On the DNA level, most fixations of new alleles are due to genetic drift. But what's the role of neutral processes in phenotypic evolution? I ask because Larry Moran is claiming (in the comments here) thar most phenotypic evolution is also due to drift. I find that hard to believe-- one of his examples, PTC tasting in humans, is certainly not drifting neutrally, and the expression levels of most genes (a "low-level" phenotype one might expect to be allowed to drift) seem to be under strict control (I reviewed some of the evidence for that here).

Good evidence for lack of selective constraint could come from mutation accumulation (MA) lines-- lines bred with a tiny effective population size for a number of generations. The small effective population size allows nearly all alleles (except the most deleterious ones) to drift randomly. One could compare a given phenotype in a number of these lines, then compare to wild isolates-- if the variance in the MA lines is about equal to that in the wild lines, you might conclude that selection is not operating on the phenotype in the wild.

Has this been done? Is anyone aware of experimental evidence for lack of constraint on a phenotype?

Labels: Evolution

The folks at the Craig Venter Institute, having patented the technology for creating a synthetic organism, now have at least part of the process working: they report that they can take an entire bacterial genome from one organism and pop it into another, essentially "re-booting" the cell as a new species. The next step, obviously, is to synthesize a custom genome that does something you find worthwhile (digests some nasty chemical, if you're feeling eco-conscious...or produces a nasty chemical, if you're feeling more war-like), and create your own bacteria.

One interesting thing (from a methodological standpoint) about this procudre is that it appears to involve inducing the fusion of the two cells (the researchers don't actually know; they just see the outcome), making it somewhat similar to procedures for creating hybrid cell types in mammals. It's something of an unexpected connection between bacterial transformation and cell fusion.

Labels: Synthetic biology

Nature Genetics has a free supplement on structural variation, with an emphasis on its role in human disease. Nothing too exciting-- structural variation is simply a type of polymorphism, albeit with some interesting issues regarding detection, but if you're looking for some background and discussion of future directions, it might be of interest.

Labels: Genetics

The Genographic Project Public Participation Mitochondrial DNA Database. This is Spencer Wells' baby. Only mtDNA, and focused more on the methods though they didn't find Neandertal lineages.

Labels: Population genetics

Another genome-wide association study:

Breast cancer exhibits familial aggregation, consistent with variation in genetic susceptibility to the disease. Known susceptibility genes account for less than 25% of the familial risk of breast cancer, and the residual genetic variance is likely to be due to variants conferring more moderate risks. To identify further susceptibility alleles, we conducted a two-stage genome-wide association study in 4,398 breast cancer cases and 4,316 controls, followed by a third stage in which 30 single nucleotide polymorphisms (SNPs) were tested for confirmation in 21,860 cases and 22,578 controls [!!!] from 22 studies... SNPs in five novel independent loci exhibited strong and consistent evidence of association with breast cancer (P < 10-7). Four of these contain plausible causative genes (FGFR2, TNRC9, MAP3K1 and LSP1).

These alleles are of small effect and in areas of the genome about which little is known, again showing that genome-wide association studies are a powerful way of opening up research into novel biology.

Labels: Association, Genetics

Early this year, I commented on a paper showing large differences in gene expression between Europeans and Asians. A letter to the editor in this week's Nature Genetics points out a major flaw in part of their analyses.

Expression arrays are tricky tools-- they don't provide a measure of absolute mRNA levels, but rather an output that corresponds to the binding affinities of the mRNA, the ambient conditions, the way the mRNA was handled, and absolute mRNA levels (and a billion and one other things). Study design is extremely important in isolating the effect of the variable you're really interested in (mRNA levels), and it's very difficult, if not impossible, to really compare the raw data from one array experiment with that from another.

The error the authors made is an unfortunate (and pretty elementary) one-- they did the array experiments on the Europeans population in 2003-2004, and the array experiments on the Asian population in 2005-2006 (they actually erroneously claimed the samples were randomized with regard to year in the paper, which would explain why it got past peer review). This means that any variation between the European and Asian populations is perfectly confounded with variation between those two batches. There's no way to correct for this; any difference in mean expression between the two populations is due to a mixture of the "real" effects and the bias from the batch effect. That's a bitch.

Luckily, the authors also did additional analyses (as they point out in their reply)-- they looked at the correlation of expression levels with genotypes. In the figure, you see the population distributions of expression for a given gene on the left, and the within-genotype levels on the right. There doesn't seem to be much of a differences between the two populations within each genotype class, but the population difference is explained almost entirely by the difference in allele frequency between the two populations.

So was their claim of finding nearly 25% of all genes differentially expressed between the two populations likely wrong? Yes. But their conclusion that allele frequency differences play a role in expression differences between populations stands-- it will just take a better-designed study to quantify the effect.

Labels: Genetics

A comment below about gluten intolerance (which is associated with problems digesting products with wheat) made me curious. In much of Eurasia this would be a serious problem since wheat is the staff of life. Hard numbers are difficult to come by. This is as good as anything else I've seen:

Celiac disease affects as many as 1 in 300 people in Italy and southwestern Ireland, but is extremely rare in Africa, Japan, and China...According to a multicenter study in 2003, there is a 1 in 133 chance that people with no risk factors or family history in the U.S. have celiac disease. Additionally, a person's risk increases to a 1 in 22 chance if they have a first-degree relative with celiac disease and a 1 in 39 chance if they have a second-degree relative...Around 60,000 Americans are diagnosed with celiac disease annually and a total of over 2 million have the disease, making it perhaps the most common genetic disorder in the United States...Celiac disease can occur at any age, and females are more commonly affected than males. Of females presenting during their fertile years, the male to female ratio is almost 3 to 1....

From Wiki:

The vast majority of coeliac patients have one of two types of HLA DQ, a gene that is part of the MHC class II antigen-presenting receptor (also called the human leukocyte antigen) system and distinguishes cells between self and non-self for the purposes of the immune system. There are 7 HLA DQ variants (DQ2 and D4 through 9). Two of these variants-DQ2 and DQ8-are associated with coeliac disease. Every person inherits two copies, one from each parent. The gene is located on the short arm of the sixth chromosome, and as a result of the linkage this locus has been labeled CELIAC1.

Coeliac disease shows incomplete penetrance, as the gene alleles associated with the disease appear in most patients, but are neither present in all cases nor sufficient by themselves cause the disease. Over 95% of coeliac patients have an isoform of DQ2 (DQA1*0501:DQB1*0201 haplotype or more simply DQ2.5) and DQ8 (DQA1*0301:DQB1*0302), which is inherited in families.

Incomplete penetrance might be due to the fact that there are other genetic actors which haven't been elucidated that are necessary for the emergence of this syndrome. Or, there might be environmental or pathogenic triggers which only affect a minority with the necessary genetic predisposition. But in any case, my first thought was gluten intolerance might be the result of an incomplete selection sweep as populations shifted from hunter-gatherer lifestyles to agricultural ones. I'm skeptical of this since populations in Africa and Australia which don't have a history of wheat agriculture don't exhibit this syndrome. Additionally, though wheat agriculture is practiced in north China this was originally a region of millet production. Finally, all the reports suggest massive underestimates of the extent of this condition within the population. Like lactose intolerance this isn't a disease with a clean set of symptoms which are easy to assay quantitatively (is there a way a metric for stool firmness?). The implication of MHC loci as necessary preconditions makes me wonder if gluten intolerance is simply a low frequency condition which is a byproduct of a disease adaptation on the genes in question which was operant in western Eurasia.

Labels: Genetics

There is a rather salty piece of correspondence in the new Nature Neuroscience from one Maureen Condic regarding Nature's editorial position on the likelihood of development of ES cell-based therapies anytime soon. Apparently, Condic has a skeptical take on the issue and Nature had some disparaging words.

The issues of immune rejection, tumor formation and hESC differentiation raised in my article are not distortions or mere polemic; they are matters of scientific fact. These same concerns have been raised in the scientific literature and voiced by leading scientists in the stem cell field. James Thomson cautioned that "major roadblocks" must be overcome before hESC-derivatives could be safely transplanted into patients, and concluded that surmounting these roadblocks will be "likely to take a long time". Similarly, Robert Lanza noted that immune rejection is a significant problem, and warned that creating hESC lines to match most patients "could require millions of discarded embryos from IVF clinics". Although the editors dismiss as "tenuous" the connection between therapeutic use of hESCs and the genetic/epigenetic abnormalities introduced during cloning, this same concern was raised by Jose Cibelli's recent article in Science.

I think it is important to hear about these obstacles and be realistic about what ES cells could provide. There are other uses of ES cells besides implantation type therapy, of course. For instance, they aid the understanding of basic cell differentiation and cell cycle regulation, topics that are important in cancer research.

The problem for me is that I find the 'moral' objections ridiculous. So if ES cells have any therapeutic or just plain scientific potential at all, then I'm all for it. Am I living in naive bliss thinking that most average people wouldn't give a damn after they really understood what a blastocyst is? Right now, I'm thinking that this is one of a few scientific areas where you could educate the public and actually impact policy in a positive way.

There appears to be a semi-lively debate underway over at the Nature Neuro news blog: Action Potential.

Labels: embryonic stem cells, es cells, politics

Macho stags have macho sons but daughters are little dears:

The findings show for the first time in animals that some genes are designed to benefit just one gender and can handicap the other sex.

It was found that the female offspring of the biggest and strongest stags were less successful at breeding and had fewer fawns during their lives than daughters of weedy males.

In The Mating Mind Geoff Miller proposed that variance in mutational load could account for the phenotypic variation in traits like intelligence. The brainy and beautiful are simply burdened with fewer deleterious alleles. But the study above suggests another reasons, traits which increase fitness in one sex may decrease it in another. The ideal is for sex dependent gene expression to modulate phenotypic expression so that female offspring of hyper-masculine males are not themselves somewhat masculinized. But the scaffolding of the genes which cause these traits by modifier loci takes time, and perhaps selective pressures are also running ahead so that the variational noise due to differential fitness across sexes is always extant within the population.

Labels: Genetics

The original human ('Old Stone Age') diet is good for people with diabetes:

In a clinical study in Sweden, the research group has now compared 14 patients who were advised to consume an 'ancient' (Paleolithic, 'Old stone Age') diet for three months with 15 patients who were recommended to follow a Mediterranean-like prudent diet with whole-grain cereals, low-fat dairy products, fruit, vegetables and refined fats generally considered healthy.

All patients had increased blood sugar after carbohydrate intake (glucose intolerance), and most of them had overt diabetes type 2. In addition, all had been diagnosed with coronary heart disease. Patients in the Paleolithic group were recommended to eat lean meat, fish, fruit, vegetables, root vegetables and nuts, and to avoid grains, dairy foods and salt.

The main result was that the blood sugar rise in response to carbohydrate intake was markedly lower after 12 weeks in the Paleolithic group (-26%), while it barely changed in the Mediterranean group (-7%). At the end of the study, all patients in the Paleolithic group had normal blood glucose.

Here's a problem I see: it is a clinical study in Sweden. It stands to reason that Swedes would not be the best test case for a Mediterranean diet. Consider that agriculture became normative in Sweden about 5,000 years ago, 5,000 years after it was the dominant mode of production in the eastern Mediterranean. Note that Sweden is also the epicenter lactose tolerance (thought that seems to have become the norm after agriculture arrived on the scene), suggesting a priori expectation of localized adaptations. In any case, I think one should be cautious about broad generalizations about diet across cultures. Not only jas there been a lot of evolution in regards to the human metabolization of nutritional intakes, we shouldn't be surprised if many of these propensities are local. Selection thinks globally, but acts locally.

Related: All diabetes, all the time.

Labels: Genetics

Reguar GNXP reader Mencius has an interesting post titled The ultracalvinist hypothesis: in perspective. Mencius is one of those rare bloggers who focuses on occasional essays where he develops his own ideas as opposed to a barrage of links and responses to the thoughts of others. Here's his introduction:

The "ultracalvinist hypothesis" is the proposition that the present-day belief system commonly called "progressive," "multiculturalist," "universalist," "liberal," "politically correct," etc, is actually best considered as a sect of Christianity.

Update: Cryptocalvinism slight tweaked, follow up post.

Labels: culture

Gene Variant Increases Risk For Alcoholism Following Childhood Abuse. We've been following this story for years in various forms. Here's the article in Molecular Psychiatry (a Nature journal). From the abstract:

The MAOA-LPR low activity allele was associated with alcoholism...particularly antisocial alcoholism...only among sexually abused subjects. Sexually abused women who were homozygous for the low activity allele had higher rates of alcoholism and ASPD, and more ASPD symptoms, than abused women homozygous for the high activity allele. Heterozygous women displayed an intermediate risk pattern...The MAOA-LPR low activity allele was found on three different haplotypes. The most abundant MAOA haplotype containing the MAOA-LPR low activity allele was found in excess among alcoholics...and antisocial alcoholics...Finally, a MAOB haplotype, which we termed haplotype C, was significantly associated with alcoholism...and to a lesser extent with antisocial alcoholism....

(the ellipses are p-values)

Labels: Genetics

The American Scene has just premiered as a new group blog with a fresh look & feel. Daniel Larison is a contributor. Now, keeping in mind that many of you use spiffy RSS readers with AJAX functionality which entails a non-trivial client side computational overhead be careful if you're on an older machine. Larison has a tendency to go "machine gun" in regards to post frequency and he might blow up your computer's CPU.

Labels: Blog

Well, turns out that The New York Times has a whole bundle of articles on evolution up right now (see the links below for some). Carl Zimmer tipped me off to this feature (he did the bug article below).

Labels: Evolution

The New York Times has a piece, Darwin Still Rules, but Some Biologists Dream of a Paradigm Shift, which alludes to rumblings under the foundations of the Modern Neo-Darwinian Synthesis. The standard allusions to evo-devo are in there, but this stuff struck me as kind of bizarre:

Transitions between species documented by the fossil record seemed to be abrupt, perhaps too abrupt to be explained by the modern synthesis. If this were generally true, it could render irrelevant much of natural selection occurring within species, because just as mutations are produced randomly with respect to the needs of a species, with selection shaping these into new adaptations, new species might evolve randomly with species selection shaping them into evolutionary trends. This challenge was greeted with less than fulsome praise by evolutionary biologists studying changes within species. The resulting hubbub has yet to fully die down. But the newer work cuts closer to the core of the modern synthesis, and is potentially more revolutionary, because it addresses the fundamental question of how really new things happen in the history of life. What brought about the origin of animals, or the invasion of land?

The bolded part, "perhaps" transforms into talk about species level selection. Frankly that strikes me as a bit much. Additionally, I think the "orthodox" view can handle rapid evolutionary changes followed by periods of stasis. Giving it a new name or added emphasis ("punctuated equilibria") does not a paradigm shift make. Evolutionary science as crystallized in the 1950s is not a canon. New findings will add nuance and insight to the pervasiveness of constraint & contingency, or the possibility of functional evolution being driven random walk processes. Perhaps you can call that a paradigm shift (i.e., it's something called science, not the the quarrel of the ancients and the moderns). But the allusive and indirect dance of the prose gets a bit tiresome. Give a paleontologist a pen and watch the erudition bleed out and obscure the potential clarity?

In other news, The New York Times has a piece about the study of evolutionary processes via microbial models. The very microevolutionary processes which the above article seems to imply might be a dead end.

Labels: Evolution

Humans Have Spread Globally, and Evolved Locally:

No one yet knows to what extent natural selection for local conditions may have forced the populations on each continent down different evolutionary tracks. But those tracks could turn out to be somewhat parallel. At least some of the evolutionary changes now emerging have clearly been convergent, meaning that natural selection has made use of the different mutations available in each population to accomplish the same adaptation.

This is the case with lactose tolerance in European and African peoples and with pale skin in East Asians and Europeans.

Nothing new to readers of this weblog, but Wade does a good job surveying the various angles.


Related articles on recent human evolution.

Labels: Evolution, Genetic

When talking about the genetics of intelligence, it's inevitable that some people feel a sense of moral outrage and grasp at any argument they can find to soothe it. Case in point:

[W]hile many behavioral traits have a heritable component, it's not anything like what the naive extremists among the cognitive science crowd think. There are no genes that specify what you will name your dog [WTF? -ed]- in fact, most of the genes associated with the brain have very wide patterns of expression and functions that are not neatly tied to behaviors: how does an allele of an adhesion factor map to your performance on a math test? It doesn't, not directly.

And how does an allele in a transcription factor map to your susceptibility to diabetes? Or how does an allele in some unknown gene map to your weight? Or how does an allele in a fatty acid gene map to Alzheimer's disease? They don't, not directly. Luckily, people are working on figuring out how that mapping function works.

This inanity was inspired by agreement with this post where some crazy...oh...wait:

So you're perfectly happy to agree that there is genetic variation in the human population which affects the facility with which various cognitive skills are learned, and so mental ability?

A: Sure.

Spontaneous Altruism by Chimpanzees and Young Children:

Debates about altruism are often based on the assumption that it is either unique to humans or else the human version differs from that of other animals in important ways. Thus, only humans are supposed to act on behalf of others, even toward genetically unrelated individuals, without personal gain, at a cost to themselves. Studies investigating such behaviors in nonhuman primates, especially our close relative the chimpanzee, form an important contribution to this debate. Here we present experimental evidence that chimpanzees act altruistically toward genetically unrelated conspecifics. In addition, in two comparative experiments, we found that both chimpanzees and human infants helped altruistically, regardless of any expectation of reward, even when some effort was required, and even when the recipient was an unfamiliar individual-all features previously thought to be unique to humans. The evolutionary roots of human altruism may thus go deeper than previously thought, reaching as far back as the last common ancestor of humans and chimpanzees.

The roots of altruism may go back quite far indeed; the elaboration and extension, not so much. After all, pigeons and rats have numeracy. Only humans have math. This might be the case where it is not the sufficiency of one necessary condition but the necessity of multiple conditions. Science Now has a summary.

Labels: Evolutionary Psychology

There have long been scholars who try to show that writing systems have been important players in world history (e.g., the Chinese system vs. the alphabetic ones). Chris of Mixing Memory reports some interesting data which suggests that these sort of conjectures need not just be hypotheses, at least on the first order level of effect:

However, recent evidence argues against this explanation. Several studies have shown that adults who learned to write in a right-to-left writing system (as in Hebrew), as opposed to left-to-right (as in English), tend to put agents on the right and patients on the left, with actions tending to be represented as moving from right to left. In other words, the inherent spatial aspect of action representations could be a product of the writing system we use, rather than the wiring of our brain....

...The fact that the children who couldn't write didn't show the bias, while adults educated in left-to-right and right-to-left writing systems showed opposite, language-consistent biases in agent placement strongly suggests that it is the writing system, and not the innate wiring of the brain, that our action representations are inherently spatial.

Labels: Cognitive Science

Martin Nowak, whose new book Evolutionary Dynamics is a must-read, recently gave an interview (PDF) for the Italian magazine Panorama. Unfortunately, it is only in Italian, so to put my break time to good use, I've translated it below. I'm fairly certain that everything is correct, but any errors are due only to me. See here for Razib's posts on Nowak's book.
- - - - -
[Headline]: Give, and ye shall receive: it's not the Gospel but Darwin
According to the American biologist and mathematician Martin Nowak, the motor of evolution and of survival of the species is altruism.
--by Chiara Palmerini

[Photo caption]: Equations of generosity. Martin Nowak. Below, the Amish, a community founded on mutual aid.

There was a pest that tormented biologists as early as Darwin: how is it that humans, and sometimes animals too, sacrifice themselves for others in a world that evolved according to the law of survival of the fittest? His successors have found some solutions. Richard Dawkins, for example, has maintained that the true selfish agents are genes, willing to do anything -- including to sacrifice an individual, for example the mother, to perpetuate themselves within the child. The problem is that altruism and generosity are not observed only among relatives. What next, then? In a singular reversal of perspective, the biologist and mathematician Martin Nowak maintains that cooperation, far from being a problem for evolution, is one of the laws that propels it, on a par with random mutation of DNA and natural selection. At Harvard, Nowak directs the program for evolutionary dynamics, in which mathematics is applied to the study of evolution. While passing through Varenna, Italy, for the conference Evolvability: the evolution of evolution, organized by the "Piero Caldirola" International Centre for the Promotion of Science, he responds to Panorama.

Why is cooperation a law of evolution?

Because it permits the construction of complexity. For example, it's cooperation between cells that leads to multicellular organisms. Without cooperation, the evolutionary process will not reach the highest levels.

Are cooperation and altruism the same thing?

According to most evolutionists, yes. But I think that the motivation should be important if it's altruism: the true altruist helps without selfish motives.

In your recent work in Science, you describe five mechanisms for the evolution of cooperation. What are they?

The first is cooperation among relatives, summed up by the motto of John B.S. Haldane: "I'd lay down my life for two brothers or eight cousins." But cooperation is also observed between people not related by blood. The rule that matters here is: "I scratch your back, you scratch mine," which still leaves out many aspects of cooperation among humans -- we help even those who will not be able to return the favor.

So then?

Then the rule of indirect reciprocity comes into play, which is typical of human societies. "You scratch my back, I'll scratch the back of someone else." Here reputation counts: helping someone serves to establish a good self-image, which will be rewarded by others. Even though some forms of indirect reciprocity are found among animals, only among humans does it develop fully. It's no accident that as a species we are very interested in gossip. Language could have evolved for acquiring information and spreading gossip, in tandem with indirect reciprocity.

Is not Darwinian generosity an oxymoron?

No, even in a situation where all compete against all, forgiveness and generosity can be a winning strategy.

You cite the Gospel as an example of indirect reciprocity: give, and ye shall receive. Evolution and religion, however, do not agree so much.

If you ask me, it's incorrect to interpret the theory of evolution as though it led necessarily to atheism.

Are you a believer?

Yes.
- - - - -

Labels: altruism, Evolution, Game Theory

Recently Razib posted on a review of sperm competition (PDF), part of which claims:

Kilgallon & Simmons [(2005)] documented that men produce a higher percentage of motile sperm in their ejaculates after viewing sexually explicit images of two men and one woman (sperm competition images) than after viewing sexually explicit images of three women.

Motile sperm are the kind that are capable of moving themselves by swimming. The idea is that if a guy watches a video with two guys and one girl, he'll try to leave more swimming sperm since they now have to compete with those of the other man (so his mind thinks). Now, the proper reaction is to think that two guys going at one girl simultaneously was probably as rare, or even more rare, in our evolutionary past than it is today, so how would we show an adaptation to it? Fortunately the study in question is available online for free -- here -- and it's only two pages long, so read it. Let's review the key findings.

In the Results, we read:

Subjects viewing images of sperm competition had a greater proportion of motile sperm in their ejaculates than those viewing images of females (52.1 +/- 7.3% versus 49.3 +/- 8.0%; F1,23=5.08, p=0.034).

That 3% difference in means is swamped by the standard-error bars of 7% - 8%, and the p-value, while under the 0.05 threshold, is uncomfortably close to it, considering the margin of error and the smallish sample size. So this result could easily be a fluke -- or not, but it warrants no confident statement that the study "documented" a pattern. "Somewhat suggested," perhaps, but gimme a break.

This equivocal data aside, it gets worse when the authors looked at the concentration of sperm per volume:

Men viewing images depicting sperm competition had fewer sperm in their ejaculate than those viewing images of females (61.35 +/- 1.27 versus 76.64 +/- 1.26 * 10^6 sperm ml^-1; F1,36=8.48, p=0.0061). [my emphasis]

Now the effect is clear, but it contradicts the hypothesis that men's bodies will make more of an effort to defeat the other male's sperm when watching "sperm competition" images. In fact, given these two findings, maybe "two guys on one girl" ought to be called "sperm anti-competition" images.

The strongest finding (read the paper for the data) was that men who thought the pornography was "more explicit" than what they'd seen previously had a much higher percentage of motile sperm and much higher concentration of sperm per volume. The authors suggest that men for whom this sort of pornography was old news had become habituated to it. That rings true anecdotally: I'm sure most guys recall how loudly their heart was pounding when they watched their first adult film.

This raises an interesting possibility: if it's largely the novelty factor that's causing men to produce more sperm, and more motile sperm, would this carry over into the case where novelty was based on the ethnicity of the girl? The study design would be pretty simple: recruit a bunch of Latino-American and Anglo-American men, and randomly assign them to two groups, one that watches a scene featuring one man and one woman of the same ethnicity as the viewer, and another that watches a scene featuring one man of the same ethnicity as the viewer and one woman of the opposite ethnicity (Latin or Anglo). Then see if "jungle fever" played any role in how much sperm the men produce. I'm assuming the actresses in all scenes would be rated beforehand to ensure that any guy would find them very attractive. That's why it has to be Latinos and Anglos -- Blacks and Anglos might not work simply because too many White men don't find Black women as attractive as women of other groups, and that could be a problem.

The other reason you might expect guys to produce more sperm when viewing a different-ethnicity girl is that throughout most of human history, including today in most parts of the world, it was incredibly rare to see someone from a noticeably different ethnic group. Even in the few cases where it happened, one of them would have been "just passing through" the other's region. Thus, the male would not know anything about her mating habits, and would have to assume the worst -- that she had a mate already. And if such encounters were fleeting, "strangers in the night" situations, then he would stand to gain everything by impregnating her. He'd never see her again, after all, so why not go the extra mile sperm-wise to make sure? Then he'd have another man raising his child: all benefit and little cost.

You could also look at sperm content from real-life interracial couples, but there could be confounding factors. Maybe if you conducted the research where there were hordes of youngsters who were more-or-less open to mating with anyone -- say, Cancun during Spring Break -- you might be able to collect enough subjects to randomly assign them to the real-life versions of the video study suggested above. "Y'know, as long as you're mating with any old person, why not take part in our study?"

Labels: Human Evolution, man-goo games