertions and deletions, mainly deletions, with no age effect and a slight maternal excess; and (iii) hot-spots occurring almost exclusively in males and rising steeply with age. Three genes--fibroblast growth factor receptor 3 (FGFR3, mutated in achondroplasia), FGFR2 (mutated in Apert's syndrome), and RET (mutated in multiple endocrine neoplasia)--are examples of the hot-spot class. In this class, genes carry mutations that are clustered at just one or two nucleotide sites.

So far, only hot-spot mutations have been amenable to direct analysis in sperm. In contrast to the analysis of FGFR3 mutations in achondroplasia (6), the data for FGFR2 mutations obtained by Goriely et al. (7) agree with clinical observations on the paternal-age effect. These authors used a sensitive technique called pyrosequencing to examine the FGFR2 mutation rate in sperm. They used a restriction enzyme that cuts near the site of the mutation in FGFR2 (nucleotide 755, normally a cytosine) and that recognizes only the normal, not the mutant, sequence. They also cleverly exploited a single-nucleotide polymorphism (SNP), dimorphic for bases A and G, about 100 nucleotides upstream of the mutation. Mutant sperm from men heterozygous for this SNP showed the expected 1:1 ratio of A and G, but the variance among men was enormous. This is consistent with premeiotic selection, because a selected mutant will carry along whichever SNP marker it happens to be linked to, thus broadening the distribution of SNP ratios. This finding, together with the enormous number of mutations at two hot-spots in FGFR2, and the fact that these are gain-of-function mutations, argues for premeiotic selection of mutant spermatogonia (7). As long ago as 1996, Wilkie suggested that mutations in sperm might be selected premeiotically (8).

Traditionalists, such as myself, are reluctant to postulate strong selection of mutant spermatogonia. Are there alternative explanations? In a 30-year-old man, some 90% of the spermatogonial divisions occur during the stem-cell phase of division, where the pattern is linear. This is followed by four exponential divisions before meiosis begins (9). By producing 16 exact copies of a mutation that occurred during the stem-cell period, this would introduce a correlation between the SNP markers, and thereby an enhancement of the variance in SNP ratio among sperm donors. With a number of exponential divisions, one would expect a Luria-Delbrück jackpot effect, that is, a tremendous difference in the mutant frequency in different men (10). A full analysis, taking mutant sperm number into account, would be complicated, yet four divisions hardly seem sufficient to explain the observations of Goriely and co-workers.

The authors offer additional evidence for selection of mutant spermatogonia. In the FGFR2 gene, the transversion, CrarrowG, is unexpectedly more common than the transition, CrarrowT. They argue that the CrarrowG mutations are rarer, but are more strongly selected. Another argument for selection is that the variance in SNP ratios is greater for the mutation with the higher frequency, an unexpected result in the absence of selection. Surprising hypotheses call for unusually strong evidence. The evidence that Goriely et al. present for the positive selection of a deleterious mutation in the testis, though indirect, is indeed strong.

Clearly, something is peculiar. If it isn't spermatogonial selection that causes these curious effects, then what does? What causes the discrepancy in results between the FGFR2 and FGFR3 studies? Measuring the mutation frequency in sperm requires very sensitive techniques, so there may be technical reasons for the discrepancy. The third hot-spot locus, RET (5), contains genes that are important for spermatogonial function (11), which may offer insights into how selection operates. Is it possible that spermatogonial stem cells do not follow the strict linear kinetics that are usually assumed for all stem cells, permitting them more stochastic variation? Stem cells in some somatic tissues have the strange and wonderful skill of directing mutant genes into cells destined to die, while maintaining normal genes in the stem-cell lineage (12). Could spermatogonial stem cells indulge in such unorthodox behavior? Happily, hot-spots such as those in FGFR2, FGFR3, and RET are amenable to further research, including linked SNPs, so we should see some answers soon. Further data on Apert's syndrome (13) are forthcoming and may help to resolve some of the conflicting data regarding the paternal age effect and premeiotic selection of mutations in achondroplasia and Apert's syndrome.

In previous examples of premeiotic selection, germinal and somatic selection act in the same direction (14). That Goriely and colleagues find favorable selection of FGFR2 mutations in the germ line, despite the fact that they cause a devastating disease, is indeed surprising. But that's how the data look.

Posted by Thrasymachus at 09:36 AM | | TrackBack

May 17, 2005

IQ Irrelevancies

Since Jensen & Rushton's article a few weeks ago (but really since Day 1 of graduate school), I've heard a lot of arguments against using IQ instruments, some are great (the best were from Jensen himself), some are mediocre (from Robert L. Williams, creator of Ebonics and the BITCH) and some I can only shake my head at, because the arguments they make are irrelevant. Some of my favorites are listed below.....

But I read an article saying X_1 group improved their performance by Z points on Y measure after a week of coaching from [usually someone with access to the assessment instrument].
So what? If they didn't gain any points, that would be the interesting point. The real question is not if X_1 group can increase their score after coaching, but, giving the same coaching to groups X_2 . . X_p is the rate of increase the same across groups1. Moreover, the score(s) at the end of the coaching are not measuring the same thing as the scores before the test, so to compare them is akin to comparing apples and doorknob handles.
Smitty took an IQ test and said s/he got X score (usually X < 80), but I think Smitty is brilliant. S/he always engages in conversation, offers lots of opinions about this, that, the other, and sounds so eloquent when s/he speaks.
So what? When did a given amount of interactions with [the person making the argument] indicate an objective, reliable way to indicate intellectual capacity?
I don't think a 2-hour exam can really give a good measure of someone's [put moral construct here, but it usually is worth].
So what? 1) No scientist would ever advocate that IQ=worth. 2) You're entitled to have whatever opinion you desire to have (whether supported or not supported by data).
IQ tests just measure performance on discrete skills. They don't really (directly) measure intelligence [usually followed by some asinine argument about why either intelligence doesn't exist or that there are so many varieties that it isn't worthwhile just to measure "1 kind"] .
So what? You can't directly measure evolution or gravity either, but few scientifically literate folks would say that they don't exist. You can quantify the constructs' effects and make (quite accurate) predictions about their potency on a given variable.
IQ researchers [in the past] have used it to discriminate against X group and say derogatory things about [the group] [The (often unstated) conclusion I am supposed to draw is that IQ/intelligence/g research should stop].
So what? People have misused fire to set women's garments ablaze, does that mean fire is bad? E-bay has been used to sell teenage boys, does that mean the Internet (or computers, in general) shouldn't be used? The ethics of a given research program and the object under investigation by the research team are two separate issues, not to mention use by folks who have no idea what they are doing with the object.

1. Note. I am not advocating the analysis of change scores.

Posted by A. Beaujean at 10:57 PM | | TrackBack

Satire: "College Profs Denounce Western Culture, Move to Caves"

This is the funniest thing I've read all year, and pretty close to the truth: "College Profs Denounce Western Culture, Move to Caves" from Iowahawk. A brief sample:

... When he earned tenure in 1991, Grok decided to broaden his philosophical research. "I realized that deconstructing literature was overly limiting. It was clear that other fields of inquiry could benefit from deconstruction."

It was then that Grok published a series of influential articles in which he deconstructed the sciences. "I initially showed that the so-called 'scientific method,' so treasured by the self-appointed high priests of science, was nothing but a bizarre ritual of the industrialist phallocracy," said Grok. "From there, it was a short intellectual leap to disprove the reality of the periodic tables, gravity and algebra." ...

Check it out!

On a side note, Razib has discussed deconstructionist theory before.

Posted by Arcane at 10:16 PM | | TrackBack

Diversity in Academia

Great piece in the LA Daily News today by Leonard Adleman. The ostensible crux of the article is to give reason why Rush Limbaugh should have received an honorary doctorate (an idea I am not necessarily super-keen on), but the subtle (and, I think, real) point behind the story is a little lower in the article....

But there is a bigger reason why I support giving him an honorary degree: Because I value intellectual diversity . . . intellectual diversity has all but vanished from America's campuses. We are failing in our duty to provide our students with a broad spectrum of ideas from which to choose. Honoring Limbaugh, or someone like him, would help to make the academy more intellectually diverse.

The great liberal ideas that swept through our universities when I was a student at Berkeley in the 1960s have long ago been digested and largely embraced in academia. Liberalism has triumphed. But a troubling legacy of that triumph is a nation whose professorate is almost entirely liberal.

In the 29 years I have been a professor, I do not recall encountering a single colleague who expressed conservative ideas [Adleman is a professor of computer science]. The left-wing accusations of Ward Churchill (Honorary Doctor of Humane Letters, Alfred University, 1992) are not the problem -- the problem is the scarcity of professors who are inclined to rebut them. It is time for the nation's universities to address this disturbing situation.

The lack of intellectual diversity in academia has been documented, much less myopic fields like my own. There is going to be a big turnover in academia in the next few years (well, in psychology/education, anyway), one can only hope that some of this functional diversity seeps through the cracks.

Posted by A. Beaujean at 09:27 PM | | TrackBack

Pinker on the gay gene

Sniffing out the gay gene by Steven Pinker.

According to Pinker, there is a reason that the recent discovery of differing reactions to odor by gay and straight men was made in Europe.

In America, the biology of homosexuality is a politicized minefield that scares away scientists (and the universities and agencies that pay for their research).

Pinker also looks at the origins to 'homophobia.'

Why didn't evolution shape straight men to react to their gay fellows by thinking: "Great! More women for me!" Probably the answer lies in a cross-wiring between our senses of morality and disgust. People often confuse their own revulsion with objective sinfulness, as when they dehumanize people living in squalor or, in the other direction, engage in religious rituals of cleanliness and purification. An impulse to avoid homosexual contact may blur into an impulse to condemn homosexuality.

What is refreshing is that there is no mention of homophobia as a socially induced characteristic.

Unfortunately he ends with a fairly good essay with a whopper.

Regardless of where homosexuality resides in the brain, the ethics of homosexuality is a no-brainer: what consenting adults do in private is nobody's business but their own.

Not true. What we do in our bedrooms, even when it does not have the obvious consequence, shapes us as individuals. Now, Pinker could have said, "we should aim to construct a society that makes it nobody's business what consenting adults do in private." Not that it's completely possible, of course. Pinker should know better than anyone that parents will always invest time in training children to behave in a certain manner. It's in our genes. People who behave differently threaten that training activity. Which in turn provokes reaction.

People threatening the social order, even if it's no fault of their own, is something that functioning societies don't tend to ignore.

Posted by Thrasymachus at 05:20 AM | | TrackBack

May 16, 2005


Miss Denmark is half-brown. Miss Norway is half-Thai. Miss Finland does not surprise (though I probably can't accuse her of being a baby-talker, seeing as she is studying in the Swedish School of Social Sciences at the University of Helsinki). No sign of Iceland, and guess what, no Miss Sweden this year. Why?

Check it:

When Scandinavian swimwear firm Panos Emporio last year bought rights to the Miss Sweden contest from TV3, its intention was to elevate the status of the the contest. However, "harassment from feminist organizations" has forced the company to cancel the competition. Thus, in 2005, Sweden will not send a contestant to the Miss Universe pageant for the first time ever.

Bizarro notes, check out Miss India, her photos make her look more Euro than Miss Denmark. Oh, and Miss Japan is 6'1.

Posted by razib at 09:01 PM | | TrackBack

The Female Orgasm

Thought that would get your attention.

The NYT also has an article on the evolutionary purpose of the female orgasm and the name of one of the scientists they quote is, get this, Dr Alcock.

Posted by jeet at 06:33 PM | | TrackBack

Class in the USA

The NYT has a series of articles this week on Class in America.

I haven't had time to read much yet but thought I'd mention it. Here is the first overview article. (Free registration may be required.)

Posted by David B at 10:52 AM | | TrackBack

Nerd alert!

Oracle and PHP in the same sentence? PHP has seen some growth over the past few years (see here or here), but security is always a headache. Probably why some webhosts are curtailing the ability to run PHP scripts under any extension.

If you want an entertaining taste of geek check out I, Cringley, sports-reporter-level-bullshit-nerd. Or, you can check out gay self-important UI nerd. And of course, philosophical self-reflective essayist nerd.

Posted by razib at 01:42 AM | | TrackBack

May 15, 2005

Theodore Dalrymple essay

Another fine essay by Theodore Dalrymple here.

(BTW the name is a pseudonym, so no relation to William.)

Comment from Razib: Read it!

Posted by David B at 02:59 PM | | TrackBack

Happy Slapping

The most alarming programme on British TV this week was an ITV report on the happy slapping craze. Moronic teenage thugs apparently find it amusing to slap complete strangers around the face while recording the incident on their video phones. In the worst cases it goes beyond slapping to punches and kicks, or even - in one case - setting a sleeping drunk alight.

I found a couple of goodish press reports on the subject, one here in a Scottish newspaper, and one in the Observer. As always, it is difficult to tell how far this is a real phenomenon and how far a media panic, of the kind that has recurred periodically since the 'Mohawk' craze of 18th century London.

Another issue that the two newspaper articles are conspicuously silent about is the ethnic aspect. In the ITV report most of the assaults seemed to be by blacks on whites. On the other hand, some of the culprits were certainly white, and in the setting-on-fire case the two culprits (now serving an inadequate 6-year sentence) were both white. I suspect that this is another case (like crack, gangsta rap, and 'hoodies') where a fashion has started among young blacks and spread throughout the underclass of feral teenage scum (if you'll excuse a non-value-neutral expression).

Posted by David B at 06:52 AM | | TrackBack

Textbook Errors

In a recent post I mentioned that there was an error in Jobling, Hurles and Tyler-Smith’s (generally very good) book on Human Evolutionary Genetics. Discussing an important measure of genetic distance (Nei’s D), the authors state that D varies between 0 and 1. I was fairly sure that this was wrong, as D is minus the log of a fraction, and the fraction can vary between 1 and 0, so it therefore seems that D can vary from 0 to infinity (that is, it increases without limit as the fraction approaches 0). I was a bit nervous about pointing this out, as I don’t like to disagree with those more expert than myself, so I was pleased to find my belief confirmed in another book, Speciation, (2004) by Jerry Coyne and Allen Orr, who say clearly (page 73) that D can range from 0 to ∞.

This isn’t by any means the first time I’ve noticed an error in a textbook. It is particularly annoying to find mathematical errors in a book aimed at students and other non-specialist readers. An expert in the field will probably be able to see immediately that something puzzling is just a careless slip or printing error, whereas a student may spend a long time trying to make sense of it, and worrying that they are missing something. I suggest that textbook authors and publishers should be fined $1,000 for every error of this kind!

Addendum from Razib: AJHG has a review of the Jobling, Hurles and Tyler-Smith book, as does Henry Harpending. I enjoyed it a great deal, though advanced readers might find it more interesting as a lead/source for a wide range of papers and texts on topics that pique their curiousity as opposed to a nuts & bolts primer. If you want something more technical, I recommend Genetics of Human Populations by Bodmer and Cavalli-Sforza, the data is out of date, but the equations are all good (and the price is really phat if you get it used).

Posted by David B at 06:30 AM | | TrackBack


Linkage disequilibrium patterns vary substantially among populations:

...Analyses of these three genomic regions provide empirical demonstration of marked differences in frequencies of the same few haplotypes, resulting in differences in the amount of LD and very different sets of haplotype frequencies. These results highlight the distinction between the statistical concept of LD and the biological reality of haplotypes and their frequencies. The significant quantitative and qualitative variation in LD among populations, even for populations within a geographic region, emphasizes the importance of studying diverse populations in the HapMap project to assure broad applicability of the results.

Linkage disequilibrium is a nonrandom association of alleles at different loci (that is, you have two forms of two genes which show up together at higher than expected frequencies assuming random mating). Two genetically very distinct populations brought together and mated would give rise to offspring with a very high level of linkage disequilibrium in the initial hybrid generation, but in subsequent generations recombination should break apart the assocations between various alleles.

You can read the full paper here (PDF).

Posted by razib at 01:17 AM | | TrackBack