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:

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!

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?

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.

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.

References:
[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.

Update:

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

[source]

"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.

Cite:

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.

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."

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.

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.

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

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.

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.

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.

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.

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?

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