Wednesday, January 31, 2007

Women in engineering   posted by p-ter @ 1/31/2007 08:59:00 PM

There has been much serious discussion on this website and others on the relative dearth of women in the fields of science and engineering. This stereotype has become so pervasive in our culture that one bold engineering program, fed up with it all, took it upon themselves to prove, conclusively, that there are indeed women in their department. Naturally, the format chosen for their demonstration was the calendar. Preview [probably NSFW] below the fold:

Thrifty genotype hypothesis   posted by amnestic @ 1/31/2007 07:46:00 PM

For the population geneticist, diabetes mellitus has long presented an enigma. Here is a relatively frequent disease, often interfering with reproduction by virtue of an onset during the reproductive or even pre-reproductive years, with a well-defined genetic basis, perhaps as simple in many families as a single recessive or incompletely recessive gene. If the considerable frequency of the disease is of relatively long duration in the history of our species, how can this be accounted for in the face of obvious and strong genetic selection against the condition? If, on the other hand, this frequency is a relatively recent pheonomenon, what changes in the environment are responsible for the increase?

-James V. Neel, "Diabetes Mellitus: A 'Thrify' Genotype Rendered Detrimental by 'Progress'?" (1962) [pdf]
The above quote is from the abstract of the highly influential paper by James Neel outlining the so-called "thrifty genotype hypothesis" for the prevalence of diabetes in modern populations. As this hypothesis is still widely cited (on this website, it has both praised and criticized), I present here my interpretation of the original paper, with comments as to how the hypothesis could be falsified or bosltered by the generation of unprecedented levels of population genetic data that we see today. I must note that this paper was written in 1962, and knowledge has certainly progressed since then. Some of the literature discussed by Neel or the paradigms he takes for granted are rather puzzling to me, and I may have missed some of the sublety of his arguments; readers are invited to peruse the .pdf linked above at their convenience and call me out on any mistakes.

I. The understanding of diabetes circa 1962

In 1962, "diabetes" was still considered more or less a single disease-- it wasn't until later that the current split between type I and type II diabetes was formalized. The adult-onset diabetes relevant to Neel is type II, so from now on, when I say "diabetes", I will be referring to type II. Further, the notion of a "complex" disease was also absent-- as is apparent from the quote above, Neel considered diabetes to be possibly caused by a single recessive allele, a situation subsequent research essentially ruled out.

In terms of the disease phenotype itself, Neel puts together a number of observations that suggest a certain advantage to the diabetic genotype. First, the children of diabetic mothers have increased birthwights as compared to the children of non-diabetic mothers. The children of non-diabetic mothers with diabetic fathers have higher than average birthweights, as well. Further, children who later develop diabtes tend to reach puberty slightly earlier, and thus could perhaps bear more children, than children who do not eventually develop diabetes. These observations, Neel suggests, indicate that the early diabetic phenotype is "thrifty", in the sense that the children are particularly efficient in their use of the resources available to them.

Of course, the eventual diabetic phenotype consists of insensitivity to insulin and the inablility to properly process carbohydrates. Neel reconciles the apparent early "thriftiness" with this eventual insensitivity with a discussion of the physiology of diabetes. In this discussion, there are two major hormonal players who, while normally in equilibrium, are thrown out of balance in diabetes. The first hormone is insulin, which moves glucose from the blood to storage, and the second Neel refers to as "anti-insulins", a class I can only assume refers to hormones like glucagon which release glucose into the blookstream.

In diabetics, then, Neel argues, there is an initial over-production of insulin, which accounts for the "thrifty" aspects of the genotype early on (the increased body weight and early menarche), which is then compensated by the stimulation of the "anti-insulins". An inbalance results, and in adulthood this is manifested by insulin insensitivity[1]. The major question becomes, why has diabetes become so prevalent now?

II. The "thrifty genotype hypothesis"

Neel's major insight in forming an answer to the above question is to note that "during the first 99 per cent or more of man's life on earth, while he has existed as a hunter and gatherer, it was often feast or famine". That is, there has been a marked change in environment in "modern" societies. He mentions three possible changes relevant to the control of the insulin/anti-insulin balance:

1. "Primitive" groups have less opportunities to overeat, have lower caloric intake, and greater physical activity than "modern" groups. This results in less stimulation of insulin, which in turn results in no over-stimulation of the anti-insulins.

2. The stress response in modern societies is less often followed by physical exertion than in primitive societies, which may disturb a "physiologic balance" established during human evolution.

3. The release of adrenaline in modern societies is also less often followed by physical exertion than in primitive societies. As adrenaline results in increased insulin production, this is an opportunity for the over-compensation of anti-insulins.

These last two are both similar in that they are involved with the stress response; indeed, Neel tentatively calls diabetes a "stress disease" along with peptic ulcers and hypertension!

In sum, the thrifty genotype hypothesis poses 1. that diabates results from a relative over-production of insulin, but more importantly 2. that "what we must now regard as an 'over-production' with unfortunate consequences was, at an earlier stage in man's evolution, an asset in that is was an important energy conserving mechanism when food intake was irregular and obesity rare."

III. The value of this hypothesis today

Now, I've noted the myriad assumptions made by Neel which are simply wrong-- the assumption of a single gene being one of them[2]. I imagine the modern view on the physiology of diabetes is quite different than his as well. So what remains of this hypothesis?

I would argue that his key insight still remains valid-- that, in population genetics, environment matters. Selection coefficients are not constant, and the way we alter our environment plays a large role in the selective forces exerted on us. More concretely, though, in terms of the genetic basis for diabetes, I can think of a couple predictions. First, any risk allele found for the disease will be ancestral-- that is, a protective allele will have arisen recently. Second, the derived protective allele will have been under recent positive selection.

The prevalence of diabetes in different populations, assuming all have more or less the same diet, should also be negatively correlated with the time since switching from a hunter-gatherer lifestyle. This is the statement that is perhaps the most contentious-- newcomers to the "modern", high-carb diet certainly have high incidences of diabetes, but it's impossible to tell whether this is due to the new availability of food or rather due to the content of the food itself. This may end up being a prediction that's impossible to test, so my instinct is to stick with the genetic evidence. Of course, I'm a geneticist, so I would say that.

[1] I am not at all familiar with modern reseatch into diabetes, and Neel's views on all of this are likely a vast simplification or even entirely wrong. I don't think, however, that this takes away from his later insights.

[2] An aside on Neel's discussion of the genetics of diabetes. I found the following passage, under the heading "Some Eugenic Considerations", to be interesing:
If the dietary and cultural conditions which elicit the relatively high frequency of diabetes in the Western World are destined to spread and persist over the entire globe, then, to the extent that modern medicine makes it possible for diabetics to propogate, it interferes with genetic evolution. But if, on the other hand, the mounting pressure of population numbers means an eventual decline in the standard of living with, in many parts of the world, a persistence or return to seasonal fluctuations in the availability of food, then efforts to preserve the diabetic genotype through this transient period of plenty are in the interest of mankind. Here is a striking illustration of the need for caution in approaching what at first glance seem to be "obvious" eugenic considerations!


Home labs   posted by amnestic @ 1/31/2007 05:31:00 PM

Coturnix made me notice that you can isolate DNA and run gels using legos and products from asian groceries. This got me thinking about what experiments I would run if I set this up. I think I could probably keep bugs of various sorts around and dissect out nervous systems. Could I select for certain traits in the right system? Could I discover anything new about biology in a DIY lab? There was a time when Rita Levi-Montalcini could make a huge contribution studying chicken embryos on a farm. What would you do with your home genetics lab? Are we at a point where the endeavor could only be a pastime or is there still something important to discover in our living room?

Monday, January 29, 2007

News to watch   posted by p-ter @ 1/29/2007 08:09:00 PM

This month's Nature Genetics has a meeting report on the Human Genome Variation 2006 conference. This little bit caught my eye:
Andrew Clark and Neil Risch provided some exciting first glimpses into these large data sets, including some remarkable findings in population genetics. For instance, Andrew Clark examined global FST in different regions of the US and noted clear evidence of a gradient of allele frequencies that could partially be explained by the demographic history. He also noted some striking differences in heterozygosity and patterns of linkage disequilibrium between HapMap Caucasians and Ashkenazi subjects from an ongoing study.
Remember that natural selection can be inferred from linkage disequilibrium patterns. Andy Clark was never too keen on the selection for Ashkenazi intelligence thing; I wonder where these LD data are taking him.

Direct measurement of the genetic contribution to the BW IQ gap   posted by the @ 1/29/2007 05:33:00 PM

To follow-up on two older posts, here is a comment on the direct tests of the genetic contribution to the Black-White IQ gap that were proposed by David Rowe and Charles Murray. Each appears to be describing the same set of experiments. The aim of these experiments is to ascertain the relative contribution of genes versus environment to the Black-White IQ gap, or put another way they aim to measure the between-group heritability (BGH) of IQ.

The easiest way to explain what they are proposing is to steal a bit of text from a paper describing the analogous experiments for a different phenotype (lung cancer):
The explanation for the observed racial or ethnic variation remains to be determined. Unmeasured environmental variations, genetic differences, or both may be involved. Dissection of disparities among racial and ethnic groups is complicated by the strong correlation between the socioenvironmental and genetic factors that differentiate these groups, with few persons differentially classified.2,8 However, a number of approaches can be taken. One approach is based on the recognition of mixed continental ancestry among persons self-identified as African American or Latino. ... Despite being genetically separable from whites, African Americans show a range of European ancestry that extends from nearly 0 percent to greater than 50 percent.9 Other studies have shown similar trends, with an average of about 20 percent European ancestry.10 Latinos are even more complex, comprising variable proportions of indigenous ancestry from three continental regions (Europe, the Americas, and Africa).11 Within these populations, individual ancestry can be estimated with the use of numerous ancestry-informative genetic markers; once established, this information can be used to examine correlations between the ancestry estimates and the trait of interest. [source]

Rowe and Murray each suggest examining the correlation between ancestry estimates (individual ancestry, or IA) and IQ. These experiments have not been done using the techniques of modern DNA genotyping, but they have been proposed for some time. Here's my question: what would be the expected correlation between IA and IQ for a given BGH? A naive answer is that r = BGH. However, this is quite unlikely to be the case.

This question has been asked in a related context, so I'll have to introduce more background to get us closer to an answer. While direct DNA genotyping has not been used to examine the IA-IQ correlation, other (less reliable) measures of IA have been used. Skin color is a prominent and notable example. Most recently, using data from the GSS, Lynn found a correlation of r=.17 between verbal IQ and skin color.[1] (I unknowingly replicated this finding in a previous post.) What is the implication of a correlation of skin-color and IQ of this magnitude to BGH? Jensen had previously considered this question.[2] In that context, Jensen estimates that the IA-IQ correlation should be around 0.5 and that the IQ-skin color correlation should be no more than about 0.2. Jensen's 0.2 figure is based on an under-estimate of the IA-skin color correlation that is found using DNA markers and electronic measurement of skin color (decades later). (However, Lynn's skin color data comes from self-estimates on a 5-point scale, and so Jensen's numbers may be appropriate.) However, Jensen does not offer an explanation for how he arrives at a value of 0.5 for the IA-IQ correlation, and so it's not clear what factors Jensen is taking into account. Jensen offers other reasons to downplay the importance of the IQ-skin color correlation as being informative about BGH. I'll again steal text from the lung cancer review to explain the point:
Such analyses are not without caveats, however. Even within an apparently homogeneous admixed group, individual ancestry may remain correlated with environmental risk factors.8 This is most likely to be the case when ancestry is apparent or known, but less likely when it is cryptic. For example, in African Americans, skin pigment is correlated with the degree of European ancestry12 and may therefore lead to residual confounding. [source]

Getting back to the question: what would be the expected correlation between IA and IQ for a given BGH? I don't know how to derive a formula to compute this directly, but it is easy enough to run simulations of the data. Jensen's estimate of 0.5 is at the upper end of the values that I computed for BGH=100%. Why not r=1? The predominant reason is that IQ varies in the African American population for reasons in addition to variation in IA. It is difficult to know how much variation in IQ occurs at a given level of IA, but a lower bound estimate comes from the variation in IQ of siblings. Full siblings share the same level of IA (more than that, they are ~50% identical by descent), but show a substantial amount of variation in IQ. A common estimate I've seen is an average difference of 12 points among white siblings. Unrelated individuals with identical IA will vary at least this much (further correction for the lower overall variance in the Black population is needed). Factors of study design will also attenuate the IA-IQ correlation. While "Black" individuals may be found at all levels of IA, the actual population distribution of IA is clustered around 20% European / 80% West African ancestry; thus the range of IA measured will probably be restricted. Also, IQ scores have excellent but imperfect reliability, further attenuating the correlation. My attempts at simulating the IA-IQ correlation suggest that even if BGH=100%, the IA-IQ correlation might be as low as r=0.25. Jensen estimates BGH in the range of 50-75%, further reducing the IA-IQ correlation.There are other caveats, and possible way around these problems (MALD). From the lung-cancer review:
Another caveat is that an estimate of individual ancestry from the entire genome may be misleading if the racial or ethnic difference is due to one or a small number of genes.13 However, this is also an attractive scenario, since the same collection of markers could be used to pinpoint specific genetic locations involved in the difference (admixture mapping).10 In this case, the likelihood of residual confounding is reduced.13 [source]

MALD may be the best hope of circumventing the confounding of skin color with ancestry -- the problem identified by Jensen, and later directed as criticism of Lynn's conclusions[3]. If black-white skin color differences are mapped to a few loci of large effect (e.g. SLC24A5) then it should be possible to examine their effects in the MALD analysis. However, this all seems far from simple.

[1] Lynn, R. (2002). Skin color and intelligence in African Americans. Population and Environment, 23, 365-375.
[2] Jensen, A. R. (1973). Educability and Group Differences. London: Methuen.
[3] Hill, M. E. (2004). Skin Color and Intelligence in African Americans: A Reanalysis of Lynn's Data. Population and Environment, 24, 209-214.


Here's a figure that explains MALD in a case-control context:

Figure 1 | Detecting disease-associated genomic regions using mapping by admixture linkage disequilibrium. a | The strategy that is used to assess the ancestral origin of chromosomal segments in mapping by admixture linkage disequilibrium (MALD)7, 13, 15 . Genotyping MALD markers is used to assess parental ancestry across a single chromosome in multiple cases (individuals with the disease of interest) versus matched healthy controls. The region indicated by the star is derived more often from one of the parental populations only in the disease cases, indicating that this region contains a disease-susceptibility locus. In the controls, the same region has an equal probability of originating from either parental population. b | A theoretical example of how an admixture signal can be detected using the MALD method for a disease with a higher incidence in one parental population (population A). The proportion of ancestry from population A in multiple individuals (both with the disease (cases) and without the disease (controls)) is shown schematically for different positions on a single chromosome. An elevated ancestry proportion from population A in cases is evident at the peak (marked by an arrow), which indicates the involvement of the corresponding genomic region in the disease. The peak can be identified by the higher (or lower; not shown) level of ancestry that is seen in cases relative to the same region in controls, and/or relative to the remainder of the genome in cases (only the neighbouring chromosomal region is shown here). Part b is modified, with permission, from Ref. 13 © (2004) The University of Chicago Press.
© 2005 Nature Publishing Group


The Pig Men Cometh   posted by Razib @ 1/29/2007 12:03:00 AM

"I wish there were pig-men. You get a few of those pig-men walking around, suddenly I'm looking a lot better."

-George Constanza of Seinfeld

Of course, a world with pig men would be a less beauteous thing. Kind of what I thought when I read Steve's most recent column on the rise of academic inequaliy, and ascendency of sub-mediocrity, in the Los Angeles school system.

Saturday, January 27, 2007

Norm of reaction and Williams Syndrome   posted by Razib @ 1/27/2007 01:40:00 PM

Despite the differences in upbringing, in both countries children with Williams syndrome were rated significantly higher in global sociability and their tendency to approach strangers than were their typically developing counterparts. But cultural expectations clearly influenced social behavior, since the sociability of normal American kids was on par with Japanese Williams syndrome kids, whose social behavior is considered out of bounds in their native country.

Norm of reaction "describes the pattern of phenotypic expression of a single genotype across a range of environments." So it seems there is a weakness in this study: Americans (mostly of European ancestry) do not share the same genetic background as Japanese. So a better test would be Japanese American children with Williams Syndrome vs. Japanese.

Icelandic fire   posted by p-ter @ 1/27/2007 12:22:00 PM

This week's Lancet has a profile of Kari Stefansson, CEO of DeCode Genetics. Regular readers have been exposed to much of the groundbreaking research done by the company, which has DNA samples from ~65% of the Icelandic population and a geneology that stretches back 1000 years. This is the group that published on the "fertility inversion", alleles that cause an ethnic-group-specific risk for heart disease, and generally has been one of the few groups to have success finding alleles that contribute to succeptibility for complex diseases like prostate cancer or diabetes.

Could anyone with a dataset as good as the entire Icelandic population pull this off? Stefansson:
"No, no, no. The real advantage is just that we are the best scientists, alright? Don't give me this bullshit about our advantage being the [Icelandic] population. Why do we have this population? Because we realised the importance of it." Although the tone of his voice suggests that he is being slightly tongue in cheek, it is clear that he is serious about the underlying message.
His repsponse to a question we've often asked interviewees-- any interest in your own genome sequence?
Stefansson says that he is not planning to follow Craig Venter's example and have his own DNA sequenced. "My mother died at the age of 62. My father died at the age of 67. And therefore I have been very diligent about avoiding to learn anything about my own disease predisposition", he says. "I want to die ignorant of my weaknesses."

Pinker on consciousness   posted by p-ter @ 1/27/2007 10:16:00 AM

Steven Pinker has an article in Time called "The Mystery of Consciousness". An extract:
What remains is not one problem about consciousness but two, which the philosopher David Chalmers has dubbed the Easy Problem and the Hard Problem. Calling the first one easy is an in-joke: it is easy in the sense that curing cancer or sending someone to Mars is easy. That is, scientists more or less know what to look for, and with enough brainpower and funding, they would probably crack it in this century.

What exactly is the Easy Problem? It's the one that Freud made famous, the difference between conscious and unconscious thoughts. Some kinds of information in the brain--such as the surfaces in front of you, your daydreams, your plans for the day, your pleasures and peeves--are conscious. You can ponder them, discuss them and let them guide your behavior. Other kinds, like the control of your heart rate, the rules that order the words as you speak and the sequence of muscle contractions that allow you to hold a pencil, are unconscious. They must be in the brain somewhere because you couldn't walk and talk and see without them, but they are sealed off from your planning and reasoning circuits, and you can't say a thing about them.

The Easy Problem, then, is to distinguish conscious from unconscious mental computation, identify its correlates in the brain and explain why it evolved.

The Hard Problem, on the other hand, is why it feels like something to have a conscious process going on in one's head--why there is first-person, subjective experience. Not only does a green thing look different from a red thing, remind us of other green things and inspire us to say, "That's green" (the Easy Problem), but it also actually looks green: it produces an experience of sheer greenness that isn't reducible to anything else. As Louis Armstrong said in response to a request to define jazz, "When you got to ask what it is, you never get to know."

The Hard Problem is explaining how subjective experience arises from neural computation. The problem is hard because no one knows what a solution might look like or even whether it is a genuine scientific problem in the first place. And not surprisingly, everyone agrees that the hard problem (if it is a problem) remains a mystery.

Friday, January 26, 2007

Anthropology on BBC4   posted by DavidB @ 1/26/2007 04:59:00 AM

People with access to the UK digital TV channel BBC4 should note that the channel has been showing a really outstanding series of programmes on anthropology. So far there have been four, on:

- Margaret Mead

- Bronislaw Malinowski

- Desmond Morris

- Tom Harrisson.

I missed the one on Margaret Mead, but I've seen the others, and they were all excellent. For me the most fascinating was the one on Tom Harrisson - titled The Barefoot Anthropologist - who was evidently a remarkable individual, though I'm ashamed to say I had never heard of him. The one on Desmond Morris was another matter: I had always vaguely dismissed him (without actually reading his books) as a pop lightweight, but Armand Leroi argued persuasively in the programme that Morris's speculations ought to be revisited in the light of more recent theories and data. As for Malinowksi, I already knew a fair amount about him, but still learned quite a lot.

I don't know if there will be any more programmes in the series, but they are likely to be repeated either on BBC4 or BBC2. [Added: There will be one on Carlos Castaneda next week.]

I don't know what the prospects are outside the UK: I suspect the programmes are too serious for Discovery Channel, but you never know.

Thursday, January 25, 2007

Blondes are not sexier: What the theory predicts and the data say   posted by agnostic @ 1/25/2007 11:42:00 PM

Steve has an interesting post on assortative mating in which he purports, in passing, that blondes have greater sex appeal, citing Peter Frost's hypothesis that blonde hair was sexually selected in Northern Europeans (I'll post on the assortative theme later). A danger in discussing which traits might be sexually selected is that the ponderer will likely go with what they personally find sexy and ask why such things might be sexually selected, rather than work from an independent angle. For example, I am very picky about the upper eyelids -- if they have that half-moon shape, that really does it for me. I've heard Michael say once that he likes this feature too -- but then, we're probably weirdos, or at least that's the conclusion until someone can show that a large fraction of guys prefer this feature, and that there's good reason to think it was sexually selected. Unlike half-moon eyes, blonde hair color receives lots of attention as a potentially sexually selected trait, but is a key prediction met -- are blondes sexier?

Below the fold, I briefly review some theory but mostly present data from all winners in three beauty contests, which indicate no overrepresentation of blondes. I conclude that hair color is of weak importance at best in accounting for sexiness, that the role of sexual selection in accounting for hair color variation is also weak at best, and that the perception that men are more likely to find blondes sexy is due to a passing fad for blondes during the decade from the mid-1970s to the mid-1980s.

First, Steve notes:
One of the most common storylines in movies is this: the blonde debutante gets engaged to the blonde fraternity president, but then she falls hard for the tall, dark, and handsome boy from the wrong side of the tracks.

The idea again is that blonde hair is sexy in females, not males. But just as common as the above scenario is the guy whose feelings for his fair-haired maiden waver once he becomes enchanted by a woman with coal eyes and raven tresses. For instance, in The Hunchback of Notre Dame (see here starting at line 57), the once pure priest Frollo describes how, after watching the gypsy Esmeralda dance and sing, he became so bewitched that he could not stem the tide of lust rising within him and fell madly in love with her. Shakespeare's "Sonnet 147" expresses a similar predicament: the speaker's got it bad for a bad girl! Not the first, nor the last. Interesting though literature and film may be, let's get to the theory and data.

Starting with the predictions from theory, the hypothesis that icy climes select for greater sex appeal is probably wrong. Gangestad & Buss (1993) showed that people in more pathogen-wracked areas emphasize "good looks" more strongly, and these are generally not icy areas. Think about the rest of the animal kingdom: where are the sexy, showy specimens with the most ornate song patterns? Same answer: mostly pathogen-infested areas, the tropics, etc. Consider the quintessential animal with exaggerated sexually selected traits -- the peacock -- whose rarer variant is native to Southeast Asia, and whose more common variant is native to the world's germ-cauldron (South Asia). Hamilton & Zuk's (1982) explanation was that these traits signaled better health to mates, no small feat in such areas. So, the prediction is that sexual selection will be very weak in Northern Europe (defined as the non-Mediterranean countries), where blondeness reaches substantial frequencies.

But even if sexual selection were a strong pressure there, what independently motivated evidence is there that blondeness is sexy, so that males who are sexually selecting would choose it over brunette hair? Again, the only good guess people have made is that sexually selected traits signal lack of being parasitized. For hair, though, this has mostly to do with the texture, lustruousness, and so on, not color -- although I'm willing to be corrected if someone knows of studies showing that blonde hair is more likely than dark hair to thwart the entry of pathogens into the scalp area. In any event, the main problem remains: in general, pathogen pressure is relatively very low in areas where blondeness is prevalent.

Turning now to the data, I recently posted about the list of who Maxim magazine ranked the hottest women for 2006, and there was no evidence of overrepresentation of blondes. The same is true for the other "lad mags" that you see in drug stores. Now I look at two other datasets that are probably more informative than who Maxim thought was hot in 2006: the winners of the Miss Universe and Miss USA beauty pageants. (The Miss America competition is not primarily a beauty pageant, as looks account for just 35% of the score). Such lists are preferable for testing the "sexy blonde" hypothesis since the individuals represent a very elite level of eminence. I looked up galleries of the winners, and if a girl's hair color wasn't clear from that, I did a Google image search for her. I judged overrepresentation based on the frequency of light hair according to Peter Frost's map at the Wikipedia entry for hair color.

For Miss Universe (gallery), there are 56 data points: 12 (21.4%) have light hair, 43 (76.8%) have dark hair, and 1 (1.8%) is pretty in-between. Now, 21.4% is surely a greater fraction of blondes than there are worldwide, but remember that Miss Universe doesn't represent the entire world -- it's mostly Europe and its offshoots, plus the white and mestizo populations of Latin America, and a tiny handful of East Asian countries (not China). For the non-Mediterranean areas of Europe, 21.4% is on the low-end of normal, but on the high end of normal for the Mediterranean (and so, for the mostly Mediterranean-looking Latin Americans who compete). I interpret this as supporting the null hypothesis of no effect of hair color on sexiness.

As for Miss USA (gallery), there are 60 data points: 17 (28.3%) have light hair, 38 (63.3%) have dark hair, and 5 (8.4%) have borderline hair. Although the fraction is larger here, remember the US is much blonder than the Mediterranean and Latin American countries who are also big contenders in the Miss Universe competition. Because the vast majority of the US population has been Northern European since the pageant began in 1952, we should determine overrepresentation based on the Northern European areas of Peter Frost's map. Doing so, we see that 28.3% is easily at expectation, and if anything is a bit on the low-end of normal for a predominantly Northern European population. Again, this result supports the null hypothesis.

In sum, we note that when put to a stringent test, blondes appear no sexier or uglier when compared to brunettes. Datasets such as Miss Universe and Miss USA are particularly instructive since the bar is set rather high. Then whence the perception that men find blondes sexier? There is an interesting temporal wrinkle in the data -- blonde winners are not evenly distributed in either dataset. For Miss Universe, from 1952 - 1974, 17.4% of the 23 winners are blonde; from 1975 - 1984, 60% of the 10 winners are blonde; and from 1985 - Present, either 8.7% or 13.0% of the 23 winners are blonde (depending on whether you are generous and code the 1 borderline girl as blonde). There thus appears to be a general lack of interest in blondes (and if anything, a dispreference for them), punctuated by a decade where blondes were very fashionable. Does the same pattern show up in the Miss USA dataset? Pretty much. From 1952 - 1973, 25% of the 24 winners were blonde; from 1974 - 1986, 50% of the 14 winners were blonde; and from 1986 - Present, 18.2% of the 22 winners were blonde. We note again the spike in blonde fashionableness from the mid-1970s to the mid-1980s.

I suggest that those who came of age during this Blonde Decade -- those who were born between roughly 1955 and 1970 -- may have unwittingly projected their perception of the sexiness of blondes onto time periods for which the view is not true. Combine this with the theoretical problems noted earlier, and it seems likely that sexual selection's role in increasing the frequency of blondeness is weak at best. That still doesn't answer the question of why blondeness evolved -- though I'll leave that for another post (or someone else can take it up). The explanation that I (and others) find most convincing for now is based on Jerome Kagan's work, starting in the mid-1980s, which has showed that light irises correlate with behavioral inhibition, suggesting that in Northern Europeans there was selection for different values of certain personality traits, which happened to also affect their eye & hair color.

Appendix: Hair color data for Miss Universe and Miss USA winners

Miss Universe (L = light, D = dark, M = borderline)

L 1952-Armi Helena Kuusela Kovo-Finland
D 1953-Christiane Magnani (Martel)-France
D 1954-Miriam Jacqueline Stevenson-USA
L 1955-Hillevi Rombin-Sweden
D 1956-Carol Laverne Morris-USA
D 1957-Gladys Zender Urbina-Peru
D 1958-Luz Marina Zuluaga-Colombia
D 1959-Akiko Kojima-Japan
D 1960-Linda Jeanne Bement-USA
L 1961-Marlene Schmidt-Germany
D 1962-Norma Beatriz Nolan-Argentina
D 1963-Ieda Maria Britto Vargas-Brazil
D 1964-Kiriaki “Corinna” Tsopei-Greece
D 1965-Apasra Hongsakula-Thailand
L 1966-Margareta Arb Arvidsson-Sweden
D 1967-Sylvia Louise Hitchcock-USA
D 1968-Martha Maria Cordeiro Vasconcellos-Brazil
D 1969-Gloria Maria Diaz Aspillera-Philippines
D 1970-Marisol Malaret Contreras-Puerto Rico
D 1971-Georgina Rizk-Lebanon
D 1972-Kerry Anne Wells-Australia
D 1973-Maria Margareta Moran Roxas-Philippines
D 1974-Amparo Muñoz Quesada-Spain
L 1975-Anne Marie Pohtamo-Finland
D 1976-Rina Messinger-Israel
D 1977-Janelle “Penny” Commissiong-Trinidad/Tobago
L 1978-Margaret Gardiner-South Africa
D 1979-Maritza Sayalero Fernández-Venezuela
L 1980-Shawn Nichols Weatherly-USA
L 1981-Irene Lailin Sáez Conde-Venezuela
D 1982-Karen Dianne Baldwin-Canada
L 1983-Lorraine Elizabeth Downes-New Zealand
L 1984-Yvonne Ryding-Sweden
D 1985-Deborah Carthy-Deu-Puerto Rico
D 1986-Bárbara Palacios Teyde-Venezuela
D 1987-Cecilia Carolina Bolocco Fonck-Chile
D 1988-Porntip Nakhirunkanok-Thailand
L 1989-Angela Visser-Holland
D 1990-Mona Grudt-Norway
D 1991-María Guadalupe “Lupita” Jones Garay-Mexico
D 1992-Michelle McLean-Namibia
D 1993-Dayanara Torres Delgado-Puerto Rico
D 1994-Sushmita Sen-India
D 1995-Chelsi Pearl Smith-USA
M 1996-Yoseph Alicia Machado Fajardo-Venezuela
D 1997-Brook Antoinette Mahealani Lee-USA
D 1998-Wendy Rachelle Fitzwilliam-Trinidad/Tobago
D 1999-Mpule Keneilwe Kwelagobe-Botswana
D 2000-Lara Dutta-India
D 2001-Denise Marie Quiñones August-Puerto Rico
D 2002-Oksana Fyodorova (Oxana Fedorova)-Russia (dethroned)
D ---Justine Lissette Pasek Patiño-Panama
D 2003: Amelia Vega Polanco-Dominican Republic
L 2004: Jennifer Hawkins-Australia
D 2005: Natalie Glebova-Canada
D 2006: Zuleyka Jerris Rivera Mendoza-Puerto Rico

Miss USA

D Jackie Loughery 1952
D Myrna Hansen 1953
D Miriam Stevenson 1954
L Carlene King Johnson 1955
D Carol Morris 1956
D Leona Cage 1957
L Charlotte Sheffield 1957
M Eurlyne Howell 1958
D Terry Lynn Huntingdon 1959
D Linda Bement 1960
D Sharon Brown 1961
D Macel Wilson 1962
L Marite Ozers 1963
L Bobbie Johnson 1964
L Sue Downey 1965
D Maria Remenyi 1966
D Sylvia Hitchcock 1967
D Cheryl Ann Patton 1967
D Dorothy Anstett 1968
L Wendy Dascomb 1969
D Debbie Shelton 1970
D Michele McDonald 1971
M Tanya Wilson 1972
D Amanda Jones 1973
L Karen Morrison 1974
D Summer Bartholomew 1975
D Barbara Peterson 1976
L Kimberly Tomes 1977
L Judi Andersen 1978
M Mary Therese Friel 1979
L Shawn Weatherly 1980
L Jineane Ford 1980
L Kim Seelbrede 1981
D Terri Utley 1982
D Julie Hayek 1983
D Mai Shanley 1984
D Laura Martinez-Herring 1985
L Christy Fichtner 1986
D Michelle Royer 1987
D Courtney Gibbs 1988
D Gretchen Polhemus 1989
D Carole Gist 1990
M Kelli McCarty 1991
L Shannon Marketic 1992
D Kenya Moore 1993
D Lu Parker 1994
D Chelsi Smith 1995
D Shanna Lynn Moakler 1995
D Ali Landry 1996
D Brook Lee 1997
D Brandi Sherwood 1997
M Shawnae Jebbia 1998
D Kimberly Ann Pressler 1999
D Lynnette Cole 2000
L Kandace Krueger 2001
D Shauntay Hinton 2002
D Susie Castillo 2003
L Shandi Finnessey 2004
D Chelsea Cooley 2005
L Tara Elizabeth Conner 2006

Labels: ,

I say inbreeding depression, you say heterosis   posted by p-ter @ 1/25/2007 05:58:00 PM

We've talked a lot about inbreeding and the its health consequences many many times before 'round these parts. Most people think of the consequences in terms of unmasking recessive disorders like rare bith defects or the inability to feel pain. But the consequences are also apparent in complex traits--a new article shows a negative correlation between heterozygosity in the genome (inbreeding causes decreased heterozygosity) and both blood pressure and cholesterol levels.
These findings, if replicated, suggest that hR [heterozygosity] be considered as a genetic risk factor in genetic epidemiological studies on common disease traits. They are consistent with the well-known effects of heterosis (hybrid vigour) described when outcrossing animals and plants. Outbreeding resulting from urbanization and migration from traditional population subgroups may be leading to increasing hR and may have beneficial effects on a range of traits associated with human health and disease. Other traits, such as age at menarche, IQ and lifespan, which have been changing during the decades of urbanization, may also have been influenced by demographic factors.

Wednesday, January 24, 2007

Sperm...cooperation?   posted by p-ter @ 1/24/2007 08:58:00 PM

A fascinating new article in PLoS One follows up on a previous paper documenting a possible evolutionary response to sperm competition-- sperm cooperation.

The idea here is simple-- if a number of males mate with a female, there are a huge number of sperm competing to be the lucky one who ends up fertilizing the egg. Selection on swimming speed and efficiency must be intense-- individuals with slow sperm just don't have any offspring. However, many of those single sperm are actually from the same individual, and are thus related; if those related sperm could somehow work together to outcompete the sperm from other individuals, they might increase their fitness. The logic here is an application of Hamilton's rule (altruism can evolve if r*B>C, where r is relatendess between two organisms, B is the benefit to cooperation, and C is the cost), except here we're talking about haploid germ cells, not diploid organisms.

Two individual sperm share, on average, 50% of their genome, giving them an r of 0.5. So altrism can evolve if the benefit of cooperation to any individual sperm is more than half the cost; if sperm competition is strong, this might not be a bad proposition. And indeed, sperm in some rodent species band together in "trains". The video they include is pretty sweet:

The puzzling thing for me about this is that, in some species, there can be 50-100 sperm in these "trains", while only those sperm at the head of the train have the opportunity to fertilize the egg. This seems like a lot, and certainly suggests a very strong benefit to forming these trains, as the cost to each sperm is likely proportional to N, the number of sperm in the train.

Another possibility is suggested by noting that the relatedness of two sperm has an expectation of 0.5; some sperm will be more or less related to each other. If there were some mechanism by which more closely-related sperm could preferentially group together, the necessary benefit for Hamilton's rule to apply would be greatly decreased, and the number of sperm willing to act altruistically greatly increased.

Imagination and memory   posted by amnestic @ 1/24/2007 07:55:00 PM

A recent paper in PNAS is getting some press. Patients with hippocampal damage and amnesia (the normal symptom) are also impaired in imagining future scenarios. The authors contend that this fits with a view of the hippocampus as necessary for creating the context in which we have rich inner experiences. The data hinge on how well you think the questions asked by the researchers reflect "imagining". The patients were given a general scenario and asked to imagine an experience there. They were usually short on descriptive richness and "spatial coherence". But they were also generally more brief, and I'm not sure this was controlled for. Some schizophrenia patients suffer from alogia (poverty of speech). They need something like a richness/detail measure.

If the hippocampus is important for vivid, rich recollection of past experience and for making up future experiences, it seems more like a setting for memories to play out in rather than a memory storage structure per se. This doesn't really sit with the systems consolidation or the multiple memory trace as far as I can see, but Nadel and Moscovitch have jumped on it as a challenge to systems consolidation. (Refresher: Systems consolidation = over time memories become less and less dependent on the hippocampus; multiple memory trace = the reduced effect of hippocampal lesions over time is due to propagation of memory traces within the hippocampus). I think it's interesting that imagination and memory recollection might have the same substrate. In efforts to eschew confabulation I often demure when asked to recollect particular details of an experience, while I have seen others in the process of storytelling give very rich, but erroneous details.

This passage from a patient's attempt to imagine himself in a museum struck me as sort of tragic. I wonder if the patient becomes as frustrated and depressed as I would failing at this task:

[pause] There's not a lot as it happens. So what does it look like in your imagined scene? Well, there's big doors. The openings would be high, so the doors would be very big with brass handles, the ceiling would be made of glass, so there's plenty of light coming through. Huge room, exit on either side of the room, there's a pathway and map through the centre and on either side there'd be the exhibits [pause] I don't know what they are [pause]...there'd be people. [pause] To be honest there's not a lot coming. Do you hear anything or smell anything? No, it's not very real. It's just not happening. My imagination isn't... well, I'm not imagining it, let's put it that way. Normally you can picture it can't you? I'm not picturing anything at the moment. So are you seeing anything at all? No.

Hippocampal subfield differentiation   posted by amnestic @ 1/24/2007 06:55:00 AM

There has been a lot written in recent years about interneuron diversity. Excitatory interneurons exist, but more often than not interneurons produce and release the major inhibitory neurotransmitter, GABA. Interneurons are locally connected, and they can control local circuit oscillations and excitability. There are about a zillion different types of GABAergic interneuron based in morphology, physiology, and molecular content. All this interneuron diversity has got me wondering about the diversity of another major neuron class, the excitatory pyramidal neuron. Look, here comes one now:

They are called pyramidal because that's how you can loosely describe the shape of their cell body. They usually have an apical dendrite that comes out of the top. The one pictured is bifurcating where the arrow is pointing. They have basilar dendrites that come out the sides near the bottom, and they have an axon that comes straight out the bottom (indicated by an arrowhead in this picture). This particular model is a CA3 pyramidal neuron, found in the CA3 subfield of the hippocampus. The hippocampus is made up of the dentate gyrus (DG) and the Ammon's horn (cornu ammonis, CA). These are two curving rows of cell bodies all lined up so their dendrites and axons are pointing the same directions. The DG curves rather sharply and makes something like a V or a crest. The CA fields together form a milder curve that still comes out something like a C. The bottom portion of the CA "C" interlocks with the DG, so you could draw something like a S to get both subregions of the hippocampus. Here's a link to a picture if my description is confusing. The CA1 field covers mostly the top arc or the "C", while the CA3 field is from more like 6 to 10 on the C clockface.

If you just look at a picture of the hippocampus, the division seems completely arbitary. CA1? CA3? And what happened to CA2? There actually are meaningful differences between the subfields though and it's not a smooth gradient. Functionally, one important distinction is connectivity. The CA3 pyramidal neurons are much more highly interconnected than CA1 pyramidal neurons. This allows them to chatter with each other and do computations locally. Some have suggested this 'recurrent network' property of CA3 places it in a role as a pattern completion computer. Morphologically, CA3 cells are bigger than CA1 cells. And this is where my knowledge sort of runs out and I don't know where to look. I'd like to know the rest of the differences between CA3 and CA1 cells. I would like to know whether one of the two is more like some class of neocortical pyramidal cell. I have one last place to check, my Hippocampus book, but I don't have it with me right now.

I did find this paper though, by Tole et al., that shows that the CA fields are specified early in development (~ embryonic day 15 in mice), and that they don't need extrinisic cues to develop properly. These brave folks managed to dissect out embryonic hippocampi (which are tiny already) and then subdivide them into even smaller "presumptive CA fields" and grow them up. The CA1 and CA3 fields still gain the proper cell morphology and cell-type markers without any help from outside sources. They also found that the differentiation of these cell-types starts at the ends of the CA layer and works its way in, so eventually there is a hole of undifferentiation in between the CA1 and CA3 specified cells. The two finally meet at about embryonic (post-conception) day 19.5 just around the date of birth. This explains CA2 as well. CA2 is where the two differentiation signals intermingle and produce some CA3-type and some CA1-type cells. The markers used in this paper are not terribly informative about function, but could perhaps be used to derive a line of mice with different colored CA3 and CA1 cells that we could grab and do genomics on. Having good specific markers for these cell-types would, in general, assist in the development of transgenic technologies to piece apart subregion contributions to hippocampal funciton. I wonder if CA3 and CA1 pyramidal cell-types can be any further subdivided or if we already understood the full-range of hippocampal excitatory diversity.

Update:The Spruston and McBain chapter in The Hippocampus Book is a treasure trove for this kind of stuff. It's going to require a whole new post. Also, Tole and Grove didn't stop publishing in 1997, so I will have to look into their more recent work.

Tuesday, January 23, 2007

Where are the freaks?   posted by Razib @ 1/23/2007 10:53:00 PM

So I've been mulling over the recent publication in Annals of Human Genetics of a review of the recent skin color genomic work. The conclusion is pretty predictable given the recent findings:

a) Dark skin is the modern human ancestral trait
b) Light skin is derived
c) The derivations are independent

There is lots of stuff to comment on, but I'll limit myself to a weird thought I've had for a while. The authors point out that East and West Eurasians (e.g., Western Europeans and Chinese) are light, in general, because of different mutations on different loci. In other words, the genetic architecture is pretty dissimilar. Even in the one case where the same locus (or genomic region) was subject to selection the haplotype differed. One would expect that there would be overlap in some of these genes being selected for since they are implicated in the same phenotype, though the allelic solution was distinct. Nevertheless, my interest is in the loci which do not overlap (most). Consider SLC24A5. It explains around 30% of the intergroup variance between Europeans and Africans, but none of the variance between East Asians and Africans, because East Asians and Africans share the ancestral allele. In contrast, MC1R is hyperpolymorphic in Europeans, constrained to the ancestral state in Africans, and being positively selected in East Asians toward fixation. And so on. Now...imagine, you have loci:

1, 2, 3, 4, 5, 6, 7, 8

...implicated in the loss of melanin production in human skin. Europeans are derived on:

1, 2, 3, 4, 5 (so ancestral on 6, 7, 8)

East Asians on

5, 6, 7, 8 (so ancestral on 1, 2, 3, 4)

Assuming that the loci are fixed, if you crossed a bunch of Asians with a bunch of Europeans (here's looking at you Hawaii!), after a few generations you could have someone who is derived on:
1, 2, 3, 4, 5, 6, 7, 8 homozygously

Greg points out that these selected genes seem to be relatively recent (agricultural?), so their shallowness means they aren't embedded in coadapted complexes which are likely to birth monsters. In fact, we know from pedigree studies that between Europeans and Africans skin color is inherited pretty much in an independent and additive fashion with 4-5 loci accounting for 90% of the between racial variance. So I am wondering if any intrepid readers want to engage in skin reflectance tests of variously racially mixed happas in Hawaii?

David Byrne = Neville Chamberlain?   posted by amnestic @ 1/23/2007 05:55:00 PM

I like David Byrne. He makes interesting music and visual art, and now he's making an interesting journal.

This is why intelligent people can be religious. That's an arrogant statement - it presumes that religion and intelligence are incompatible, that anyone with any sense wouldn't believe in unproven supernatural faith-based scenarios. But of course that is not the case. I personally might believe (believe!) that many religious beliefs are irrational and verge on lunacy - but I can both see their efficacy - their attraction and usefulness - and sense their beauty. One does not have to be a Catholic to stand in awe of the Sistine Chapel ceiling; be Muslim to hear the lure of the soulful cry of the muezzin and sense the power of the mass dance of the faithful in prayer; be Hindu or Jewish to read and enjoy a text that is often chock full of amazing and surprising metaphors and analogies. These dances, music, images, metaphors are, I sense, deep-rooted - they are like the neural propensities for grammatical structures that Chomsky goes on about - and are therefore similarly genetically inheritable. The dance that is religion has evolved within us, to be released and expressed in a thousand different forms, none of which make logical sense, and all of which, if looked at literally, require a large helping of denial. God is in the wiring, bequeathed by the genes.

To me, this is why the current (tiny) wave of atheism - the recent books by Dawkins, Dennett and Harris, for example - are also in denial. They deny that this propensity for people to believe is innate. Yes, they admit that religion offers many comforts and assurances, security and community - very attractive and seductive - but they stop short at admitting that we are genetically predisposed to believe, that it is in our very nature, a part of what it means to be human. Maybe an illogical part, but that all our innate evolved characteristics are not practical forever (context changes, the world changes) or even rational, from some points of view (does the peacock's tail have to be THAT big? Isn't all that just a wee bit of a wasteful allocation of resources?)

More on GNXPy business:

Among recent evidence for continuing evolution are the Ashkenazi Jews. It seems that possibly as a result of being banned from many labor and work opportunities over the last 1000 years, this mainly Eastern European gene pool has evolved a higher than average intelligence (12-15 points higher than average). The blowback from repression is the creation of a super race. Poetic justice of a twisted sort.

Other evidence:

Gene CCR5-Δ32 a gene found in certain parts of Africa affords some protection against HIV.

Gene DRD4 is the dopamine receptor gene. It has become more common in the last few thousand years. It is positively selected for, so it will probably become even more common as time goes by. It is also associated with attention deficit disorder and hyperactivity. Why humans should evolve FAVORING those conditions is still a mystery. My guess is that those conditions are the flip side of a genetic coin whose face side offers a more obvious suitability and advantage and, being linked on the same gene, you unfortunately get the bad along with the good. Aren't the dopamine receptors also somehow related to the pleasure centers of the brain?

This could also be like the schizophrenia/creativity link mentioned in an earlier posting, or the genius-geek/autism link. A taste of Fugue gives a nice buzz, but too much and it's your last meal.

Super race? "Never yet has there been a superman. I have seen them both naked, the greatest and the smallest men:—and they are still all-too-similar to one another. Verily, even the greatest I found to be all-too-human."

Dendrite evolution   posted by amnestic @ 1/23/2007 05:37:00 PM

Trawling the net, I came across this chapter from the forthcoming 2nd edition of the Dendrites monograph: Phylogeny and Evolution of Dendrites by Gayle M. Wittenberg and Samuel S.-H. Wang (pdf). I was hoping to find something about the origin of dendrites and maybe something about differences in primates or humans. Unfortunately, there isn't much to report. From reading this review, you'd get a definite impression that dendritic architecture is not the target of selection. The dendrites either don't scale at all with brain size or they scale in such a manner as to preserve the "isoelectric" distance from the soma. In other words, even when dendrites grow, they preserve computation and communication to the soma. We get three leads to follow if we want to know about novel primate dendritic architectures:

Another place in which unusual dendritic specializations may occur is the neocortex of great apes, which show unusual social and cognitive complexity. These animals have several types of giant neocortical neurons, including Betz cells (Sherwood et al., 2003), Meynert cells (Sherwood et al., 2003), and spindle cells (Nimchinsky et al., 1999). These giant cells may have arisen in great apes as extreme adaptations of pyramidal neurons. Among primates their somata show distinct scaling relationships relative to brain and body size. Like other neocortical pyramidal neurons (Elston et al., 2001), they may vary in dendritic extent and synapse number across species as well. At present, however, little is known about their dendrites.

We know a reasonable amount about molecular determinants of dendritic branching:

The commonly held view of dendritic morphogenesis is that general structural features result from genetic instructions, whereas fine connectivity details rely mostly on substrate interactions and functional activity. During early dendritic maturation, dendritic growth cone formation produces new branches at all dendritic roots. The second phase is growth cone independent and afferent input dependent, during which branching is limited to high order distal dendrites. During the third phase, activity-dependent synaptic maturation occurs with limited or subtle remodeling of branching.

So it seems like maybe some molecular phylogeny could point us in the direction of good hypotheses. It would sure be nice to know when dendrites first arrived though. Does anyone know? Were cells excitable first or polar first (polar meaning having separate extremities with distinct function)? I assume it happened back in flatworms or something but I haven't got a clue.

Storms and Teacups   posted by DavidB @ 1/23/2007 03:12:00 AM

As GNXP's only British contributor I feel bound to say a few words about the Big Brother controversy. For the past week Britain - and perhaps also India - has been gripped by a bout of collective insanity. I'm not sure how far the rest of the world has taken any interest in the affair, so here is a report from CNN.

In commenting I am somewhat hampered by having hardly watched the show - honest - but it has been impossible to escape it entirely. As far as I can judge, the alleged 'racism' has been hugely exaggerated. Tensions of social class and personality were far more important, though it would be difficult to deny an undercurrent of racism in some of the comments about Shilpa Shetty. But it is worth pointing out that the only overtly racist comment was made by Jermaine Jackson, whispering to Shilpa (perhaps underestimating the sensitivity of the microphones) that "we are people of color, they [Jade and her friends] are just white trash". Shilpa, a high-caste Hindu, does not seem to have been overjoyed by this gesture of solidarity.

Which brings me to my main point: I question the smug assumption among the liberal commentators, including those of Asian origin, that racism is somehow a preserve of the white working classes. The commentators can hardly be unaware that prejudice exists in all ethnic groups, but with a few honourable exceptions, like Yasmin Alibhai-Brown here, there seems to be a tacit conspiracy to ignore it.

Monday, January 22, 2007

10 Questions for György Buzsáki   posted by amnestic @ 1/22/2007 11:00:00 PM

György Buzsáki is Board of Governors Professor at the Center for Molecular and Behavioral Neuroscience at Rutgers University. His recent book, Rhythms of the Brain, is a clear explication of the study of network-level dynamics in the nervous system, ranging from innovations in extracellular recording to theoretical solutions to the binding problem. Rather than list his numerous awards and accomplishments, I direct you to the hundreds of research articles and reviews which have placed him at the forefront of the rapidly progressing field of systems neuroscience. Chris Chatham of Developing Intelligence and I collaborated to bring you the following ten questions.

1. Modeling necessarily requires simplification. In your view, what features of biological neural networks are so important that they must be captured in any accurate artificial neural network model? For instance, do you believe it is enough to supplement firing rate-coding units with a parameter for "phase," or do computational models need to simulate biological neural networks at a lower level?

Models can be useful in at least two different ways, inferential and inductive. Inferential class modeling is analogous to statistics. In the simplest scenario we measure two variables and compare their relationship by e.g., a t-test. When the system under investigation is complex and the multiple measured variables are not related to each other in an obvious way, testing the statistical validity of the individual and interactive contributions can become a daunting task. Here models can be invaluable because they may explicitly illustrate which variables we believe are critical. Such model-based summaries can be conveyed to others much more rigorously and effectively than using words and pencil drawings typical of the 'old days'. Models in the second class can extrapolate from a limited set of observations, so that only a few test points are needed to verify the validity of the extrapolation. These models can (or rather should) address the issue of 'scaling'. A good model is not about the reproduction of the observations but about its ability to predict how the network/system should grow to preserve the functions and timing of the smaller size network. For example, if a network of 100 neurons can generate gamma oscillation, what should be the rule to generate the same coherent rhythm when the network is scaled up to 1,000 or 10,000 neurons.

Every model, as any biological system, must have a 'goal', to be meaningful and interpretable. It is not the 'biologically realism' or 'detail-equivalence' that matters in most cases but the inductive power of the computational model. If I gain new insights from a model, I like it no matter its ingredients. I gained a lot more insights about oscillations from models over the past decade than from my own experiments. Experiments provide the constraints and the model should provide alternatives.

2. Contextual fear and simple context learning have become standard assays for hippocampal functioning and plasticity, but it is difficult to reconcile the use of this behavioral tool with the theories that arise from unit recording. What is the relationship of hypotheses concerning episodic and semantic memory and types of navigation to context or contextual fear memory? Is a context (or configural representation) a sequence or a map?

I believe, along with many other evolutionary biologists, that a computational algorithm introduced by nature in a small network does not change drastically when the network grows. I believe that the fundamental nature of computation is the same in the hippocampus of mice, rats and humans. This is why I keep working with rodents. I pointed out that the computations used for dead reckoning (or path integration) and map-based navigation in the rat are perhaps identical to the computations used for episodic and semantic memories in humans, respectively. Both dead reckoning navigation and episodic memory rely on self-reference and require a unique spatio-temporal context, in contrast to the self-independent (explicit) map and semantic information. Since fear is custom-tailored and does not exist outside the brain, and it is both contextual and self-referenced, the connections between these man-invented terms are perhaps not so remote as they presently appear.

3. You have invested much time and effort developing and refining the silicon probe for multi-unit recording. This investment seems to be paying off now in a series of remarkable findings only achievable through the recording of large numbers of neurons. What is the next level of refinement needed in this technology? For that matter, do we need to record and isolate more units or do you think that we have reached the point of diminishing returns?

With some effort several laboratories could record from a thousand or more neurons simultaneously even from a small brain with existing technologies. But this in itself is not interesting. One can place hundreds of wires in the neocortex and other structures and increase the n. The emphasis is not on gigantic numbers but on statistically representative samples of neurons that can provide insight into the nature of the computation. Accordingly, my strategy is to record from two or more representative populations of local neurons without inflicting detrimental damage to the network. This task cannot be achieved effectively with wire electrodes but silicon probes can provide progress. Multiple-site probes allow not only measuring the spike output of neurons but also provide information about intracellular and intradendritic events brought about by the inputs, and all this can be done in the behaving animal. Only when both inputs and outputs of the networks are monitored simultaneously can one hope to infer the underlying computation.

4. What is 1/f organization and what does it imply about a system?

It shows that a system is organized at multiple temporal levels, none of which is unique when assessed over large time periods but at any instance some temporal scale dominates, and that the pattern at each time point is a function of the past history of activity. Interestingly, the brain seems to generate these dynamics from a finite number of discrete oscillators with a unique, asymmetric relationship between them: slow oscillators affect faster ones but the reverse relationship is much weaker. We learned about the properties of 1/f systems from other disciplines but appreciation of these features in the brain is quite recent. These properties imply that e.g., cortical networks can be 'sensitized' to environmental inputs with extreme efficacy but this tuning depends strongly on the self-organized (ongoing) brain activity. At the same time, the dynamics can shift transiently to a dominant oscillation which, in turn, allows for precise timing and, therefore, prediction of events.

5. In the Science review of your book, Pascal Fries noted that Hungarian neuroscientists were highly represented. You, in fact, became an honorary member of the Hungarian Academy of Sciences in 2001. Is there a special emphasis on the study of neuroscience in Hungary, and if so, what is the reason?

Admittedly, part of it is just cultural chauvinism. But as in any self-organized system, weak links can have large effects. If you read the recently published 'Martians of Science' you will realize that these five men of physics were as diverse as any five can be. But they were linked by similar experiences: E.g., they were forced to change countries multiple times, shared an exceptional degree of enthusiasm about science, and it also helped their interactions - and relative isolation from others - that they were fluent in Hungarian and much less so in German or English. The result of mutual information exchange among them might explain why the knowledge they generated as a group exceeded so much the sum of their individual contributions.

But even if you are aware of this truism, you do not rationally form networks. You just happen to be in one of the participants in a spontaneously emerging web of links. In my early life, high school and science education was strong in Hungary under the communist regime and there were limited channels of communications with the West. Hard sciences were all strongly linked to the military technology of the Soviets. Neuroscience (apart from Pavlovianism) was a new and non-partisan field. After the war, only two individuals (János Szentágothai and Kálmán Lissák at the University of Pécs) in the entire country had the necessary connections at home and abroad, a unique protection from the political system and the personal charisma to form active neuroscience groups. These seeds attracted all motivated students who wanted to carry out brain-related research and have become parts of the same web. What also helped our generation is that by ending up living in different countries and continents we were not competing for the same limited sources of funding so we could 'afford' to share some complementing views and technical abilities.

6. Your discussion of the brain's first rhythm could make one feel that we are close to understanding when meaningful cognition begins. Does your knowledge of EEG patterns and their underpinnings influence your thinking about beginning-of-life, end-of-life, or even animal rights debates?

I believe that cognition begins once the 1/f features of cortical rhythms emerge because this dynamics represents global (i.e., distributed) computation and only structures with these features appear to generate conscious experience. The ontogenetic appearance of 1/f dynamics coincides with the emergence of long-range cortico-cortical projections. In the newborn human the 1/f global feature of the EEG is already present. On the other hand, in preterm babies, depending on the gestation age, long seconds of neuronal silence alternate with short, spatially localized oscillatory bursts (known as "delta brush"), like in sharks and lizards. These localized intermittent cortical patterns in the premature brain, and similar ones in the strictly locally organized adult cerebellum, cannot give rise to conscious awareness, no matter the size. From this perspective, the structure-function relations between the small world network-like features of the cerebral cortex and the resultant global rhythms appear as necessary conditions for awareness. Earlier developmental stages without these properties simply do not have the necessary ingredients of the product we call cognition.

7. You've suggested that sleep disturbances associated with psychological disorders might be a cause rather than a symptom. Aside from the disturbance of circadian rhythm, do you think differences in the magnitude or frequency of other oscillations could be at the root of any particular psychological disorders?

Timing and network synchronization are the essence of all cortical computation, and the timing ability of cortical networks is reflected in the rhythms they produce. We have shown that deterioration of synchrony of hippocampal assemblies, e.g., induced by the active ingredient of marijuana, is reflected quantitatively by the field rhythms. In turn, the degree of impaired hippocampal oscillations is correlated with the deterioration of memory performance. Alterations of gamma oscillations observed repeatedly in schizophrenic patients may also reflect impaired assembly synchronization. Oscillations constitute a robust phenotype that reliably 'fingerprint' an individual and expected to alter in most psychiatric disorders. Often such changes are most pronounced in sleep.

8.What paper or presentation has most impressed you in the past 6 months, and can you explain why?

Jan Born and my ex-postdoctoral fellow Lisa Marshall from Lubeck, Germany reported in November that by applying weak electrical fields through scalp electrodes at 0.75 Hz during slow wave sleep enhanced the retention of hippocampus-dependent declarative memories in student volunteers. They speculated that the effect is due to the enhancement and regularization of slow (< 1 Hz) cortical oscillations. Since we have shown earlier that the cortical slow oscillations can trigger hippocampal sharp waves and possibly determine the neuronal content of these events, their findings provide support for the active role of these sleep patterns in memory consolidation. This is good news for us, of course. However, what fascinates me most about the work is that such a weak stimulation was able to entrain a cortical oscillator. The effect of the stimulus-induced electrical field in the brain must be extremely weak since the current is strongly shunted by the parallel resistance of the skin, subcutaneous tissue and cerebrospinal fluid. If you had asked any able biophysicist (or me) whether such an experimental plan would make sense, they would have told you that it would never work. Yet, if the finding is confirmed, it is a perfect demonstration that oscillators can indeed synchronize at an extremely low cost of energy that may not exert any measurable effect on anything else. It also implies that the electrical fields produced by the synchronously active neurons may exert a temporal constraint to the same population that gave rise to the field. The broader implication of this study is even more exciting. The effect of stimulation on memory retention was detected in young students who have large amounts of slow oscillations during sleep. However, the power slow of oscillations decreases rapidly after forty years of age. Thus, in individuals like me the density of slow oscillations is quite low and their effect on memory consolidation, therefore, must be quite limited. The cheap and simple method of electrical field-induced entrainment may revert sleep patterns to the young adult form with the hope that the induced field effects can bring about even larger improvement of memory compared with young subjects. So I can become as smart again as my postdocs and students. Isn't this fascinating?

9. You seem to endorse Mountcastle's idea that the cortex is relatively homogenous and "uniformly organized". You do this by suggesting that Mountcastle's claim is well supported, and by pointing to various features like the scale-free and small-world nature of cortical networks. However, the book also spends a lot of time discussing the diversity of interneuron types, and various other details that can make the cortex seem very heterogenous. Can these characterizations be reconciled?

Many years ago, while I was a postdoc in Canada, a friend of mine of Chinese origin planned to visit Europe. I prepared a list of things for him to see in Budapest and Vienna. When he returned from the trip, I learned that he spent only a few hours in Vienna and headed back to the train station after concluding that Vienna was just the same as Budapest. Back then I was shocked by his statement as would be any citizen of either Budapest or Vienna. This story nicely illustrates the important point that boundary problems, typically reflected by our terms of similar and different or integration and segregation, in fuzzy systems like the brain are hard to define because the boundaries can dynamically shift depending on function. Numerous scientists are interested in the common or similar features of cortical circuits and computation. E.g., the similarity of cortical computation in the visual, auditory and somatosensory cortices is probably more striking than the differences among these regions. Others look for differences and keep finding them. Thus, the issue of functional integration and segregation always depends on the context and perspective. With regard to the rich family of interneurons, their diversity seems to be quite similar in all parts of the cerebral cortex.

10. If you were back at the undergraduate or graduate level, would you choose the same course of study or would you make different choices now that you're older and wiser?

We do not quite understand where our curiosity and motivation come from. Occasionally, we dream up an ideal life with constant happiness and success but attempts to define universal happiness and success always fail. Even if I confine your question to the “most effective road to systems neuroscience’, it is hard to make up an ideal curriculum. Perhaps, I wish I had learned more math and engineering, and got exposed to a world-class laboratory environment from the beginning. But whereas possession of tools is useful in answering questions, the critical factors in science seem to relate to asking an important question and building up a sufficiently intense motivation to solve it. Living in a suppressive regime at the time when my interest in the brain emerged made me focus on inhibition. This may not have happened under other conditions. Hardship and failure can be as formative of character and creativity as a barrage of positive feedback and supportive advisors.

Crime and Religion   posted by DavidB @ 1/22/2007 05:10:00 AM

Having seen Razib's post below, I thought it would be interesting to look at the British Prison Statistics, which include a breakdown of the religious affiliation of people in prison. The bottom line is that atheists do seem to be a relatively wicked lot, but the religious can hardly claim to be above temptation. Some religious groups in particular seem to be well above average in criminality.

For male prisoners (the great majority), the percentage of prisoners in the main religious groups (in 2002, England and Wales) is as follows:

Roman Catholic.......17
Free Church...........2
Other Christian.......3
(total Christian.....58)
Other religions.......3
No religion..........32

'Other religions' include Hindus, Buddhists, Sikhs and Jews, each with less than 1% of the prison population, though Hindus and Buddhists come close to 1%.

Of course, these figures are meaningless without some comparative figures for proportions in the general population. The 2001 Census for England and Wales for the first time included a question on religious affiliation. The results are broken down by sex and broad age group (Census Table S107) [Added: correction, it should be Table S103]. For comparison with prisoners, it is probably most appropriate to take the group of males aged 25-49. There is a complication that about 7% of respondents declined to answer the question. If we exclude these from the total, the percentages of the main religious groups among those who did reply to the question were as follows:

No religion...23

No other group had more than 1 % of the population

It therefore does seem that those claiming 'no religion' are statistically somewhat over-represented among the British prison population, compared to those in the general population, while Christians and Hindus are under-represented. On the other hand, Muslims are heavily over-represented. [Added: it has been pointed out that some of these will have converted to Islam while in prison. See the comments board.] Buddhists, with less than 0.5% of the general population, but nearly 1% of the prison population, are also over-represented. This may be partly because Buddhists tend to be serving long sentences, which puzzled me until it occurred to me that they would include Chinese and South East Asian drug smugglers and Triad gangsters. I suspect that among Christians, Roman Catholics, with 17% of the prison population, are also somewhat over-represented. The general population Census does not break 'Christians' down into denominations, but it is usually reckoned that between 10% and 15% of the population are Catholics.

I wouldn't take any of this very seriously as evidence for the effect of religion on criminality (or vice versa), as so many other factors would be involved.

Labels: ,

Sunday, January 21, 2007

Religious Americans commit fewer crimes   posted by Razib @ 1/21/2007 10:49:00 PM

Ron Gunhame has the goods.

Screw you, "America's team"   posted by p-ter @ 1/21/2007 04:07:00 PM

What was up with the New Orleans Saints becoming a symbol of all that is good and right in this country? As far as I'm concerned, that's reason enough to be satisfied that they got crushed.

Saturday, January 20, 2007

Evolutionary psychology, technology, and virtual sex   posted by p-ter @ 1/20/2007 01:32:00 PM

"Why chicks don't dig the singularity". The interviewee mentions that Huey Newton (of the Black Panthers) was interested in sociobiology; it's true, he actually published an article on self-deception with Robert Trivers--read it in Natural Selection and Social Theory.

(via ALDaily)

Friday, January 19, 2007

Robert Trivers wins the Crafoord Prize   posted by Razib @ 1/19/2007 06:49:00 PM

Bob Trivers just won the Crafoord Prize in bioscience! For those who would like to become more familiar with Trivers' work, I highly recommend Natural Selection and Social Theory. Genes in Conflict is also a good read if you want some molecular level evolutionary exposition. Finally, Trivers looms large in both Mother Nature and Defenders of the Truth. If you don't know anyting about Trivers, I suggest this Edge Special Event.

Anti-science mad libs   posted by the @ 1/19/2007 03:53:00 PM

If there is one trend in American life that most irks [group], it is probably [inconvenient truth]. It's not the [inconvenient truth] itself that bothers them... It is the perception of [inconvenient truth] and, worse, the ... discussion of [inconvenient truth] that is so irritating. It offends their view of [philosophy], helps justify all sorts of nefarious [disliked policies], and makes the [group adjective] agenda ... appear [bad thing]. They would very much like for it not to be true. Failing that, they would like for the public not to believe that it's true--or, at the very least, not to be sure whether it is true or not. This is where [skeptic] comes in.

[Lack of appropriate intellectual credentials of skeptic.]

[Claims made by skeptic.] In other words, [group] aren't sure whether [inconvenient truth is true or not], and they don't really care if it is. Their primary concern is that newspapers treat the question as a matter of dispute rather than a settled fact.

If this sounds like the conservative stance on global warming or evolution, it shouldn't come as a surprise. Like those two issues, the [inconvenient truth] is beyond dispute among academics who study it. This applies even to [group academics] with strong [group] pedigrees. ([Example]) And so the ambition of the [group] counterestablishment in these areas is not to overturn the scholarly consensus but simply to make the topic appear so complicated that laypeople and the press don't know what to believe.

And the science of [inconvenient truth], like most sciences, is subject to complicating details. [Explain.]

That was [skeptic's] cue to spring into action. In [skeptic's] [group magazine] op-ed, [skeptic] lists a series of potential flaws in the [data that strongly supports inconvenient truth]. Most of the complaints are simply picayune details. [Example.] All these points are true enough. But is there any reason to think they would change the overall picture very much? Not really, unless you think [absurd scenario].

And some of [skeptic's] critiques are simply mistaken. [Example] This sounds sensible enough, but it is wrong on several levels. [Explain]... so, even if [skeptic] were right about [Example], it would very likely make [inconvenient truth] look even worse.

But whether the [trivial problem] would make [inconvenient truth] look worse or better is really beside the point. [skeptic's] role is merely to point out that the data is imperfect. The skeptic challenging the expert consensus must be fluent enough in the language of the experts to nibble away at their data. (The evolution skeptic can find holes in the fossil record; the global-warming skeptic can find periods of global cooling.) But he need not--indeed, he must not--be fluent enough to assimilate all the data himself into a coherent alternative explanation. His point is that the truth is unknowable.

You might suppose that somebody in [skeptic's] position would do everything he could to mask his own ideological preferences in order to lend credibility to his research. But [skeptic] is completely up front about his beliefs, which are on display in the [frequency publications] he churns out. He is a [group] of the [philosophy] variety. [Quote], he wrote last year in a typical passage. [Quote continues] ([Witty and ironic take down of quote.])

This is not a slip-up. Introducing ideology into a debate is one of the think-tank hack's strongest weapons. It demystifies a complicated issue, moving it from the realm of science into the realm of politics. The think-tank hack confesses he has his biases but then claims that his opponents in academia or government do, too. Evolution is the secularist science establishment's campaign to discredit religion; global warming is being pushed by regulators who would gain enormous power from new pollution controls; et cetera.

Since the goal is not winning these debates but merely achieving symmetry, the hack's most effective technique can be taking the accusation that would seem to apply to him and hurling it at his opponents. [Quotes accusing other side of malfeasance.] So, while you might think [skeptic] is a hack mining the data for results that would conform to his political preferences, he has already made the same charge against the other side. Who can tell who's right?

Source material

Thursday, January 18, 2007

Sign up for A Week of Science   posted by Razib @ 1/18/2007 08:59:00 PM

There is now a sign up page for A Week of Science. Basically I'll take the feeds and load them up on with Feedpress the day before the 5th. You can see the current list here. You can insert the sign up page with this code into your own site (remove the styling if you wish of course):
<form action="" method="GET">
#justScienceInputs { border:#CCCCCC thin groove; width: 250px; padding:5px;
background-color:#FFFFCC; font-family:Arial, Helvetica, sans-serif; font-size:12px;}
input {width:150px;}
<div id="justScienceInputs">
<b>Sign up for Just Science 2007!</b><br/>
<input type="text" name="blogName" value="" />Blog name<br/>
<input type="text" name="blogEmail" value="" />Email contact<br/>
<input type="text" name="blogURL" value="" />Blog URL<br/>
<input type="text" name="blogFeed" value="" />Blog Feed<br/>
<input type="submit" name-"blogSubmit" value="Sign me up" /><br/>

Submitting this information means that you will be signed up for the aggregator
blog site for the week of February 5th to the 11th.

Murray on education and intelligence   posted by the @ 1/18/2007 02:31:00 PM

Charles Murray has a three-piece series of op-eds in the WSJ. They describe education policy recommendations for three levels of the IQ distribution:
  1. Intelligence in the Classroom: Half of all children are below average, and teachers can do only so much for them.
  2. What's Wrong With Vocational School? Too many Americans are going to college. 
  3. Aztecs vs. Greeks: Those with superior intelligence need to learn to be wise. 

The only criticism I can offer is the lack of citations/footnotes to support the many empirical claims made, especially in the first article, but I understand the venue does not permit it.

You can find plenty of criticisms on the web. At the Corner, Jonah Golderg criticizes Murray for being "dismissive of alternative or competing definitions of intelligence". Golberg's criticism is somewhat missing the mark by his framing in terms of "competing definitions of intelligence", but the IQ's corner blog offers a critique (and follow up) that appears to capture the spirit of Jonah's remark in more precise language. Jonah also confuses intelligence with wisdom -- a mistake worth pointing out. Hopefully Murray will find time to address his critics and publish a response in a venue where the underlying data can be examined more fully.

Another aspect of this worth pointing out: it is generally agreed that it is distinctly impolite to discuss differences in intelligence in public. However, this doesn't stop intelligence from being discussed in private, and is an unfortunate hamper to an important debate. In the comment threads of several recent posts we've discussed the issue of public discussion of non-PC topics. I would suggest that the intersection of intelligence and education falls into the class where the benefits of open debate far out weight the costs. As for getting over our discomfort with intelligence differences, I note that pharmaceutical companies have made major strides by getting commercials for embarrassing medical conditions onto prime time TV.


Wednesday, January 17, 2007

A week of Just Science, what it's about   posted by Razib @ 1/17/2007 09:08:00 PM

RPM and Chris have hit most of the points in regards to the Just Science project. To be short, what it's not about is anti-science. Just one week, that's all. It certainly isn't about traffic or comment response. It isn't about ease of posting, expressing a clever opinion, but rather a tight exposition of a difficult concept. And it isn't about any one blogger, and it isn't about you, it's about science. Myself, I don't have the marginal time to spend writing one deep scientific post a day, so I'm putting things in the queue right now. I'm going to set up Just Science as an aggregator weblog. In other words, for a week in early February the website will bring together scientific content from all the blogs who take up the challenge, and you can then use that feed to keep track of the posts.

Four Stone Hearth   posted by Razib @ 1/17/2007 04:27:00 PM

Martin has Four Stone Hearth up, go check it out!

Imagine, what if there was no anti-science?   posted by Razib @ 1/17/2007 09:51:00 AM

A Week of Science. More later (We're on board here @ GNXP)....

Tuesday, January 16, 2007

Daniel Larison & the Doppelganger   posted by Razib @ 1/16/2007 08:53:00 PM

I started reading Daniel Larison because he is pretty clear headed about the Mitt Romney candidacy. But wow, I seem to have caught a blogger at his peak. I know whereof I speak, there is a time in one's blogging "career" when the posts come fast and furious, unbidden, demanding release. The blog brooks no argument in regards to time or priority, there is no life, it is life. It seems that at the pace Larison is keeping he is at that stage, so enjoy it while it's good, because the flower of youth always fades and the passion to speak abates as fires of cogitation withdraw to recoup. In any case, lots of interesting stuff, where else could you find someone who curses John Locke and the Enlightenment in one breath and backhands the Intelligent Design movement then next? Definitely an army of one.

On a different note, a few months ago I was in California at a burrito shop and I was face to face with someone behind the counter who looked just like me. Same height, same skin color, same short cropped hair, similar features, and get this, same cut and color of shirt! I could tell he was as unnerved as I, and even though I tried to be calm and eat I noticed that he kept looking my way in a really strange manner. I hope I never see him again....

I don't smell it   posted by Razib @ 1/16/2007 08:46:00 PM

Over at Genetics and Health Hsien-Hsien Lei tells the tale of a friend who can't smell:
The Anosmia Foundation says that approximately two to five million American adults have disorders of taste and smell, which is a serious problem because they're not able to smell burning fires, poisonous fumes, leaking gas, or spoiled food. Not being able to taste or smell anything can lead to weight loss (especially in the elderly) and even depression.

Just to show you what a freak I am, I immediately thought that perhaps these individuals would be greats controls to check and see if their partner's MHC profiles don't exhibit the same patterns we see in the smelling population. Meanwhile, Churchill posts on olfactory genes.

The thousand dollar genome   posted by p-ter @ 1/16/2007 07:44:00 PM

Via Genetics and Health, I see Nature Genetics has posted answers to their "Question of the Year" from a number of notable geneticists:
What would you do if it became possible to sequence the equivalent of a full human genome for only $1,000?
Read it to see what the big shots in the genetics world would (will?) do with more data than you can shake a stick at.

Slicer structure, piRNAs, and so much more   posted by amnestic @ 1/16/2007 06:39:00 PM

Nature Chemical Biology has a bunch of free content up in the form of an RNA Focus. There is, for instance, this review of some of the most recent advances in understanding RNA interference.

Small interfering RNAs are cut out of larger precursors by an enzyme called Dicer. From there, they are loaded into the RNA-Induced Silencing Complex (RISC). RISCs silence complementary, target RNAs either by sequestering them in processing bodies (P bodies) or by snipping them in two. This latter activity is carried out by a component of RISC called Argonaute. Since Argonaute can carry out the central "Slicer" activity of RNA interference, there has been much interest in its catalytic mechanism. Crystallization and mutagenesis studies have winnowed the active site down to three central amino acids in a chunk of Argonaute called the PIWI domain. Conservation of these amino acids ("the Slicer catalytic motif is moderately degenerate and should be defined as Asp-Asp-Asp/Glu/His/Lys") is necessary but not sufficient for the Slicer activity, but Argonautes without them can still perform the other form of translational repression.

I haven't yet taken the time out to read the literature on Piwi-interacting RNAs (piRNAs), but the review gives a nice concise description. These RNAs are slightly larger than your usual siRNA. They have mainly been studied in mouse testes. There are a ton of them and they don't match up to known mRNAs so who they should be targeting. The Argonaute associated with piRNAs has the right amino acids and is a Slicer, but we don't know what it is slicing just yet. There are also sections on the process of handing off newly produced siRNAs from Dicer to Slicer and Slicer function in another form of RNA-induced silencing that happens in the nucleus.

ASPM, Microcephalin, and intelligence   posted by p-ter @ 1/16/2007 04:05:00 PM

One of the papers mentioned before on the lack of association between the derived haplotypes at ASPM and Microcephalin and intelligence is now out. Here's the abstract:
Recent studies have made great strides towards identifying putative genetic events underlying the evolution of the human brain and its emergent cognitive capacities. One of the most intriguing findings is the recurrent identification of adaptive evolution in genes associated with primary microcephaly, a developmental disorder characterized by severe reduction in brain size and intelligence, reminiscent of the early hominid condition. This has led to the hypothesis that the adaptive evolution of these genes has contributed to the emergence of modern human cognition. As with other candidate loci, however, this hypothesis remains speculative due to the current lack of methodologies for characterizing the evolutionary function of these genes in humans. Two primary microcephaly genes, ASPM and Microcephalin, have been implicated not only in the adaptive evolution of the lineage leading to humans, but in ongoing selective sweeps in modern humans as well. The presence of both the putatively adaptive and neutral alleles at these loci provides a unique opportunity for using normal trait variation within humans to test the hypothesis that the recent selective sweeps are driven by an advantage in cognitive abilities. Here, we report a large-scale association study between the adaptive alleles of these genes and normal variation in several measures of IQ. Five independent samples were used, totaling 2,393 subjects, including both family-based and population-based datasets. Our overall findings do not support a detectable association between the recent adaptive evolution of either ASPM or Microcephalin and changes in IQ. As we enter the post-genomic era, with the number of candidate loci underlying human evolution growing rapidly, our findings highlight the importance of direct experimental validation in elucidating their evolutionary role in shaping the human phenotype.


Monday, January 15, 2007

1st edition of Oekologie is up at Infinite Sphere   posted by Matt @ 1/15/2007 07:51:00 AM

Go see it here: a blog carnival devoted to the best ecology and environmental science posts from across the blogosphere. This might be a nice complement to Tangled Bank...

Sunday, January 14, 2007

Variation in gene expression between Africans and Europeans   posted by agnostic @ 1/14/2007 08:26:00 PM

Speaking of race, literally on the heels of a separate study (by a separate lab) on variation in gene expression between European and East Asian populations, a new study in the AJHG quantifies within- and between-population variation in gene expression for Africans and Europeans, an open question at the end of Rik's post on the Euro vs East Asian differences.

We find extensive variation in gene-expression levels and estimate that ~83% of genes are differentially expressed among individuals and that ~17% of genes are differentially expressed among populations.

The latter percentage is smaller than the corresponding estimate from the Euro vs East Asian study, where it was ~26%. Contrary to proclamations (originally stemming from Lewontin's Fallacy) that such fractions are "small," imagine you observed that, despite most of the employees at the numerous stores of two corporations being mostly identical (there are mail clerks, receptionists, etc.), some of the actions of certain positions varied from one store to another. Suppose 83% of these variations were idiosyncratic: say, the mail clerks in all stores of corporation X tended to wear their hair in ways different from one another, and likewise for the mail clerks in all stores of corporation Y, with no clear split. But then suppose 17% of the variations were mostly X vs Y differences: some might be boring, like X employees wore blue uniforms while those of Y wore red uniforms. Other differences would not be boring, especially differences in "management style" -- who gave what orders to whom. You'd have to dig up lots of data to see how large of an effect these between-group differences had on observable characteristics for each corporation (such as gross revenue, market share, and other finance terms I don't know the meaning of). But the point is simply that it might "only" require the "small" amount of 17% to make a noticeable difference in such characteristics.

Next, the authors looked up the biological pathways that the differentially expressed genes fell into (using PANTHER). Their Table 1 shows that genes in 2 pathways were expressed differently among individuals, while genes in 11 pathways were expressed differently between Africans and Europeans:

Inflammation mediated by chemokine and cytokine
T-cell activation

Inflammation mediated by chemokine and cytokine
Histamine H1 receptor-mediated signaling pathway
Toll-receptor signaling pathway
Fibroblast growth factor-signaling pathway
Vascular endothelial growth factor-signaling pathway
T-cell activation
EGF receptor-signaling pathway
B-cell activation
Notch-signaling pathway
Enkephalin release
5HT2 type receptor-mediated signaling pathway

All p-values were less than 0.05, though only the first one listed in "Between-populations" remained significant after a Bonferroni correction. I'm no bioinformaticist, but it seems that "multiple tests" here might not be so multiple if, for example, several differentially expressed genes were all involved in combatting a particular pathogen -- then we have 1 hypothesis (different expression to combat a pathogen) which has several facets whose p-values we might add up, on the idea that the facets constitute a partition of the main trait, rather than multiply each p-value by 100 (or however many "tests" we ran). For example, the 4 p-values of the third through sixth entries in the "Between-populations" list add up to 0.0459 -- still significant -- although here none of their p-values withstands the Bonferroni correction. NB: I don't claim these 4 pathways are linked to a single purpose; I'm just showing how several typical p-values can add up to less than the standard 0.05 significance level. Obviously, though, the input of professional statisticians is worth more than my wonderings.

Finally, on a molecular bio level (my square brackets:

To better understand the molecular basis for the observed [between-population] difference in expression [for SH2B3], we asked whether the expression level of one allele was different from the other in heterozygous individuals. If so, this provides evidence of cis-regulatory effects.26 There was a significant difference [P = 0.00118] in expression between alleles in heterozygous cDNA versus genomic DNA, strongly suggesting cis-regulatory effects (fig. 5b).

And as for signatures of selection (my square brackets):

Interestingly, these observations coincide with patterns of genetic variation at SH2B3, since there are 13 SNPs with large allele-frequency differences [Fst greater or = 0.45] between the CEU and YRI samples (fig. 5c). Five of these highly differentiated SNPs occur in conserved regions, as determined by alignment of 17 vertebrate genomes, making them strong candidates for future functional studies. We calculated the empirical probability of observing a SNP with a pairwise [Fst greater or = 0.45] between the CEU and YRI samples, on the basis of all autosomal markers contained in Hap-Map release 21, to be ~0.05, and this magnitude of allele frequency difference is consistent with a signature of local adaptation.7,39 SH2B3 also possesses unusually large levels of linkage disequilibrium compared with the rest of the genome,40 which provides additional support for the hypothesis that this locus has been subject to adaptive evolution, although additional studies will be necessary to make more-definitive inferences about its evolutionary history.

Race: the current consensus   posted by p-ter @ 1/14/2007 04:58:00 PM

There has been surprisingly little outrage in the internets over Steve Hsu's argument that the concept of "race" has a biological basis. But still, it might be worth going over in a bit more detail the evidence supporting him, so that's what this post will aim to do; it will hopefully be worthwhile to have this all compiled in a single spot.

First, an important preliminary-- there are millions of places in the human genome where any two given people could possible differ, either by a single base change, the addition of an entire chunk of DNA, the inversion of a chunk of DNA, or whatever. Keep that in mind: millions and millions of places (for a database of many of the single base changes, see the HapMap). Now, the intuitive argument: after humans arose in Africa, they dispered themselves throughout the world. By both chance and in response to selection due to their new environments, populations in different parts of the world ended up with different frequencies of those millions of DNA variants. Simple enough. Now, below the fold, I will present the evidence that 1. the patterns of genetic variation form clusters on a world-wide scale, 2. genetic clusters coincide with what is commonly called "race", and 3. genetic variation between clusters is relevant phenotypically.

I. Genetic variation in humans forms clusters that correspond to geography

The fact that one can cluster humans together by geography based solely on their genetic information was most convincingly demonstrated in two papers (the second one is open access) by a group out of Stanford. These studies looked at several hundred variable places in the genome in 52 populations scattered across the globe. The hypothesis was as follows-- on applying a clustering algorithm to these data, individuals from similar geographic regions would end up together. I've put a representation on the right, where colors represent poplations-- on top is a pattern of variation that would lead to no clustering (the colors all blend one into the next) while on the bottom is a pattern of variation that would lead to clustering (there are subtle but noticable jumps from yellow to green, for example, though there is much variation within each color). Note that the lack of clustering would not mean that all populations are genetically the same (in the top figure, yellow and orange are not "the same" even though you couldn't find a fixed boundry between them). But indeed, the researchers found the situation corresponding to the bottom figure-- the individuals formed five clusters which represented, in the authors' words, "Africa, Eurasia (Europe, Middle East, and Central/South Asia), East Asia, Oceania, and the Americas". Some populations were exceptions, of course (there are always exceptions in biology)-- they seemed to be a mix between two clusters, or could even form their own cluster in certain models.

But in general, the second model in the figure is a good fit for human variation based on the spots in the genome used by these researchers-- continents correspond to clusters, and geographic barriers like the Himalayas or an ocean correspond to those areas where a "jump" from one cluster to the next occurrs.

II. Clusters and race

The fact that humans cluster together based on genetic information could, in theory, be entirely orthoganal to the concept of race. However, at least in the United State (where this has been explicitly tested), this is not the case. The most important reason for this, in my mind, is that the ancestors of European-Americans and African-Americans were not randomly sampled from the globe (there's a bias towards points on the globe that are quite distant), and this non-random sampling accentuates the genetic differences between the two groups. But in any case, the reasons for this are irrelevant to the argument; let's look at the data.

The basis for this assertion comes from a paper (open access) by a different set of researchers at Stanford, who assembled a group of Americans who identified themselves as either African-American, white, East Asian, or Hispanic. They followed a similar protocal as the studies in the first section-- they took DNA from all individuals, looked a hundreds of different DNA variants, and applied a clustering algorithm. They then looked to see if their clusters corresponded to self-reported group. And indeed, in 3631 out of 3636 cases (99.85%), the individuals were clustered by the algorithm into the "correct" racial group.

This result is obviously only valid in America, but presumably it could be repeated in other parts of the world (though there is some evidence that skin color and genetic ancestry are becoming independent in Brazil). But it is certainly the case that knowing someone's race will give you some probabilistic insight into their genetics[1].

III. Genotype and Phenotype

Once one accepts that genetic information clusters people together according to geography and that these clusters sometimes correspond to race, the next question is, do these genetic differences add up to phenotypic differences? The answer to this question is slowly emerging, and in the shadows I see the outline of a "YES".

All of the studies I will cite are based on the HapMap, a resource with genetic data as well as cell lines for individuals from four populations-- one of Western European ancestry, an Nigerian population, a Chinese population, and a Japanese population. Does the Nigerian population represent all populations in the African cluster, or the European population represent all the populations in the Eurasian cluster? Of course not, but analyzing them certainly gives an insight as to what makes one population different from any other.

First, the genetic data from the different populations can be analyzed to search for areas of the genome that have been under recent selection-- i.e. that have recently become beneficial for Nigerians, or Chinese, or whichever group. That analysis was done by two groups (both papers are open access), though I will discuss the second one. What they found was that each of the populations (they group the Chinese and Japanese together into a single population) has been under, and probably continues to be under, natural selection. It would be theoretically possible (if remarkable) to find that all humans are undergoing the same selective pressures and responding identically to them, but that is not the case. I've posted on the right a Venn diagram from the paper showing that most of the loci identified as under selection are detected in only one of the three groups, indicating that selection is causing people in different parts of the globe to become more distinct. The precise effects of the genetic variation between populations is unclear, but (as it's under selection) it's certainly phenotypically relevant. And lest you think the genes under selection are related only to "boring" physiological traits, note that one of the papers found that a number of genes involved in "neuronal function" have been under selection.

Even more recently, another group analyzed gene expression in both the Asian HapMap samples and the European HapMap samples and found that around 25% of the genes in the two were differentially expressed, and that this differential expression is due to genetic differences in many cases. The road from genotype to phenotype goes through gene expression, so this is a major step in connecting genetic variation to phenotypic variation.

So it's clear that populations differ genetically and that these differences are relevant phenotypically and informative about race. So, do genetic differences explain racial differences in any given phenotype? I hope that for phenotypes like eye color and skin color people accept the answer as obviously yes; these sorts of things have been convincingly demonstrated. For other phenotypes like IQ or personality, if you're inclined to react negatively, I say wait a few years before you get too confident; the study of human genetic variation is in its infancy, and once it hits adolescence it's going to start becoming a real pain in the ass.

[1]A note on race being a societal construct. To some extent, of course it is--some people that would be called "black" in the US might not be called "black" in France, for example (and not because of the language difference, for all you smartasses. The word "black" in French specifically refers to racial classification). I have enough faith in human intelligence to think that the first person who called race a societal construct did not mean that it had no biological component as well--note that the Wikipedia entry on adolesence refers to it as a "cultural and social phenomenon" but also "the transitional stage of human development in which a juvenile matures into an adult". People seem to somehow be able to keep the cultural and biological aspects of adolescence in their heads at the same time, as I imagine the first sociologists to study race were able to do (I may, of course, be wrong), yet somehow the fact that biological differences are interpreted through a cultural lens has somehow morphed into the idea that the biological differences don't exist to begin with (see, e.g. the ASA statement on race). Weird.

The Alevis of Turkey   posted by Razib @ 1/14/2007 11:32:00 AM

Ruchira Paul points me to this article about the Alevis of Turkey. CIA factbook says of Turkey: "Muslim 99.8% (mostly Sunni)." The articles suggests that about 20% of Turkish citizens are Alevi (I say "Turkish citizens" because many Alevis are Kurds, not ethnic Turks). It goes on to describe their religion, which is hard to pin down and is assumed to be vaguely Shia (mostly because anything non-Orthodox seems to be thrown into the Shia bag). I've noted before that it is likely they have some relationship to the Alawites of Syria, this must remain conjecture since both are operationally crypto-religions. That being said, it doesn't really matter much...except for the fact that the Middle East matters...because of oil and international politics....

Addendum: My own awareness of Alevis comes from taking a course on ethnic minorities in Germany as an undergraduate. The Alevi-Sunni schism is pretty evident in the Turkish Diaspora as the Alevis no longer have to dissimulate and kow-tow to the Sunni establishment. It is important to know this when an ethnic Turk attempts to represent Turks in Germany, and it turns out they're Alevi and so have no influence amongst most Turks.

France no longer Roman Catholic?   posted by Razib @ 1/14/2007 11:23:00 AM

Via Jim Kalb, France is No Longer a 'Catholic' Country. A google translation of a summary of the original report is here. Two points:

1) In keeping my earlier contention, a decline in the dominant organized confession doesn't mean that all defectors are turning to atheism. A vague (pan)theism remains in place (the translation summary seems to imply that some are switching from "Catholic" to generic "Christian").

2) Muslims were 4% of respondents. I'm assuming this excludes the non-religious of ethnicities traditionally Muslim (since they form around 10% of the population).

Heather Mac Donald interview responses   posted by Razib @ 1/14/2007 10:51:00 AM

Just an FYI for readers, lots of comments on the Heather Mac Donald interview can be found on technorati. A link from Arts & Letters Daily has resulted in a new spike of interest. Larry Auster probably has the most serious commentary. Many liberal bloggers praised her atheism but were blasphemed by Heather's conservatism, while many conservative bloggers now seem to believe she is a crypto-liberal.

Saturday, January 13, 2007

APOE4: a blessing and a curse   posted by amnestic @ 1/13/2007 11:04:00 PM

The APOE gene comes in a number of varieties in humans. The ancestral primate allele (APOE4) still hangs out in humans at a low frequency and is most famous for increasing risk for Alzheimer's. I noted a paper a few months back suggesting that the APOE4 allele is protective for severe childhood diarrhea. I just found another paper showing an association between APOE4 and better episodic memory. So you have better memory when you're young, but you pay for it when you get older. It seems like learning was just easier for APOE4 carriers. In the fMRI portion of the study they showed reduced hippocampal signal, interpreted as "more efficient" use of neural resources. The authors note that the memory phenotypes of humans are paralleled by LTP phenotype in an APOE4-carrying transgenic mouse strain. LTP is enhanced in young mice, but gets worse as they get old. Apparently, APOE4 is capable of stimulating CREB activation unlike other alleles. CREB is a heavily studied transcription factor thought to be important for inducing expression of genes needed for memory consolidation. At one point, the authors seem to suggest that this ability might help explain the greater hippocampal efficiency in APOE4 carriers, but the whole transcriptional activation and cellular consolidation program involving CREB is supposed to take several hours if not a whole day, while the changes in hippocampus activity took place within an hour. So maybe better LTP induction could be part of the explanation, but I doubt CREB is part of the equation. I wonder if the pattern of memory performance (young = above avg.; old = below) can be observed regardless of APOE genotype. Maybe this is more mechanical such that if your memory system is overclocked you are likely to burn it out.

NIH videos - dirty laundry   posted by amnestic @ 1/13/2007 07:59:00 AM

I rediscovered the NIH videocasting site last night. Looks like they finally made the transition to downloadable content.

This one promises to be interesting:

Issues and Approaches in Genome-Wide Association Mapping

Program date: Wednesday, December 13, 2006, 3:00:00 PM
Presented by: Nancy J. Cox, Ph.D., University of Chicago Department of Medicine


I will air some of the "dirty laundry" in conducting genome-wide association studies with current platforms, and provide an overview of approaches that we have been developing in applying in GWA studies on type 2 diabetes. In addition, I will address some of the reasons that I believe GWA studies for complex phenotypes will be just as challenging as all other genetic studies of these phenotypes have been.

Nancy Cox is a quantitative human geneticist with a primary interest in the relationship between genotypes and complex phenotypes. Research in the lab focuses simultaneously on the development and extension of analytic approaches for identifying and characterizing genotype - phenotype relationships and on the application of those approaches to a variety of complex phenotypes including type 1 and type 2 diabetes and related phenotypes.

Audio or Video

Their vast library is still only available in realmedia. Some good ones should be David Amaral, Michael Hasselmo, Karel Svoboda, Paul Glimcher, and Gyorgy Buzsaki.

Friday, January 12, 2007

International Obesity   posted by Razib @ 1/12/2007 09:35:00 PM

The Inductivist has a hilarious post on obesity rates. Americans are the fattest of course....

Building better beef   posted by p-ter @ 1/12/2007 06:31:00 PM

Mad cow disease is caused by the misfolding of a protein called the prion protein. One might imagine, then, that a cow without said protein would be resistant to mad cow. And indeed, that is the case:
Prion diseases are caused by propagation of misfolded forms of the normal cellular prion protein PrPC, such as PrPBSE in bovine spongiform encephalopathy (BSE) in cattle and PrPCJD in Creutzfeldt-Jakob disease (CJD) in humans. Disruption of PrPC expression in mice, a species that does not naturally contract prion diseases, results in no apparent developmental abnormalities. However, the impact of ablating PrPC function in natural host species of prion diseases is unknown. Here we report the generation and characterization of PrPC-deficient cattle produced by a sequential gene-targeting system. At over 20 months of age, the cattle are clinically, physiologically, histopathologically, immunologically and reproductively normal. Brain tissue homogenates are resistant to prion propagation in vitro as assessed by protein misfolding cyclic amplification. PrPC-deficient cattle may be a useful model for prion research and could provide industrial bovine products free of prion proteins.
Will it one day be considered irresponsible to produce beef that is not genetically modified?

Thursday, January 11, 2007

Race site   posted by Razib @ 1/11/2007 08:05:00 PM

I've received several emails about this website, Understanding Race. Here is a article about the project. I don't have much to say, the readers of this blog can decompose assertions like this easily enough I assume:
The pattern of DNA across populations shows a nested subset. African populations harbor some alleles (gene variations) that are absent in non-African populations; however, all of the alleles that are common in non-African populations are also common in African populations.

The English here is peculiar. If African populations are more polymorphic, wouldn't it stand to reason that the common (derived) alleles in non-Africans must be less common in Africans? (since you can't have more than 100%?) In any case, loci such as MC1R invert this stark narrative. In attempting to replace an outmoded racial typology derived from Victorian imaginations and social contexts anti-racists construct their own ghostly strawmen which are a mirror of the old Platonic constructs.

I have little more to say than to exhort you to hold truth close to your hearts, the follies of the deceivers will then stand naked before you.

Update: Newsflash, Steve Hsu is evil.

Women advertise to potential extra-pair mates   posted by Matt @ 1/11/2007 01:59:00 PM

In an interesting paper published in the Jan, 2007 issue of Hormones and Behavior, researchers describe a phenomenon they claim is unique to human females; their overt display of fertilty. Specifically, around the time of maximum fertility, women show enhanced "self-grooming" behavior and dress in a more provacative manner in an apparent attempt to solicit copulations. Even more interesting, and in support of a claim I have made previously, is that even females in long term "monogamous" relationships exhibit these behaviors. (difficult to imagine how or why behaviors like this would evolve under the humans are monogamous hypothesis)

I'll just remind people that while the idea of unconscious regulation of overt behavior that enhances host reproductive opportunities, there are even cooler stories where parasite infection effects sexual behavior similarly.

While this is an intersting study, one might ask the following additional questions:

  1. Does the magnitude of solicitation depend on the quality of either the existing mate or extra pair mate? If this is an adaptive behavior, you would predict that solicitation should increase as existing partner quality decreases or as extra-pair mate quality increases.
  2. Is there a difference in male perception of this solicitation when looking acoss male quality or relationship status?
  3. Does solicitation vary with MHC genes? (Do Women with rarer alleles solicit less?)
  4. How might one get a judge-jobs? "hot-woman photograph evaluator"

Any interest in replicating this here at GNXP?
Women- submit randomly chosen photos to me or to Razib, one just after your period (low fertility), one about 2 weeks later (peak-fertility). We can assemble an "expert panel" of judges to evaluate ...

Paper Abstract (and doi)
Humans differ from many other primates in the apparent absence of obvious advertisements of fertility within the ovulatory cycle. However, recent studies demonstrate increases in women's sexual motivation near ovulation, raising the question of whether human ovulation could be marked by observable changes in overt behavior. Using a sample of 30 partnered women photographed at high and low fertility cycle phases, we show that readily-observable behaviors – self-grooming and ornamentation through attractive choice of dress – increase during the fertile phase of the ovulatory cycle. At above-chance levels, 42 judges selected photographs of women in their fertile (59.5%) rather than luteal phase (40.5%) as “trying to look more attractive.” Moreover, the closer women were to ovulation when photographed in the fertile window, the more frequently their fertile photograph was chosen. Although an emerging literature indicates a variety of changes in women across the cycle, the ornamentation effect is striking in both its magnitude and its status as an overt behavioral difference that can be easily observed by others. It may help explain the previously documented finding that men's mate retention efforts increase as their partners approach ovulation.

Haldane's Selection Theorem   posted by DavidB @ 1/11/2007 02:08:00 AM

Razib has several times mentioned an important theorem of population genetics, credited to J. B. S. Haldane, that the probability of a single favourable mutation surviving and spreading throughout a population is approximately 2s, where s is its selective advantage relative to other alleles. So for example if a mutation has a selective advantage of 1 per cent, it will have approximately a 2 per cent chance of ultimately sweeping through the population. This may seem a low probability, but if the same mutation recurs more than a few dozen times in the species, it is virtually certain to be successful. A recent paper by John Hawks and Greg Cochran makes a central use of Haldane's theorem.

As a matter of historical curiosity I wanted to see Haldane's original statement of this principle, and how he derived it.

Hawks and Cochran give the citation 'Haldane, J. B. S. (1927): A mathematical theory of natural and artificial selection, part v: Selection and mutation. Proceedings of the Cambridge Philosophical Society, 28, 838-44.' I find that the correct volume number is 23, not 28. The same incorrect citation is given by Crow and Kimura's An Introduction to Population Genetics Theory (1970).

The paper is also reprinted in Selected Genetics Papers of J. B. S. Haldane, edited with an introduction by Krishna R. Dronamraju, Garland Publishing, NY, 1990, at pp. 90-96. I have transcribed the key passage from the paper below. Incidentally, Haldane uses k, rather than s, for the selective advantage, but this is a trivial matter of notation. More important, Haldane's theorem only applies where the population is sufficiently large. If the breeding population n is very small (less than about 50) there is a significant chance that a single mutation will be fixed by genetic drift before selection has had much effect. For a single neutral or favourable mutation there is always a probability of at least 1/2n that it will ultimately be fixed, since in the absence of recurrent mutation one of the 2n genes in the population will ultimately be the ancestor of all surviving genes.

It is interesting that Haldane himself does not claim great novelty for his 1927 theorem, but presents it as an application of the methods set out by R. A. Fisher in his 1922 paper 'On the dominance ratio'. Fisher himself later gave a more elaborate treatment of the same problem in a 1930 paper, 'The Distribution of Gene Ratios for Rare Mutations', Proceedings of the Royal Society of Edinburgh, 1930, 50, 205-20. (Like most of Fisher's papers, this is available online from the Fisher archives at Adelaide.) This includes the conclusion that:

The probability of a mutant, enjoying a small selective advantage a, spreading until it establishes itself throughout the entire population is thus found to be 2a/(1 - e^-4an); it is easy to see that with an indefinitely large population, or in any case if 4an [population size x selective advantage] is large, this expression reduces to 2a. Thus a mutation conferring a selective advantage of 1 per cent will have practically a 2 per cent chance of establishing itself.

In 1930 Fisher, rather characteristically, did not cite Haldane's 1927 treatment of the selection problem. Sewall Wright, in his 1931 paper on 'Evolution in Mendelian populations', states a similar proposition and credits Fisher, but not Haldane, with prior publication. This might raise a question whether Haldane or Fisher should be given the main credit for the theorem. As far as I can judge, Haldane does make a heavy use of Fisher's 1922 methods, but Fisher himself did not (in 1922) explicitly calculate the probability that an advantageous mutation would survive, and Haldane's application of Fisher's methods in 1927 was by no means as easy as falling off a log. I think therefore that Haldane does deserve the credit for the theorem itself.

In any case, as often turns out in issues of priority, there are neglected earlier candidates. As early as 1873, the Rev H. W. Watson, in response to a request from his friend Francis Galton, had published a method for calculating the 'extinction of surnames' which contains much of the technique later used by Fisher for calculating the random extinction of genes. And even earlier, in 1845, a French mathematician called Bienayme had published a brief paper with results suggesting that he may have discovered some of the same methods, though he did not give details. (See Michael Bulmer, Francis Galton: Pioneer of Heredity and Biometry (2003), pp.156-60.) There is nothing to suggest that Fisher or Haldane knew of these earlier efforts.

The following extract from Haldane's 1927 paper contains his proof of the theorem. I cannot reproduce all of the mathematical notation, so I will use S to indicate summation, x^n to indicate the n'th power of x, and x_a (etc) to indicate subscripts. I have added some comments (in square brackets) and notes in an attempt to explain the derivation, as far as I can follow it myself. No doubt much of this will be self-evident to expert mathematicians, but expert mathematicians have a tendency to underestimate the difficulty of following mathematical proofs for the rest of us.


...the treatment of Fisher [1922] is followed.

In a large population let p_r be the chance that a factor [allele] present in a zygote at a given stage in the life-cycle will appear in r of its children in the next generation. If the individual considered is homozygous, this is the chance of leaving r children, if mutation is neglected. Let S p_r(x^r) = f(x) [note 1]. Therefore f(1) = 1, f(0) = p_0 [note 2], the probability of the factor disappearing, while f ' (1) = S rp_r, [note 3] i.e. the probable number of individuals possessing the factor in the next generation. The probability of m individuals bearing one each of the factors considered leaving r descendants is clearly the coefficient of x^r in [f(x)]^m, if we neglect the possibility of a mating between two such individuals, which we may legitimately do if m is small compared with the total number of the population. If then the probability of the factor being present in r zygotes of the nth generation be the coefficient of x^r in F(x), the corresponding probability in the (n + 1)th generation is the same coefficient in F[f(x)]. Hence if a single factor appears in one zygote, the probability of its presence in r zygotes after n generations is the coefficient of x in S(x) [S has subscript f and superscript n], i.e. f(f(f...f(x)...)), the operation being repeated n times [note 4]. The probability of its disappearance is therefore LtS(0) [note 5]. By Koenigs' theorem this is the root of x = f(x) in the neighbourhood of zero [note 6].

Now in the case of a dominant factor appearing in a population in equilibrium, and conferring an advantage measured by k, as in Part I(5) [of Haldane's series of papers] f ' (1) = 1 + k. Since f ' (x) and f '' (x) are positive, x = f(x) has two and only two real positive roots, one equal to unity, the other lying between 0 and 1, but near the latter value if k be small [note 7]. Hence any advantageous dominant factor which has once appeared has a finite chance of survival, however large the total population may be.

If a large number of offspring is possible, as in most organisms, the series p_n approximates to a Poisson series, provided that adult organisms be counted, and since
f'(1) = 1 + k, f(x) = e^(1 + k)(x - 1). Hence the probability of extinction 1 - y is given by 1 - y = e^-(1 + k)y [note 8].

Hence (1 + k)y = -log(1 - y) [note 9]

and k = y/2 + (y^2)/3 + (y^3)/4 + ... [note 10]

and if k be small, y = 2k approximately [since the terms after y/2 are orders of magnitude smaller]. Hence an advantageous dominant gene has a probability 2k of survival after only a single appearance in an adult zygote, and if in the whole history of the species it appears more than log_e2/2k times [the natural logarithm of 2, divided by 2k] it will probably spread through the species. But, however large k may be, the factor may be extinguished after a single appearance. Thus, if k = 1, so that the new type probably leaves twice as many offspring as the normal, the probability of its extinction is still .203. If in any generation there are m dominant individuals the probability of extinction is reduced to y^m, where y is the smaller positive root of x = f(x). When k is small this reduces to (1 - 2k)^m. Hence if in any generation more than log_e2/2k adult dominants exist, the factor will probably spread through the whole population.


[Note 1] Summation is over values of the subscript r from zero to infinity. Since r is the number of an individual's offspring, it can only take integer values.

[Note 2] The sum is p_0(x^0) + p_1(x^1) + p_2(x^2) + p_3(x^3)... For the value x = 1 this equals p_0 + p_1 + p_2 + p_3... , which sums to 1, since the probabilities are mutually exclusive and cover all possible outcomes. For the value x = 0 the terms from p_1(x^1) onward are all equal to zero, so the series reduces to p_0(0^0), which = p_0 if we accept that 0^0 = 1. I am not sure that there is any agreed convention on this point, as the usual proofs that x^0 = 1 (e.g. 1 = (x^a)/(x^a) = x^(a - a) = x^0) break down for the case x = 0. Fisher, in his formulation of the series, presents it as p_0 + p_1(x^1) + p_2(x^2) + p_3(x^3), which avoids any doubt on this point.

[Note 3] Summation is over values of r from zero to infinity. The expression f ' (1) evidently means the first derivative of the function f(x) with respect to x, for the value x = 1. Each term in the sum f(x) has the form p_r(x^r), so by elementary calculus its first derivative is rp_r(x^(r - 1)), and the first derivative of the sum f(x) as a whole is the sum of the first derivatives of its component terms. But for the value x = 1 these each reduce to rp_r, so the first derivative of f(x) is equal to S rp_r, as in Haldane's formula.

[Note 4] Haldane's treatment here is closely based on Fisher, but uses different notation.

[Note 5] Lt is the limit as n goes to infinity, in other words as the function is iterated indefinitely with its own previous value as argument.

[Note 6] This part of the derivation evidently requires advanced knowledge of the theory of functions, and I can only take it on trust. Haldane gives the cryptic reference 'Koenigs. Darb. Bull. (2) 7, p.340, 1883.' I wondered if 'Koenigs' might be an error for 'Koenig', possibly Julius Koenig, but on consulting the Dictionary of Scientific Biography I found an entry for a French mathematician, Gabriel Koenigs (1858-1931). Among his many accomplishments, according to the DSB, Koenigs was 'one of the first to take an interest in iteration theory'. Koenigs was also a pupil of Gaston Darboux, founder and editor of the Bulletin des Sciences Mathematiques et Astronomiques, sometimes known as 'Darboux's Bulletin'. So Haldane's cryptic reference to 'Darb. Bull.' is probably to an article by Gabriel Koenigs in the Bulletin des Sciences Mathematiques et Astronomiques, 2nd series, volume 7, 1883, at p.340. I find that there is indeed an article by Koenigs, 'Recherches sur les substitutions uniformes', at the cited place, but its mathematics is far beyond me.

[Note 7] Haldane does not consider the trivial cases p_0 = 1, where the gene is always extinguished immediately, or p_1 = 1, where it always produces one and only one offspring per generation. In the first case f(x) would have the value 1 for all values of x, while in the second case it would have the value x for all values of x. For non-trivial cases the value of the function f(x) increases continually and at an increasing rate with increasing x, so the first and second derivatives of f(x) are positive. Haldane also states that the equation x = f(x) has two and only two real positive roots, one of which is 1, and the other between 0 and 1. I am not sure I could give a rigorous proof of this, but I suggest the following approach. If we plot a graph of the function y = f(x), for real positive values of x, then f(x) = y = x wherever the curve representing the function touches or intersects a line through the origin at 45 degrees to the axes. As f ' and f '' (the first and second derivatives) are both positive, the curve is concave upwards, i.e. it has just one 'bend', with the inner part of the bend on its upper side. The curve must start from the y axis at the value p_0, since we know that f(0) = p_0, which is somewhere between 0 and 1. We also know that f(1) = 1, so the curve must touch or intersect the 45 degree line at x = y = 1, which is accordingly a real positive root of x = f(x). The curve must therefore pass in some way from the point (x = 0, y = p_0), which is above the 45-degree line, to the point (x = 1, y = 1), which is on that line. As the curve is concave upward, it cannot touch or intersect a straight line in more than two points. Since it touches or intersects the 45-degree line at the point (x = 1, y = 1), there are three possible ways of doing so: (a) it is a tangent to the line at that point; (b) it intersects the line at that point from above the line (in its approach from its starting point on the y axis); or (c) it intersects the line from below the line. But it cannot be a tangent to the line at that point, because the first derivative of the function would then be equal to the slope of the line, which is 1, whereas by assumption the first derivative at that point is 1 + k, with non-zero k. Possibility (a) is therefore excluded. Possibility (b) can be excluded for a similar reason. If the curve intersects the 45-degree line from above, a tangent to the curve at that point must make an angle of less than 45 degrees with the x axis. But this means that the first derivative of the function at the point of intersection must be less than 1, whereas by assumption it is greater than 1. This leaves only possibility (c), that the curve intersects the line from below, which is consistent with the fact that the first derivative is greater than 1, so that a tangent to the curve would have an angle greater than 45 degrees. But this implies that in passing from (x = 0, y = p_0), which is above the line, to (x = 1, y = 1), it has first intersected the line at some other value of x between 0 and 1, which is another real positive root of x = f(x), as required by Haldane's proof.

[Note 8] Here Haldane follows Fisher closely, but with a significant modification. Fisher (1922) had given the formula f(x) = e^m(x - 1), where m:1 is the ratio of the total population in generation (n + 1) to the population in generation n; in other words he allows for the growth of a neutral allele in line with any expansion of the population as a whole. Haldane's significant innovation is to allow for genes which increase in numbers because of a selective advantage, k, relative to other genes in a static population. Fisher's f(x) = e^m(x - 1) then becomes Haldane's f(x) = e^(1 + k)(x - 1), and Haldane is able to find an explicit expression for the chance of survival in terms of the selective advantage k (see Note 9).

[Note 9] Haldane denotes the probability of the gene surviving as y, so the probability of extinction is 1 - y. But the probability of extinction is the appropriate root of the equation x = f(x) = e^(1 + k)(x - 1). So substituting 1 - y for x we get 1 - y = e^-(1 + k)y. In the right hand side of this equation the expression -(1 + k)y is the (natural) logarithm of the left hand side, which is 1 - y, so, taking the negative of both sides, (1 + k)y = -log(1 - y).

[Note 10] Here Haldane assumes knowledge of a theorem equivalent to -log(1 - y) = y + (y^2)/2 + (y^3)/3 + (y^4)/4: see this Wiki article on logarithms. Given this theorem, we have

(1 + k)y = -log(1 - y) = y + (y^2)/2 + (y^3)/3 + (y^4)/4 ...

therefore, dividing both sides by y and then subtracting 1 from both sides, we get

k = (y^2)/2y + (y^3)/3y + (y^4)/4y ... = y/2 + (y^2)/3 + (y^3)/4 + ...

as stated by Haldane.

Slatkin   posted by Razib @ 1/11/2007 12:26:00 AM

If any readers are associated with Montgomery Slatkin's lab, could you email me? (contactgnxp -at- Thanks.

Tuesday, January 09, 2007

A whole new squirrel   posted by amnestic @ 1/09/2007 10:59:00 PM

Squirrels lose half of their synapses when they go into hibernation. The synapses fall apart in relation to temperature changes. The proteins aren't destroyed. They are just detached, possibly as protein complexes floating in the cytoplasm. They get more synapses when they wake back up, but it's not clear that they are the same ones. In fact, they are impaired in recognizing squirrels they've met before after hibernation. Can you imagine? Half of synapses in thalamus, hippocampus, and cortex? If Synaptic Self is at all appropriate book title, do squirrels lose their squirreldentity every winter? Maybe some place holder protein is left behind so the synapses can grow back how they're supposed to. It's not easy to tell that you got the same synapses before and after hibernation. Guess you could induce in vivo LTP and see if it can be maintained over that span. Or use one of Svoboda's fancy window-on-the-brain techniques.

For King or Parliament?   posted by Razib @ 1/09/2007 09:48:00 PM

I am currently reading The English Civil War. When I read God's War, a history of the Crusades between 1100 and 1400, it was a rather detached affair. My conscious partisanship toward the West expressed itself in a mild sentimental bias toward its medieval Christian percursor.1 Nevertheless the medieval period is a distant land and it was a survey of a shadow alien landscape from which I wished to glean facts in the service of a general understanding of human affairs and action. Yet my reading of The English Civil War is different, I seem to always "root" for the Roundheads against the Cavaliers. Perhaps this is because I am an American, and will always smile upon the tribunes of the plebs who have the gall to rise against the armies of the king, but sometimes I wonder if the sentiment does not have deeper origins. In Albion's Seed David Hackett Fisher identified "Four Folkways" in the United States which derive from the pre-1776 British Settlers:
Families of zealous, literate Puritan yeomen and artisans from urbanized East Anglia established a religious community in Massachusetts (1629-40); royalist cavaliers headed by Sir William Berkeley and young, male indentured servants from the south and west of England built a highly stratified agrarian way of life in Virginia (1640-70); egalitarian Quakers of modest social standing from the North Midlands resettled in the Delaware Valley and promoted a social pluralism (1675-1715); and, in by far the largest migration (1717-75), poor borderland families of English, Scots, and Irish fled a violent environment to seek a better life in a similarly uncertain American backcountry.

My own personal background is at the nexus between the Puritan and Midland folkways. I once told a friend that when going through the Civil War period I always knew who the good guys were. (the Blues of course!) Only later on with the awareness of adulthood did I comprehend the nature of "the Lost Cause," or the reality that the Roundheads were arguably more tyrannical than the Cavaliers. Other biases lurk in my mind, when I read The Reformation I leaned toward the Protestants, even though I knew the rough sketch of the outcomes. This, though I am aware of, and attempt to ward myself from, the sin of anti-Catholic prejudice which suffuses the Anglo-American intellectual tradition.

I am immigrant, strictly speaking, to this nation. Though schooled nowhere else I am visibly different from the majority of the citizens, and was a conscious alien as a child. Nevertheless, it is clear that I have internalized the subtle biases and outlooks of the "the Yankee," whatever that is. Part of the explanation perhaps lay with the thesis of The Nurture Assumption, my peers have generally been northern Yankees, and so I became. Additionally, my teachers always knew who the "good guys" were, even if they wouldn't say it in so many words. I am curious, what biases do readers feel themselves stumbling upon? In our society we are taught to reflect & explore "latent" bias on the dimensions of sex and race, but what about the unconscious "folkways" which we imbibe through the banal processes of socialization?

1 - Though I have admitted a faint and reflexive attraction to the harmonies of the call to prayer because of childhood memories, in general I find Islamic civilization a cold and dour affair and am not particularly disposed toward it.

Monday, January 08, 2007

The human ecosystem   posted by p-ter @ 1/08/2007 09:25:00 PM

Bacteria treat pain?
Abdominal pain is common in the general population and, in patients with irritable bowel syndrome, is attributed to visceral hypersensitivity. We found that oral administration of specific Lactobacillus strains induced the expression of mu-opioid and cannabinoid receptors in intestinal epithelial cells, and mediated analgesic functions in the gut—similar to the effects of morphine. These results suggest that the microbiology of the intestinal tract influences our visceral perception, and suggest new approaches for the treament of abdominal pain and irritable bowel syndrome

Brain size review   posted by amnestic @ 1/08/2007 06:34:00 PM

So Chris at DevIntel had a post a few days ago about a Barbara Finlay paper from 2001 that examined the ordering and relative length of phases of neurogenesis in mammals. I haven't got a copy of the paper, but it appears that she's arguing that the pattern of brain development is highly constrained and that changes through evolution will be quantitative rather than qualitative. This is evidence for a domain-general view of human evolution wherein first we get extra tissue and (i'm not sure of my usage here) we exapt it into human-specific brain parts.

I remembered a study from a while back suggesting that humans had a disproportionate amount of white matter in the prefrontal cortex. The author of that study (Schoenemann) has a thick 2006 review (pdf) covering many areas of human brain evolution available on his website. There are sections on cranial capacity, the fossil record, and behavioral evolution, but the bulk of the most interesting data are in the comparative internal allometry section and the genetic correlations between brain size and behavior. Neither are my specialty, but I'm really out of my league in the genetic correlations area, so I'll give you the brain size business and you can study the other part on your own.

Brain size scales with body size in a log-log relationship. You can determine the normal parameters of this relationship by sampling brain and body sizes across primates, for instance. You can get an idea of the relative increase in brain size controlling for body size by taking the ratio of observed brain size to that expected from this line of best fit. Compared to the rest of the primates, human brains are 3.1 times too big.

Brain regions evolve at different rates. For instance, in the boring case, the motor and somatosensory cortices could grow to accommodate larger bodies leaving other regions behind. We can compare the relative region sizes across primates and control for brain size, so we know how big the region should be "for a primate brain of our size". I like this measure more than the body size comparison because it seems to show how the brain has specialized. Thus, the human olfactory bulb, visual cortex, primary motor cortex, and premotor cortex are smaller than expected. As an aside, Michael Graziano is scrambling all of our distinctions about primary and pre- motor areas and moving away from the homunculus model that you see in your intro to neuroscience books. All these regions scale with body size reasonably, and we know we can see and move pretty well. Not only that, but the frontal lobe (which contains the motor cortices) scales properly while the motor parts lag. What is making our brains so big and raising the expectations for all these poor workhorse regions? The prefrontal cortex is what.

It turns out that measuring the prefrontal cortex (PFC) is messy because there aren't clear markers for the boundaries. Some MRI studies have used the area in front of the corpus callosum. This underestimates the size, but does so more for humans than for other primates. Using measures such as this, we find that the human PFC is larger than expected compared to brain and body size. There are some more detailed techniques outlined in the review. Three studies in 2005 morphed common chimp, bonobo, and macaque brains into human brains and came to the conclusion that human PFCs were expanded. Also, based on traditional cytoarchitectural markers of PFC areas, specific subregions within the PFC scale at different rates. He didn't mention any area that lags behind though, so it can't really help us focus yet. One interesting point that runs through the analysis is that you shouldn't write off a change in absolute size just because you can account for it using these scaling relationships. We get two examples (abstract rule learning and object-discrimination) that are better explained by absolute brain size than any relative measure.

In a semi-related note, Buzsaki suggested that a constraint on overall brain size may be axonal conduction delays. Certain cognitive feats may require synchronized oscillations in different cortical areas. While the networks can adjust to some out-of-phase inputs, there must be a certain degree of incoherence that they just can't handle. The idea is that Neandertal brains could possibly've gotten too big for their bridges. If this interests you, look into gamma oscillations and binding. I don't understand it yet well enough to explain it.

Update:Mindblog discussed a paper about long-range synchrony last week.

Monday Morning Satire   posted by Matt McIntosh @ 1/08/2007 05:12:00 AM

Aaron Haspel gives away the recipe for a productive* career in the social sciences.

* Measured the same way Alexandre Dumas got paid.

Sunday, January 07, 2007

Three cheers for Dr. Benbow   posted by Alex B. @ 1/07/2007 08:27:00 PM

I received my latest APS Observer in the mail, and one of the main articles reports that 3 psychologists have been placed on the National Science Board, one of whom is Camilla Benbow.

This is significant for multiple reasons. While Dr. Benbow's academic record is exemplary (here are some pdfs), her record of research on sex differences and mathematics (along with Stanley and Lubinski) ranks her among the few in this area who do not fall into the "there are no differences" camp (a la Hyde; pdf). Moreover, her writings on the cogency of cognitive ability and its influence in educational and life outcomes (no doubt stemming from her many years working with precocious youth) is very much in line with the general London School mindset. (must read: Benbow, C. P., & Stanley, J. C. (1996). Inequity in equity: How current educational equity policies place able students at risk. Psychology, Public Policy, and Law, 2, 249-293.). Consequently, I think this is the first time in the NSB's History an Individual Differences researcher is on board. I am not sure what, if any, changes are in store at the NSF, but this a big step for the field of differential psychology and (hopefully) a sign of things to come.

Three cheers for Dr. Benbow!

Short guys: thank environmental heterogeneity   posted by agnostic @ 1/07/2007 05:49:00 PM

At Steve Sailer's blog, there's an interesting discussion on height in music stars, with some evidence that country singers are taller on average than rock musicians. The mean for rock stars is ~5'10", although personal observations in the comments suggest exaggerated heights among the shorter rock stars like Mick Jagger. I looked through the CelebHeights website for height data on "pretty boys" (e.g., Johnny Depp), and they too appear to be at or below the male population average of 5'10" (see list at the end of this post). If the apparent trend is real, it would be a nice illustration of why all males aren't the same ideal height: there may be some ideal height, but those falling on either side of ideal will still have some niche to fill. Thus, selection is likely more of the balancing type -- it keeps heights within a tolerable range, in this case normally distributed.

Just because you're within 1 SD of the mean on the below-average side doesn't mean you're doomed -- you can excel in areas where being short is more advantageous, such as bouncing around on stage as a musician, generating pretty boy / heartthrob appeal, or honing your skills as a dancer (which becomes more difficult as your center-of-gravity increases and your limbs become longer). This assumes the below-average individual possesses independent other appealing traits, which is why the height distribution isn't uniform -- guys who are 5'7 and otherwise unappealing will be selected against, so 5'7 males will be less frequent than 5'10 males, but enough of the former can rely on other qualities to find mates that their frequency won't be close to zero.

Now, it may sound strange to lump being a rockstar and being a good dancer into the same category, but that just proves the point: just one generation ago during the disco era, dancing skills were highly valued in males. Now, not really. Stochastic environments tend to result in a more diverse range of phenotypes -- unlike, say, the constant environment of oxygen in the air, which will weed out human lungs designed to process anything other than oxygen. So, it seems that predicting fitness based on a guy's height is chancy enough that non-ideal phenotypes aren't mercilessly purged from the genepool.

This scenario predicts that human height will show moderate-high heritability, since directional selection isn't at work and so doesn't exhaust genetic variance in the trait, and since height is not so fitness-neutral that there is nearly unconstrained variance among individuals. Sure enough, h^2 = 0.65 [see Note1]. All this said, I'm no expert on life history theory, so there are surely some subtleties that I'm missing.

As a final thought, complex modern societies open up many more niches to be exploited by yesteryear's outcasts (asocial introverts for one), and the accelerated pace at which aspects of social life change in such societies -- especially due to technological changes -- introduces greater environmental stochasticity. Aside from the disco example, consider the present-day greater fitness of lesser-IQ individuals compared to higher-individuals: in the mid-19th C., who could've rationally predicted that the less intelligent would turn the Darwinian tables on the more brainy? If we ended welfare state policies that support large families among lower-IQ individuals, the trend could snap back to the way it was in 1850. This greater unpredictability of life compared to that of hunter-gatherer societies tells us that phenotypic variance should have exploded not long after the transition to agriculture roughly 10,000 years ago. Concluding where we began with height, Greg Cochran coined a nice mneumonic for remembering the take-home lesson here: "The bow begat the Bushmen."

Pretty Boys

Gael Garcia Bernal 5'6.5
Tom Cruise 5'7
Wilmer Valderrama 5'7
Scott Wolf 5'7
Johnny Depp 5'8
Ryan Phillippe 5'8
Jon Bon Jovi 5'9
Jared Leto 5'9
Dave Navarro 5'9
Scott Baio 5'10
Orlando Bloom 5'10
Leonardo DiCaprio 5'10
Matt Damon 5'10
Colin Farrell 5'10
Jude Law 5'11
Brad Pitt 5'11
Mark McGrath 5'11
Jake Gyllenhaal 6'
Freddie Prinze Jr. 6'1
Gavin Rossdale 6'1
Josh Hartnett 6'3

Median = 5'10. Sex appeal doesn't tail off as height decreases in this sample: look who's 5'9 or shorter. I'm sure there are other data points, but I'm only going to tolerate looking up so much data on pretty boys in the interests of science. I randomly thought of as many as I could, then Googled websites showcasing pretty boys, so if anyone is going to add more data, try to make it random rather than only looking for confirming or disconfirming data points. I think I covered the real heartthrobs, though, which are the most important data. I invite those more inclined to study this -- such as our legions of teenage girl readers -- to pick up where I'm leaving off.

Note1: Falconer & Mackay give two references for heritability of human height, one of which is here, and the other of which is:

Huntley (1966). Heritability of intelligence. pp. 201-18 in Meade & Parkes (eds.), Genetic and Environmental Factors in Human Ability. Oliver and Boyd: Edinburgh.


Differences in gene expression between Asians and Europeans   posted by p-ter @ 1/07/2007 04:43:00 PM

Different populations have different traits-- the distributions of hair color, skin color, behavior, etc., all vary between groups, and some of this variation is certainly genetic in origin. This much is clear. But how does genetics cause these population-level differences?

A new paper in Nature Genetics (see the news story here) is a start towards answering this question-- the authors find a huge percentage of genes have different levels of expression in Europeans and Asians, and that these expression differences are due to common genetic variation. In addition, clustering by expression profile led to almost perfect clusters according to ethnicity (those are the two clusters--Europeans and Asians--in the picture) Here's the abstract:
Variation in DNA sequence contributes to individual differences in quantitative traits, but in humans the specific sequence variants are known for very few traits. We characterized variation in gene expression in cells from individuals belonging to three major population groups. This quantitative phenotype differs significantly between European-derived and Asian-derived populations for 1,097 of 4,197 genes tested. For the phenotypes with the strongest evidence of cis determinants, most of the variation is due to allele frequency differences at cis-linked regulators. The results show that specific genetic variation among populations contributes appreciably to differences in gene expression phenotypes. Populations differ in prevalence of many complex genetic diseases, such as diabetes and cardiovascular disease. As some of these are probably influenced by the level of gene expression, our results suggest that allele frequency differences at regulatory polymorphisms also account for some population differences in prevalence of complex diseases.
1. This provides a neat mechanism for ethic differences-- a number differentially expressed genes act in a network to give various phenotypes-- be they diseases, skin colors, behaviors, or anything else with a genetic component.

2. It's also possible that different regulatory networks have evolved in the two populations:
In addition to the variation analyzed above, some variation in expression phenotypes between populations can probably be attributed to different regulatory mechanisms. For four phenotypes, we found significant cis association in the CHB+JPT [Asian] sample but not in the CEU [European] sample.

3. The elephant in the room: The authors used cell lines from the HapMap for these studies. Besides the European and Asian samples, there's another population in the HapMap which was not included in this paper-- that of an African population from Nigeria. If a full quarter of genes have different expression profiles in Europeans and Asians, then this African population is likely to be even more different. The authors of this study certainly have the African cell lines and have probably done the expression analysis. So where's the data?

Cal Tech wins!   posted by Razib @ 1/07/2007 04:38:00 PM

Brainy Caltech gets first NCAA victory since 1996:
Coach Roy Dow and his squad of brainy -- as opposed to brawny -- Beavers beat Bard College of New York 81-52 on Saturday night, ending a mathematically improbable run of 207 consecutive NCAA Division III losses.

Saturday, January 06, 2007

Richard Dawkins eats small children   posted by p-ter @ 1/06/2007 02:07:00 PM

So the internets are abuzz about Richard Dawkins's op-ed lamenting Saddam Hussein's death from a scientific standpoint. There's a lot of outrage out there, for myriad reasons. Some seem to think Dawkins is advocating experimental manipulation of Saddam's brain or some crazy shit like that, but I think anyone calmly reading the article would come to the conclusion that he's talking about doing interviews and maybe drawing some blood. "Psychological research" might have negative connotations for some, but observation is also research.

John Hawks and Chris at Mixing Memory have more reasonable objections related to the potential scientific utility of having Saddam around and/or the issue of informed consent. There are presumably ethical guidelines in place for research on prisoners, so I'm going to simply skip over that (Dawkins isn't writing this for an IRB, but rather the LA Times, so give him a break). It is true, however, that it's not immediately obvious what Hussein's actual scientific worth would be, at least to me, a geneticist. But I imagine historians would love to ask him about his regime (sure, he might not be entirely truthful, but when is any primary source perfect?) and psychologists would love to add another well researched test case of crazy-ass dictator syndrome to the literature. And in any case, whenever there's data available, someone will be clever enough to ask an interesting question of it-- it's not likely to be John, Chris, or I, but people are constantly researching things I'd never thought of, and I'm not bold enough to ever argue against collecting data because I can't think of any use for it.

John Hawks's final point is perhaps the most relevant:
I guess the reason why I am so revulsed is that Dawkins explicitly sets his interest in scientific inquiry above the cause of justice...I'd say that far more important to our future is the value of justice over science. Certainly, many people believe that Saddam's execution did not serve justice. But scientific value should not be part of that calculation
That's a valid objection, but I'm not sure I entirely agree. The problem is that justice can be served in a number of ways. Imgaine a less incendiary example: there are 1000 people convicted of drug related crimes who, according to the law, must be punished. Now there are a couple ways the punishment can be meted out-- a certain amount of time in prison, for example, or treatment for drug abuse in some clinic. There's a scientfic question to be asked there: which punishment has the best outcome, i.e. which reduces the future probability of being arrested the most. The experiment is obvious-- assign 500 people to each punishment and follow them for X number of years, but it implies that scientific questions are considered in the selection of the punishment.

Now, this is not exactly analogous to Saddam's case, but still, I'm not so quick to discard scientific value in the calculation of a punishment. If you've of the opinion that death was the only just punishment for Saddam's crimes, then this argument isn't for you. If, on the other hand, you think there are multiple ways justice could have been served, then I think scientific value could have been one criteria for making that choice.

A love of worms is essential   posted by p-ter @ 1/06/2007 07:58:00 AM

PLoS Genetics has an interview with Sir John Sulston, otherwise known as the guy who mapped all the cell lineages of C. elegans using only a microscope, some pens, and a lot of paper. A representative sheet of his notes is on the right.

Friday, January 05, 2007

More on "variables must vary"   posted by agnostic @ 1/05/2007 04:50:00 PM

Returning to a previous post of p-ter's, a common fallacy in popular discussions that involve statistics is to assert that "variable" X doesn't predict outcomes in Y very well, so X is of little consequence when we're talking about Y, despite the fact that the values of X didn't vary that much to begin with in the sample on which we based our conclusion. So, tautologically, variation in X will account for a pitiful fraction of the variation in Y or anything else. You have to allow X to vary to see what influence it's capable of. Imagine you looked at variation in height among NBA players, and it turned out that it was a poor predictor of MVP status. It would be silly to conclude that height is of little importance here -- just ask the 99.9% of male adults who are below the mean height in the NBA of 6 ft 7 in (cite; assume normal distribution with pop mean and SD = 70 in and 3 in). If you let height vary as it does in the population by letting anyone play in the NBA, of course it would be a good predictor of excellence in basketball.

On that note, there's an NYT article about some new algorithms Google is developing -- not those that deliver the most relevant sites given your search query, but ones being developed to best predict success within the company. That way, managers can cut out a lot of the guesswork involved in hiring. In short, they adminstered a battery of questions to their employees, gathered performance data on these employees, and looked for which "biodata" variables best predicted success. As for academic performance:

Among the first results was confirmation that Google's obsession with academic performance was not always correlated with success at the company.

"Sometimes too much schooling will be a detriment to you in your job," Dr. Carlisle said, adding that not all of the more than 600 people with doctorates at Google are equally well suited to their current assignments.

Well, sure, and height is "not always" correlated with success in the NBA, and "not all" of the NBA players with collegiate MVP awards are equally well suited to their professional assignments. But at a firm like Google, standardized mean and variation in academic performance, book smarts, or g must be similar to those of height in the NBA, or else Google wouldn't be the giant that it is. Thus, the fact that engineer A got an 800 on the Math GRE and a 3.8 GPA, while engineer B got a 780 and 3.7, is not going to tell you much about who is more likely to come up with the next big idea -- presumably the behavior and personality variables would do more of the work, such as if one of the engineers is curious and the other is close-minded. But as with socialist basketball, in a Google where anyone was free to work as an engineer, g and its correlates would account for a hefty portion of the variance in performance. Linda Gottfredson has many free articles on g in the workplace at her webpage. I doubt that these subtleties are lost on the people at Google, but journalists could cure much of their innumeracy with a handful of weekend workshops on statistical fallacies common in reporting.

Thursday, January 04, 2007

Sex difference in g   posted by the @ 1/04/2007 09:25:00 PM

A new La Griffe is up: Intelligence, Gender and Race.

Inspired by Jackson and Rushton (Intelligence 34 (2006) 479-486), La Griffe (Prodigy?) seeks to use a version of the "method of thresholds" to estimate the female distribution of g relative to males. The details are well spelled out in the article. Combining a variety of data sources, the article arrives at a least-squares estimate of the parameters defining the distribution of g first for blacks and then for women.

A white-black mean difference in g of 1.09 SD exists in favor of whites, equivalent to 16 IQ points. The black g distribution is narrower than the white, with a variance ratio (B/W) of 0.888.

A male-female mean difference in g of 0.164 SD exists in favor of men, equivalent to 2.46 IQ points. The female g distribution is narrower than the male, with a variance ratio (F/M) of 0.916.

Contrast the sex-difference estimate with Jackson and Rushton's estimate of 3.63 IQ points. At the time of publication of the Jackson and Rushton paper, I noted that no attempt was made to take into account the very well documented difference in variability of IQ between men and women. We can now compare Jackson and Rushton's estimate with La Griffe's. Above a +1 sd threshold, women would make up only 40% of the population using Jackson and Rushton's estimate and assuming equal variance. Notably, using La Griffe's estimates of mean and variance, women would make up 39% of the population above a +1 SD threshold.

Even small differences in mean and variance can have large effects at the tails. To give an idea of the effects, I've generated a table listing the percentage of women in a population above +1 SD for values of female mean in standard units (listed in the first column) and the ratio of female to male SDs (listed in the first row).

1 0.975 0.95 0.925 0.916 0.9 0.875 0.85
0 50% 49% 48% 47% 46% 46% 44% 43%
-0.025 49% 48% 47% 46% 45% 45% 43% 42%
-0.05 48% 47% 46% 45% 44% 43% 42% 41%
-0.075 47% 46% 45% 44% 43% 42% 41% 39%
-0.1 46% 45% 44% 42% 42% 41% 40% 38%
-0.125 45% 44% 43% 41% 41% 40% 38% 37%
-0.15 44% 43% 42% 40% 40% 39% 37% 36%
-0.164 44% 42% 41% 40% 39% 38% 37% 35%
-0.175 43% 42% 41% 39% 39% 38% 36% 34%
-0.2 42% 41% 39% 38% 37% 37% 35% 33%
-0.225 41% 40% 38% 37% 36% 35% 34% 32%
-0.242 40% 39% 38% 36% 36% 35% 33% 31%
-0.25 40% 39% 37% 36% 35% 34% 33% 31%
-0.275 39% 38% 36% 35% 34% 33% 31% 30%
-0.3 38% 37% 35% 34% 33% 32% 30% 28%


Borat out of character   posted by Razib @ 1/04/2007 08:21:00 PM

Terry Gross interviews Sacha Baron Cohen.

Wednesday, January 03, 2007

Morality   posted by Razib @ 1/03/2007 11:49:00 PM

Below we were talking about morality, and where it comes from. Check out this story:
The reason for the controversy is this: three years ago, when Ashley began to display early signs of puberty, her parents instructed doctors to remove her uterus, appendix and still-forming breasts, then treat her with high doses of oestrogen to stunt her growth.

In other words, Ashley was sterilised and frozen in time, for ever to remain a child. She was only 6.


Afflicted with a severe brain impairment known as static encephalopathy, she cannot walk, talk, keep her head up in bed or even swallow food. Her parents argued that "keeping her small" was the best way to improve the quality of her life, not to make life more convenient for them.

In other news, I've just spent considerably more than a "the cost of a cup of coffee every day" [over a year] on surgery for my cat. I don't regret it at all, it was the "right thing to do." No need for casuistry here.

A Mormon in the Whitehouse, not yet, though someday....   posted by Razib @ 1/03/2007 09:11:00 PM

I finally read Damon Linker's piece, The Big Test, where he expresses worries about the possibility of Mitt Romney becoming president (my post on Romney & Mormonism from last fall). I am generally rather skeptical of Linker's piece, though he is an erudite fellow it seems to me that he misses the details while surveying all from the intellectual commanding heights (his background seems to be in history and philosophy).

1) Linker suggests that while Protestantism and Catholicism have given rise to sophisticated liberal forms, Mormonism might not be capable of this because of its prophetic nature (he makes an analogy to Islam). My first caution would be that the Mormonism of Joseph Smith already has: the Community of Christ was until recently called The Reorganized Church of Latter Day Saints. Though far less numerous than the Utah Mormons, this midwestern branch of the church has basically morphed into a moderate Protestant denomination. There are plenty of other splinter sects, most of them far crazier than the Utah Mormon church derived from Brigham Young's leadership. The point is that Linker suggests that there is a structural deficiency in Mormon beliefs which prevents them from changing, but I have a hard time not seeing how their very prophetic nature (continuous revelation) can't but make them pretty adaptable to the times. The Mormons who remained in Missouri eventually assimilated into the Middle American religious culture and lost their distinctiveness, suggesting that geographical separation, as opposed to a specified set of beliefs, is what really set Utah Mormonism off on its different path.

2) The fact that Mormons have an attenuated theology and by and large reject Greek philosophy as a modality of their faith is not looked upon positively by Linker. That the Mormon God is a physical being who has a wife and lives embedded within this universe might seem really bizarre to most sophisticated believers, but I have come to believe that this is actually far closer to the mental conceptualization of God that is genuinely accessible to the human mind than the definitions of most "higher religions." Mormons believe that God was once a human being, that righteous Mormon males will become Gods and rule their own universes, and that the New World was once populated by white skinned Jews. This all seems bizarre to most people, but let's compare it to Transubstantiation, Tawhid or Nirvana. One reason that Mormonism is so bizarre is that it is so intelligible! The basic Mormon canon of beliefs seems ludicrous and falsifiable, but it is such precisely because it is accessible to conventional analysis (i.e., Mormonism is clearly false, many other theisms have fled into incoherency and semantical obfuscation to escape critique). The Mormon God is a constrained being, though far grander than you or I. Mormonism does not make recourse to a complex theology to justify a Trinity, they simply accept a multiplicity of divine entities. God did not mysteriously withdraw revelation from the world thousands of years ago, in Mormon belief God speaks directly through their prophet as he always has and always will (until they change their minds of course).

3) We shouldn't neglect the fact that Mormonism is an American religion which can be comprehended in part by understanding its social historical background, and that of Joseph Smith. Smith was from the region of upstate New York and New England which was the scene of much religious revival in the early 19th century. Some aspects of Smith's background are evident in the Mormon religion. There is some consideration as to whether he was involved in Universalism, which rejects hell. To this day Mormons do not accept hell, and non-Mormons who are righteous may not become Gods, but they will not be consigned to eternal damnation. It is important to remember than in many ways at its core Mormonism is rather liberal and adventurous because of its historical origin, even though socially it has a conservative air about it because of the character of the believers.

4) I will not elaborate much on this point, but I do not believe that Damon Linker properly frames the psychological complexity which religious belief is. He seems to read it straight from texts, professed creeds and historical councils. The fact is that the average Mormon is as engaged with his or her theology as the average Protestant, Catholic or Jew. Not much. I really don't know what the fact that Mormons don't draw from the thoughts of classically educated church fathers tells us in terms of their behavorial tendencies.

This does not mean that I think that Romney can become president. Though I don't believe in the functional significance of theology, it does have a role in demarcating barriers. I believe that like Catholics, Mormons will be accepted by other Protestant Christians over time. But the mental reconciliation won't happen overnight. Mitt Romney's run for the presidency will be futile, but it will serve as the building block for the future absorption of his demonination into the American mainstream.

Update: Daniel Larison has 12,000 posts on Mormonism & Romney. He also reports on polling data which shows that anti-Mormonism matters.

DNA "spectral lines"   posted by Fly @ 1/03/2007 05:08:00 PM

DNA no-no's

Elements can be detected in the solar energy spectrum because elements absorb specific wavelengths creating dark lines in the hot body radiation spectrum. By analogy "forbidden" DNA sequences would form "dark lines" in the expected DNA sequence frequency spectrum. Find interesting stuff by what is missing. Neat.

"COULD there be forbidden sequences in the genome - ones so harmful that they are not compatible with life? One group of researchers thinks so. Unlike most genome sequencing projects which set out to search for genes that are conserved within and between species, their goal is to identify 'primes': DNA sequences and chains of amino acids so dangerous to life that they do not exist."

Tuesday, January 02, 2007

10 Questions for Heather Mac Donald   posted by Razib @ 1/02/2007 03:35:00 PM

Heather Mac Donald is John M. Olin fellow at the Manhattan Institute. Well known for her realist take on immigration reform and law enforcement, of late she has been the center of a small controversy precipitated by a piece in The American Conservative where she expressed her atheism rather forcefully. Below are 10 questions and Heather's answers (here is an exchange Heather had with Luke Ford from a few years back).

1) OK, I'll get this out of the way. What prompted you to "come out" as an atheist in The American Conservative earlier this year? A friend of mine suggested that you might have become frustrated with the lack of a "reality based" conservatism during this administration, in particular in its attitude toward immigration. Is he going down the right track?

I wrote The American Conservative piece out of frustration with the preening piety of conservative pundits. I attended a New York cocktail party in 2003, for example, where a prominent columnist said to the group standing around him: "We all know that what makes Republicans superior to Democrats is their religious faith." This sentiment has been repeated in print ad nauseam, along with its twin: "We all know that morality is not possible without religion." I didn't then have the courage to point out to the prominent columnist that quite a few conservatives and Republicans of the highest standing had no religious faith, without apparent injury to their principles or their behavior.

Around that time, I had started noticing the puzzling logic of petitionary prayer. What was the theory of God behind prayer websites, for example: that God is a democratic pol with his finger to the wind of public opinion? Is the idea that if only five people are praying for the recovery of a beloved grandmother from stroke, say, God will brush them off, but that if you can summon five thousand people to plead her case, he will perk up and take notice: "Oh, now I understand, this person's life is important"? And what if an equally beloved grandmother comes from a family of atheist curs? Since she has no one to pray for her, will God simply look the other way? If someone could explain this to me, I would be very grateful.

I also wondered at the narcissism of believers who credit their good fortune to God. A cancer survivor who claims that God cured him implies that his worthiness is so obvious that God had to act. It never occurs to him to ask what this explanation for his deliverance says about the cancer victim in the hospital bed next to his, who, despite the fervent prayers of her family, died anyway.

As I was pondering whether any of these practices could be reconciled with rationality, the religious gloating of the conservative intelligentsia only grew louder. The onset of the Iraq war expanded the domain of religious triumphalism to transatlantic relations: what makes America superior to Europe, we were told by conservative opinionizers, is its religious faith and its willingness to invade Iraq. George Bush made the connection between religious beliefs and the Iraq war explicit, with his childlike claim that freedom was God's gift to humanity and that he was delivering that gift himself by invading Iraq.

I need not rehearse here how Bush's invocation of the divine gift of freedom overlooks the Bible, the persistence throughout history of hierarchical societies that have little use for personal autonomy, and the unique, centuries-long struggle in the West to create the institutions of limited government that underwrite our Western idea of freedom. Suffice it to say, the predictable outcome of the Iraq invasion did not convince me that religious belief was a particularly trustworthy ground for political action.

So in the American Conservative piece I wanted to offer some resistance to the assumption of conservative religious unanimity. I tried to point out that conservatism has no necessary relation to religious belief, and that rational thought, not revelation, is all that is required to arrive at the fundamental conservative principles of personal responsibility and the rule of law. I find it depressing that every organ of conservative opinion reflexively cheers on creationism and intelligent design, while delivering snide pot shots at the Enlightenment. Which of the astounding fruits of empiricism would these Enlightenment-bashers dispense with: the conquest of cholera and other infectious diseases, emergency room medicine, jet travel, or the internet, to name just a handful of the millions of human triumphs that we take for granted?

My hope in writing the piece was that the next time a conservative pundit, speaking for and to other conservatives, assumes that he is surrounded by like-minded believers because of course to be conservative is to be religious, that for just a moment a doubt might pass through his mind whether some in his audience may be without faith. And the worst part would be: he couldn't tell who they are.

2) How exactly did you find yourself on the political Right? I recall that you were a liberal while in college, what happened that resulted in your political shift? Was in a "Eureka!" moment, or a gradual affair?

First I realized that I had wasted my college education on the literary theory known as deconstruction, being as I was then too stupid to grasp that nearly everything deconstruction had to say about language was lunatic and fictional. When multiculturalism hit the academy (several years after I had graduated), I was appalled that barely literate students were allowed to trash the most astounding creations of Western civilization before which we should all be on our knees. I came to New York in 1987, in the midst of a particularly craven period of capitulation to racial extortionists. Taking up journalism in the early 1990s exposed me to the total disconnect between liberal dogma about the underclass poor and the reality of their self-defeating behavior. I still have no idea how New York Times reporters can visit the same homeless shelters and welfare offices that I have and remain confident that the "clients" of those facilities are the victims of racism, rather than their own bad decisions. So I would say that reporting on social problems provided the coup de grace for liberal pieties. (I write about my political evolution at greater length in a forthcoming book of essays by various journalists called Why I Turned Right)

3) You've covered many absurd fads and fashions, from the banalities of teacher's colleges to the rise of "relevant" hip-hop curriculum. Of the various topics is there one that has struck you as an exemplar of all that is wrong with our culture?

First of all, I'm in such a period of doubt regarding the conservative establishment right now that I am not sure that I would still use the phrase: "all that is wrong with our culture." My recoil from contemporary conservatism is undoubtedly an overreaction, but even the cultural declinism that is one of its standard features--and which I have endorsed in the past--now strikes me as possibly overwrought.

That having been said, the most idiotic practice that I have come across remains the entire foolishness of progressive pedagogy: the insanity of having students "teach" each other (translation: sit around in class talking about the latest sneakers while the teacher-oops, I mean, "facilitator"--looks on benignly); the dismissal of knowledge as an essential legacy that a teacher must convey to his students; and the rejection of memorization and drilling as necessary to learning.

And having just read a hair-raising column in the New York Times (December 29, 2006) on parent-endorsed "talent shows" that feature 10-year-old girls simulating pole dancing, I am nearly ready to join the jeremiad against American cultural decline again.

And yet, I look around for signs that such pedagogical stupidities and parental cluelessness are retarding our progress, and I can't find them. For all the barbarity of popular entertainment and the historical ignorance of the American public, American civilization and the West generally are at the top of their games-contrary to war on terror hysteria that holds that we face an "existential threat" from Islamists. The rate of technological innovation is higher than at any point in human history and will undoubtedly only accelerate in the future. We are reaping a whirlwind of unfathomable benefits from scientific research.

Would I prefer it if our elites had the taste of 18th century aristocratic patrons and were subsidizing the likes of Mozart, Haydn, and Tiepolo, instead of Jeff Koons and Richard Prince? A thousand times, yes! But as much as I yearn to live in a world that could produce such beauty, I have to recognize that this is the best of all possible times to be alive. I don't know how many of us would give up our astounding array of choices, despite their costs above all in family stability, to go back to a time of more restricted individual autonomy.

4) You've taken a hard look at Latino "family values." When I say "hard," I must be frank and admit that it doesn't seem like it is that difficult to scry that Latin American cultures do not exhibit the sort of family values typical of the Anglo-American tradition, rather, you simply read out the data as it was. Do you think that facts can eventually supersede the cant on this issue?

Given that the liberal elites have ignored the 70% black out-of-wedlock birth rate for decades in discussing the causes of black poverty, I am confident that open borders conservatives will prove just as capable of ignoring the 48% Hispanic out-of-wedlock birth rate as they perpetuate the myth of redemptive Hispanic family values.

5) Do you think that the Bush administration was bad for conservatism? If so, how bad?

Since Bush was not a conservative, arguably he did no harm to conservatism. His failings were not those of conservatism but rather of a Wilsonian absolutism: faith in the universality of his favorite religiously-based abstractions and in the ability of government to impose those abstractions globally.

6) Do you take a particular interest in the natural human sciences? For instance, evolutionary psychology, behavioral ecology, neuroscience, and so on.

I have not read much evolutionary psychology, but I take it that it may come in very handy in rebutting the claim that human altruism proves God's existence (as Francis Collins recently proposed at the 92nd St. Y in New York City, before leading the audience in a sing-along to You Really Got a Code On Me," a tribute to the genome and God, set to Beatles music). As for neuroscience, I am in awe of its power. If I could be any kind of scientist, I would study the brain.

7) You've labelled yourself a 'skeptical conservative.' Would you also say you are hopeful about the trajectory that this republic might take into the future, or do you warrant that the corner is likely turned and we'll be fighting a rearguard action for most of our lives?

I will interpret your question to mean whether I think secularism will strengthen in the U.S. over time. I am not ordinarily an optimist, but I take heart from the incensed response to the existence of a mere three contemporary books debunking religion. While the proportion of Americans who believe in Biblical revelation remains depressingly high and doesn't yet show much sign of decline, the reaction of religion's conservative apologists to a few atheists sticking their heads out of the foxhole suggests to me a possible nervousness about religion's hold in the future. First Things editor Joseph Bottum calls secularists "superannuated," in the aforementioned book Why I Turned Right. Wall Street Journal columnist Dan Henninger claims a religious provenance for the following "American" virtues: "fortitude, prudence, temperance, justice, charity, hope, integrity, loyalty, honor, filial respect, mercy, diligence, generosity and forbearance." Yet Classical philosophers and poets celebrated many of these "religious" virtues as vigorously as any Evangelist or Christian divine, and these ideals are in any case human virtues, which is why religion can appropriate them. As for Henninger's suggestion that mercy and hope had to wait upon Christianity to make their appearance on the scene, I would need more evidence. Do these overbroad claims for the necessity of religion suggest that the theocons are running scared? Perhaps.

Up to half of the conservative writers and thinkers whom I know are non-believers. And yet because of the rule that one may never ever question claims made on behalf of faith, they remain in the closet. At some point, however, they may emerge to challenge the idea that without religion, personal and social anarchy looms.

8) If you are 18 and figuring out what course of study to pursue for the next 4 years what changes would you make to your educational path now that you have some hindsight?

I would study a lot more history. Thanks to my college's refusal to tell its ignorant students what an educated person should know-heaven forbid that it actually exercise intellectual authority!-I was required to study no history and didn't know enough to do so on my own.

9) John Derbyshire has offered in the past that evangelical religious conservatives aren't really reliable conservatives in a Burkean sense considering that evangelicalism was aligned with progressive and radical causes in the past. What's your opinion of this assessment, is the Religious Right here to stay as part of the grand conservative coalition?

I defer to John Derbyshire in all things. But given the view of conservative spokesmen that they need the patina of piety, I can't see anyone drumming the Religious Right out of a "grand conservative coalition" in the future, even if the RR were to suddenly embrace the cause of global warming, say. And since our current reigning Republicans are not particularly worried about expanding government, I don't see how anything the RR might want in that arena would get it in trouble.

I have always been amazed that the liberal media is willing to let stand the right's equation between "religious voters," "values voters," and opposition to gay marriage, abortion, and stem cell research. There is no necessary relation between being religious, having values, or opposition to stem cell research or gay marriage, in my view. That having been said, the current obsession with homosexuality on the part of the Religious Right would seem to assure it a political relevance for the Republican Party for some time.

10) Were you surprised at all at the reactions to your piece about your atheism?

I had led such a sheltered life that I had never come across people like the letter writer who chastised me for not mentioning "God's sacrifice of his Only Begotten Son" in my discussion with Michael Novak. For the letter writer, this sacrifice constituted unassailable proof of Christianity. That type of reasoning was new to me.

As for the conservative intelligentsia, I was surprised-but that is my fault. I was ignorant and naive enough that somewhere in the back of my mind, I think, I might actually have assumed that presenting what strike me as pretty strong empirical arguments against the claim that God is just and loving, say, would end the matter. And I was unaware of the depth of commitment to the idea that religion is the source of values and that conservatism and religion are inseparably linked. For me, conservatism was about realism and reason.


The evolution of the human brain: gene regulation is key   posted by p-ter @ 1/02/2007 02:42:00 PM

A few days back, Razib linked to a paper in PLoS Biology claming that the evolution of genes expressed in the brain has slowed down along the lineage leading to humans. As this paper is at odds with a paper I've commented on before which claimed to show an acceleration of brain-expressed genes along the human lineage, I thought I'd add my two cents:

This is indeed an excellent paper--the genome sequencing juggernaut has produced a wealth of new data over the last couple years and this analysis, which is more rigorous than previous analyses, shows a slight decrease in the evolutionary rate of change of brain-expressed genes. This raises the intriguing possibility that the complexity of regulatory networks in the brain constrains protein-coding sequence while accentuating the effects of regulatory changes. I see through Chris Chatham at Developing Intelligence that other people are coming to the same conclusions:
As Barbara Finlay and coauthors wrote in this 2001 Behavioral and Brain Sciences article, the order of neurogenesis and ultimate size of various brain regions is highly conserved across all mammals, suggesting natural selection largely works not by selecting for specific "modules" or components in the nervous system as appropriate to a particular organism, but instead "by adjusting the parameters of a 'standard' developmental program."
Changes in gene expression will definitely account for some of the particular evolutionary features of the human brain. That said, it's incredibly frustrating to see a sentence like this:
Our results do not contradict the finding of accelerated amino acid changes in some brain-expressed genes [6,31,32]. Deviations from the general trend are expected. In fact, these deviations may be the most interesting cases.
So which genes are the interesting ones!? There's no list, no Supplementary Table, nothing! I'm hoping they're just saving those results for a later paper, we'll see...

Atheism is not robust   posted by Razib @ 1/02/2007 01:13:00 PM

Recently I had an email exchange with a friend about the nature of religion, and whether Communism could serve as a religion-proxy. The basic idea being that messianic political movements are godless religions. I don't dismiss this analogy, and I do believe that there is a significant intersection between the cognitive states of those who are passionate about God and those who are passionate about political justice. But I don't believe there is one 'God module,' and I suspect that 'religion' is a catchall term for a range of beliefs and mental states common in our species which emerge from convential human psychology (e.g., 'agency detection'). On some of these traits messianic political movements and supernatural organized religion intersect, and the idea that socialism is secularized Christianity is true insofar as I believe that many political movements exhibit the characters of radical religion shorn of supernaturalism. That being said, I tend to believe that supernatural religion is far more robust than messianic political movements because God does not die, but Stalin or Castro do. In other words, I believe that the emotional locus of a charismatic leader is essential to these movements (operationally a "God-king"), and when that leader dies unless there is a replacement the political movement is liable to lose its vigor. In contrast, gods never die but persist, and so the emotional attachment can transcend generations and develop powerful cultural staying power.

The reason I bring this up now is that Derb pointed me to some data from Russia which suggests a massive revival of Orthodox religiosity within the last 15 years. You can read the google translation here. The important point is that 16% of Russians now call themselves atheists. I have seen data that a plural majority were avowed atheists in 1990 (e.g., 30-40%). If you look closely at the data the massive revival of religion is to some extent notional and nominal, but the point is that all it took was 15 years for the reassertion of the traditional religious sentiments of the population in name if not action. This polling data is a bit extreme in its findings, but I've seen other surveys which confirm its general result, that religion exhibited a massive and almost immediate bounce back after the fall of Communism. What does this tell us? Note that the Soviet Union went through 3 generations of disincentives toward supernatural religiosity, and yet people seem rather casually to flip back toward an Orthodox confession in half a generation (both Yelstin and Putin were public converts to Orthodoxy from a secular-atheist background). I think this goes to my above point, religion is natural and robust. Messianic political movements devoid of supernaturalism can fill the same vacuum, but over the long term I believe they are at a disadvantage and relatively epiphenomenal.

Watson in Esquire   posted by Razib @ 1/02/2007 01:02:00 PM

I've received several emails about this interview by James Watson in Esquire. Here is a representative sample:
I've wondered why people aren't more intelligent. Why isn't everyone as intelligent as Ashkenazi Jews? And it may be societies work best when there's a mixture of abilities-the bright people would never be an army. Or has our intelligence been limited by leaders killing off any potential competitors? I suspect time is not a factor. The Ashkenazi Jews have a thousand years. So these are the sorts of things we'll find out-how many mutations would you need to be more intelligent?

IQ → Academic Achievement   posted by Alex B. @ 1/02/2007 03:30:00 AM

Count 'em: one, two, three new studies on the relationship between IQ and academic achievement in the latest issue of Intelligence (volume 35, issue 1)

Before the studies' precis, a little background on why such studies are necessary. More than anything, such studies are needed because folks such as S. Ceci and R. Sternberg (very prominent and oft-cited) advocate that (traditional) IQ tests are just measuring little more than school related achievement. So, IQ and academic achievement are only related because, for reasons X, Y, and Z (pick your own environmental variables), some folks get more out of school, and it just so happens that the same folks do well on IQ tests due largely (if not entirely) because school achievement and IQ tests are measuring the same thing. Consequently, g is an irrelevant artifact of those damned psychometricians.

An alternative hypothesis (explicated nicely in Jensen1,2), however, is that due largely to genetic factors (which influence both individual differences and environmental influences), people enter school with wide variability in cognitive ability and "readiness to learn." This initial variability then heavily influences (although not completely determines) the amount a given student will pick up as he/she matriculates. As a student gains more information, his/her initial ability and the new information acquired then interact so he/she is able to expand his/her knowledge further, and so on and so forth. Therefore, while one needs access to "information," the child's general cognitive ability is the engine driving his/her educational achievement.

Don't miss the point here. These are two separate, testable, hypotheses. (A) IQ and academic achievement are synonymous. That is, people are smart (or not so smart) almost solely because they had (or did not have) a good education. (B) IQ is independent of academic achievement, although the former significantly influences the latter. That is, you can come from a good school, but not be so bright, and do poorly on achievement tests; likewise, you can come from a school that is not so good, (but meets some very minimum standard), but be bright, and do very well on academic achievement tests.

Now, the studies.......

1) Treena Eileen Rohde and Lee Anne Thompson: Predicting academic achievement with cognitive ability

This study is likely the weakest only because they used a group of college students from an elite university. Not that there is anything wrong with this, but when you see the samples in the studies below, it is a noticeable concern.

Their major contribution was that in predicting (standardized) academic achievement, speed of information processing and spatial ability can explain small, but significant, amounts of variance unexplained by general vocabulary (Mill Hill) and perceptual organization (Raven's Matrices), although the latter two tests, hands down, did the best in predicting academic achievement across various indicators.

In their own words:
General cognitive ability measures (Raven's, Vocabulary) and specific cognitive abilities (working memory, processing speed, spatial ability) collectively accounted for between 16% [GPA] and 54% [SAT] of the variance in academic achievement.

2) Marley W. Watkins, Pui-Wa Lei and Gary L. Canivez: Psychometric intelligence and achievement: A cross-lagged panel analysis

This study had 3 advantages over the former: (1) it is longitudinal, (2) the data is from a much wider scope of IQs, and (3) the data comes from all over the US. The drawback, and major caveat, is that the data is all from special education (broadly defined) testing, so the applicability to the entire population is in question. Still, the mean Full Scale IQ score from the WISC-III (the IQ instrument used) is 90 with a SD of 15 (in the general population it is 100 and 15), and the subtest scores hover around 8 with SDs that hover around 3 (in the general population it is 10 and 3).

Because they have longitudinal data on both standardized IQ and standardized achievement tests, they can specifically test the IQ--->Achievement hypothesis (see preamble). What do they find?

This notion of intelligence estimating a student's ability to succeed in school assumes the temporal precedence of intelligence to achievement. . . Regardless, the present study supports the view that intelligence, as measured by the VC [Verbal Comprehension] and PO [Perceptual Organization] dimensions of the WISC-III, influences or is related to future achievement whereas reading and math achievement do not appear to influence or are not related to future psychometric intelligence.

Stated more bluntly:

. . . the present study provides evidence that psychometric intelligence is predictive of future achievement whereas achievement is not predictive of future psychometric intelligence. This temporal precedence is consistent with the theoretical position of Jensen (2000)[1] that intelligence bears a causal relationship to achievement and not the other way around.

3) Ian J. Deary, Steve Strand, Pauline Smith and Cres Fernandes: Intelligence and educational achievement

Before getting on to the study, a brief word about Dr. Deary. He is the current badass of differential psychology. Because of his background (degrees in medicine and psychology), he is able to investigate psychometric, chronometric, genetic, and neurological aspects (often concurrently) of both intelligence and personality (look at the range on his vita). As if that were not enough, he has challenged the whole field of differential psychology by obtaining multiple population level, longitudinal data sets. So instead of trying to infer from a sample a few hundred to the target population, he is gathering population level samples of thousands of individuals. Case in point:

Deary's study looked at how cognitive ability measured at age 11 predicted academic achievement at age 16. Unsurprisingly, the IQ-Achievement correlations for the Sciences are around .6 (math highest, chemistry lowest), with similar coefficients form Arts/Humanities and Social Studies. Surprisingly, for practical fields (e.g., P.E., Art) the coefficients are a little lower, but not that much, averaging around .5. Here is a pic of the correlation table: (the n is in parentheses; it obviously changes as not every student took every class)

Deary took the analysis a step further however and did a little latent variable modeling. As the IQ test had three components/subtests (verbal, nonverbal, quantitative), he correlated a latent g factor with a latent academic factor using the following subtests: English, English Literature, Math, Science, Geography, French (n=12519). The correlation between the latent factors was .81. That is: 66% of the variance in latent (general) academic achievement can be explained by latent cognitive ability---measured 5 years previously. While he hypothesizes that such things as "school ethos" and "parental support" are good areas to search for the other 34%, based on Rohode's work, it is likely going to be found in residual, first order factors (see Carroll or McGrew).

Take home message: While general cognitive ability and academic achievement are not isomorphic, the former is necessary for the latter, while the converse is not necessarily true. Spearman suggested this more than a century ago, and, to quote the last sentence in Deary's work,
These data establish the validity of g for this important life outcome.

1. Jensen, A. R. (2000, August). The g factor and the design of education. Paper presented at the annual meeting of the American Psychological Association, Washington, DC.

2. Jensen, A. R. (1989). The relationship between learning and intelligence. Learning and Individual Differences, 1, 37-62.


Monday, January 01, 2007

Happy New Year to Bob Skipper   posted by Razib @ 1/01/2007 03:43:00 PM

Robert Skipper is back! (or will be soon) Put him back into your RSS everyone....