Category Archives: evolution

E. O. Wilson is Wrong Again — not About Math, but About Collaboration

So, stop me if you’ve heard this one.

Q: What’s the difference between E. O. Wilson and a stopped clock?

A: A stopped clock does not have unlimited access to a national media platform to push its ridiculous ideas on the public.


A couple of weeks ago, E. O. Wilson published a piece in the Wall Street Journal, where he argued that you don’t need math to be a great scientist. There are two parts of the argument. First, that science is more about conceptual thinking that does not require mathematical formalism to get at great ideas. Second, that when it comes time to mathematize, you can always find a mathematician to collaborate with.

He has already been taken to task in places like Slate and Huffington Post. The criticism in these pieces and most of the grumbling I’ve heard around the internet has been something along the lines of, “Nuh uh! Math is too important!” More specifically, that the era of math-free scientific discovery is over. That to operate at the frontier of science in the twenty-first century, you have to be able to grapple with the mathematical and statistical concepts required in the days of big data.

There’s something to that.

On the other hand, I’m sympathetic to what Wilson is trying to do here. I would hate to see anyone drop out of science because they don’t feel that they can keep up with the math. Of course, that’s partly because I think most people can do more math than they think they can, if you know what I mean.

But what I want to focus on here is Wilson’s view of collaboration. This, even more than math, is going to be the must-have talent of the twenty-first-century scientist. The thing about science is, an awful lot of it has been done. To get to the frontiers of human knowledge requires years of study, and, for those of us without super powers, a lot of specialization. At the same time, the most interesting and important problems often lie between areas of specialization, and require contributions from more than one area. Those most interesting and important problems are going to be solved by teams and networks of people who bring different skills to the table, and who are able to integrate their skills in a way that leads to a whole that is greater than the sum of the parts.

It’s that integration bit, I think, that Wilson does not really get. Wilson’s view of collaboration seems to go something like this: you make some observations about some biology, come up with some ideas, then you go find someone who can translate those into the language of mathematics.

Here’s the thing about translation, though. It can’t be unidirectional, or rather, it shouldn’t be unidirectional. At the risk of something or other (obscurity? pretentiousness?), I’m going to dip into poetry here. Robert Haas (Poet, Berkeley Professor, and Occupy hero), in addition to writing a bunch of his own extraordinary verse, has translated seven volumes of poetry by Czech Nobel laureate Czesław Miłosz. Or, more accurately, he collaborated with Miłosz to produce those translations.

After Miłosz’s death, Haas included their translation of Czesław Miłosz’s poem “O!” in his own volume Time and Materials. The poem is prefaced with this note about the translation process:

In his last years, when he had moved back to Kraków, we worked on the translation of his poems by e-mail and phone. Around the time of his ninetieth birthday, he sent me a set of poems entitled “Oh!” I wrote to ask him if he meant “Oh!” or “O!” and he asked me what the difference was and said that perhaps we should talk on the phone. On the phone I explained that “Oh!” was a long breath of wonder, that the equivalent was, possibly, “Wow!” and that “O!” was a caught breath of surprise, more like “Huh!” and he said, after a pause, “O! for sure.”  Here are the translations we made:

Now, if you’re not a writer and/or avid reader of poetry, it may seem strange to fuss over the difference between “Oh!” and “O!” But worrying about the difference between “Oh!” and “O!” is precisely the sort of thing that differentiates poetry from other forms of writing. Robert Frost famously defined poetry as “what gets lost in translation.” One way to unpack that statement is to say that translation can typically capture the basic meaning of words and phrases, but the part of writing that is poetry is the part that goes beyond that basic meaning. Poetry is about subtle differences in meaning. It is about connotation and cultural resonance. It is about the sounds that words make and the emotional responses that they trigger in someone who has encountered that word thousands of times before, in a wide variety of contexts.

These things almost never have simple one-to-one correspondences from one language to another. That means that a good translation of poetry requires a back-and-forth process. If you have a translator who is truly fluent in both languages — linguistically and culturally — this back-and-forth can happen within the brain of the translator. But, if your translation involves two people, who each bring their expertise from one side of the translation, they have to get on the phone every so often to discuss things like the difference between “O!” and “Oh!”

Doing mathematical or theoretical biology is exactly like this.

The theories and observations that build up in the biological domain exist in a language that is profoundly different from the language of mathematics. For theory in biology to be both accurate and relevant, it has to stay true to both of these languages. That means there has to be a vibrant, even obsessive, back-and-forth between the biological observations and concepts and the mathematical representations that attempt to capture and formalize them.

As in the poetry case, if you, as an individual scientist, have a deep understanding of the biology and a fluency in the relevant mathematics, that back-and-forth can happen in your own brain. Where E. O. WIlson is right is in his assertion that, if you don’t have the math, you can still make a contribution, by focusing on building your deep understanding of the biology, and then by finding yourself a mathematician you can collaborate with.

But there’s a trick.

If you’re going to follow this route, you have to sit down with your mathematician, and you have to walk through every single equation. You have to press them on what it means, and you have to follow the thread of what it implies. If you’re the mathematician, you have to sit down with your biologist and say, “If we assume A, B, and C, then mathematically that implies X, Y, and Z.” You have to understand where, in the biology, A, B, and C come from, and you have to work together to discover whether or not X, Y, and Z make any sense.

Basically, each of you has to develop some fluency in the other’s language, at least within the narrow domain covered by the collaboration. If you’re not willing to put in this level of work, then yes, you should probably consider a different career.

Now, maybe you think I’m being unfair to Wilson here. After all, he doesn’t explicitly say that you should hand your ideas over to the mathematicians and walk away. And obviously, I don’t have any privileged access to the inner workings of Wilson’s brain or the nature of his collaborations.

But let’s go back to a couple of years ago, when he collaborated with Martin Nowak and Corina Tarnita to write a controversial paper in which they argued that modeling the evolution of social behaviors based on “kin selection” was fundamentally flawed. That paper elicited a response from the community that is rare: multiple responses criticizing the paper on multiple fronts, including one letter (nominally) co-authored by nearly 150 evolutionary biologists.

I won’t go into the details here, as I have written about the paper and the responses multiple times in the past (here and here, in particular, or you can just watch my video synopsis of the criticism here).

Briefly, the controversial article (published in Nature, arguably the most prestigious journal for evolutionary biologists), completely misinterprets, misrepresents, and/or ignores the work done by other people in the field. It’s a little bit like if you published a physics paper where you said, “But what if the speed of light is constant in different frames of reference? No one has ever thought of that, so all of physics is wrong!” That’s an exaggeration, of course, but the flaws in Wilson’s paper are of this general type.

The weird thing about the paper is that it includes an extensive supplement, which cites much of the literature that is disregarded by the main text of the paper. It is exactly the sort of error that happens when you have something that is written by a disconnected committee, where the right hand does no know what the left hand is doing. Basically, it is hard to imagine a scenario in which someone could actually have understood the papers that are cited and discussed in the supplementary materials, and then turned around and, in good faith, have written that paper.

That leaves us with a few possible explanations. It could be that the authors were just not smart enough to understand what they were talking about. Or it could be that they deliberately misrepresented prior work to make their own work seem more original and important. For the purposes of our discussion here, let’s assume that neither of these explanations is accurate.

Instead, let’s assume that everyone involves is fundamentally competent, and was acting in good faith. In that case, perhaps the problem came from a failure of collaboration. E. O. Wilson probably knows more than just about anyone else in the world about the biology underlying the evolution of social behavior — especially among eusocial insects. Martin Nowak is a prominent and prolific mathematical biologist. Corina Tarnita was a postdoc at the time, with a background primarily in mathematics.

Wilson, as he acknowledges, lacks the mathematical skills required to really understand what the models of kin selection do and do not assume and imply. Tarnita, I imagine, has these skills, but as a young researcher coming out of math, perhaps lacked the biological knowledge and the perspective on the field to understand how the math related to the prior literature and the state of the field. Nowak, in principle, had both the mathematical skills and the biological experience to bridge this gap. He’s a curious case, though, as he, rather famously in the field, is interested in building and solving models, and has little interest in what has been done by other people, or in chasing down the caveats and nuanced implications of his work.

Among the three of them, Wison, Nowak, and Tarnita have all of the skills and knowledge required to write an accurate analysis of models of kin selection. But if assembling the requisite skills was all that was necessary, that Nature paper would have been very different — in much the same way that you could dump a pile of gears, shafts, and pistons in my driveway, and I could drive away in a Camaro.

The challenge of interdisciplinary collaboration is to combine your various skills in a way that creates something greater than the sum of the parts. If you can master this, you’ll be able to make great contributions to whatever field you apply your skills and interests to.

In the case of Wilson’s disastrous paper, what we got was a situation where the deficits that each of the researchers brought to the table combined to create something greater than the sum of the parts. Sadly, I get the feeling that Wilson does not understand this difference, that he thinks collaborating with mathematicians means explaining your intuition, and then waiting for them to “prove” them.

So, yes, you can be a great scientist in the twenty-first century, even if you don’t have great mathematical skills yourself. But, just as Robert Haas called up Czesław Miłosz on the phone to discuss the difference between “O!” and “Oh!” maybe you’re going to have to call up your mathematician collaborators to talk about the difference between O(x) and o(x). You don’t necessarily have to understand the difference in general, but you do need to understand the difference and its implications in the context of the system you’re studying, otherwise you’re not really doing science at all.

Two more from Fisher and Haldane

So, previously I introduced you to Darwin Eats Cake’s two newest characters, R. A. Fisher’s Pipe and J. B. S. Haldane’s Mustache. Well, the comedy duo have provided two more installations of their series, tentatively entitled, “Stuff Sitting in Jars on a Shelf, Talking.”

I would not necessarily have predicted this, but as it turns out, Fisher’s Pipe has a really juvenile sense of humor.

It’s sort of sad, really.

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Epigenetics and Homosexuality

So, last week featured a lot of news about a paper that came out in the Quarterly Review of Biology titled “Homsexuality as a Consequence of Epigenetically Canalized Sexual Development.” The authors were Bill Rice (UCSB), Urban Friberg (Uppsala U), and Sergey Gavrilets (U Tennessee). The paper got quite a bit of press. Unfortunately, most of that press was of pretty poor quality, badly misrepresenting the actual contents of the paper. (PDF available here.)

I’m going to walk through the paper’s argument, but if you don’t want to read the whole thing, here’s the tl;dr:

This paper presents a model. It is a theory paper. Any journalist who writes that the paper “shows” that homosexuality is caused by epigenetic inheritance from the opposite sex parent either 1) is invoking a very non-standard usage of the word “shows,” or 2) was too lazy to read the actual paper, and based their report on the press release put out by the National Institute for Mathematical and Biological Synthesis.

That’s not to say that this is a bad paper. In fact, it’s a very good paper. The authors integrate a lot of different information to come up with a plausible biological mechanism for epigenetic modifications to exert influence on sexual preference. They demonstrate that such a mechanism could be favored by natural selection under what seem to be biologically realistic conditions. Most importantly, they formulate their model into with clear predictions that can be empirically tested.

But those empirical tests have not been carried out yet. And, in biology, when we say that a paper shows that X causes Y, we generally mean that we have found an empirical correlation between X and Y, and that we have a mechanistic model that is well enough supported that we can infer causation from that correlation. This paper does not even show a correlation. It shows that it would probably be worth someone’s time to look for a particular correlation.

As a friend wrote to me in an e-mail,

I found it a much more interesting read than I thought I would from the press it’s getting, which now rivals the bullshit surrounding the ENCODE project for the most bullshitty bullshit spin of biology for the popular press. A long-winded-but-moderately-well-grounded-in-real-biology mathematical model does not proof make.


Okay, now the long version.

The Problem of Homosexuality

The first thing to remember is that when an evolutionary biologist talks about the “problem of homosexuality,” this does not imply that homosexuality is problematic. All it is saying is that a straightforward, naive application of evolutionary thinking would lead one to predict that homosexuality would not exist, or would be vanishingly rare. The fact that it does exist, and at appreciable frequency, poses a problem for the theory.

In fact, this is a good thing to keep in mind in general. The primary goal of evolutionary biology is to understand how things in the world came to be the way they are. If there is a disconnect between theory and the world, it is ALWAYS the theory that is wrong. (Actually, this is equally true for any science / social science.)

Simply put, heterosexual sex leads to children in a way that homosexual sex does not. So, all else being equal, people who are more attracted to the opposite sex will have more offspring than will people who are less attracted to the opposite sex.

[For rhetorical simplicity, I will refer specifically to “homosexuality” here, although the arguments described in the paper and in this post are intended to apply to the full spectrum of sexual orientation, and assume more of a Kinsey-scale type of continuum.]

The fact that a substantial fraction of people seem not at all to be attracted to the opposite sex suggests that all else is not equal.

Evolutionary explanations for homosexuality are basically efforts to discover what that “all else” is, and why it is not equal.

There are two broad classes of possible explanation.

One possibility is that there is no biological variation in the population for a predisposition towards homosexuality. Then, there would be nothing for selection to act on. Maybe the potential for sexual human brain simply has an inherent and uniform disposition. Variation in sexual preference would then be the result of environmental (including cultural) factors and/or random developmental variation.

This first class of explanation seems unlikely because there is, in fact, a substantial heritability to sexual orientation. For example, considering identical twins who were raised separately, if one twin is gay, there is a 20% chance that the other will be as well.

Evidence suggests that sexual orientation has a substantial heritable component. Image: Comic Blasphemy.

This points us towards the second class of explanation, which assumes that there is some sort of heritable genetic variation that influences sexual orientation. Given the presumably substantial reduction in reproductive output associated with a same-sex preference, these explanations typically aim to identify some direct or indirect benefit somehow associated with homosexuality that compensates for the reduced reproductive output.

One popular variant is the idea that homosexuals somehow increase the reproductive output of their siblings (e.g., by helping to raise their children). Or that homosexuality represents a deleterious side effect of selection for something else that is beneficial, like how getting one copy of the sickle-cell hemoglobin allele protects you from malaria, but getting two copies gives you sickle cell anemia.

It was some variant of this sort of idea that drove much of the research searching for “the gay gene” over the past couple of decades.  The things is, though, those searches have failed to come up with any reproducible candidate genes. This suggests that there must be something more complicated going on.

The Testosterone Epigenetic Canalization Theory

Sex-specific development depends on fetal exposure to androgens, like Testosterone and related compounds. This is simply illustrated by Figure 1A of the paper:

Figure 1A from the paper: a simplified picture of the “classical” view of sex differentiation. T represents testosterone, and E represent Estrogen.

SRY is the critical genetic element on the Y chromosome that triggers the fetus to go down the male developmental pathway, rather than the default female developmental pathway. They note that in the classical model of sex differentiation, androgen levels differ substantially between male and female fetuses.

The problem with the classical view, they rightly argue, is that androgen levels are not sufficient in and of themselves to account for sex differentiation. In fact, there is some overlap between the androgen levels between XX and XY fetuses. Yet, in the vast majority of cases, the XX fetuses with the highest androgen levels develop normal female genitalia, while the XY fetuses with the lowest androgen levels develop normal male genitalia. Thus, there must be at least one more part of the puzzle.

The key, they argue, is that tissues in XX and XY fetuses also show differential response to androgens. So, XX fetuses become female because they have lower androgen levels and they respond only weakly to those androgens. XY fetuses become male because they have higher androgen levels and they respond more strongly to those androgens.

This is illustrated in their Figure 1B:

Sex-specific development is thus canalized by some sort of mechanism that they refer to generically as “epi-marks.” That is, they imagine that there must be some epigenetic differences between XX and XY fetuses that encode differential sensitivity to Testosterone.

All of this seems well reasoned, and is supported by the review of a number of studies. It is worth noting, however, that we don’t, at the moment, know exactly which sex-specific epigenetic modifications these would be. One could come up with a reasonable list of candidate genes, and look for differential marks (such as DNA methylation or various histone modifications) in the vicinity of those genes. However, this forms part of the not-yet-done empirical work required to test this hypothesis, or, in the journalistic vernacular, “show” that this happens.

Leaky Epigenetics and Sex-Discordant Traits

Assuming for the moment that there exist various epigenetic marks that 1) differ between and XX and XY fetuses and 2) modulate androgen sensitivity. These marks would need to be established at some point early on in development, perhaps concurrent with the massive, genome-wide epigenetic reprogramming that occurs shortly after fertilization.

The theory formulated in the paper relies on two additional suppositions, both of which can be tested empirically (but, to reiterate, have not yet been).

The first supposition is that there are many of these canalizing epigenetic marks, and that they vary with respect to which sex-typical traits they canalize. So, some epigenetic marks would canalize gonad development. Other marks would canalize sexual orientation. (Others, they note, might canalize other traits, like gender identity, but this is not a critical part of the argument.)

The model presented in this paper suggests that various traits that are associated with sex differences may be controlled by distinct genetic elements, and that sex-typical expression of those traits may rely on epigenetic modifications of those genes. Image:

The second supposition is that the epigenetic reprogramming of these marks that normally happens every generation is somewhat leaky.

There are two large-scale rounds of epigenetic reprogramming that happen every generation. One occurs during gametogenesis (the production of eggs or sperm). The second happens shortly after fertilization. What we would expect is that any sex-specifc epigenetic marks would be removed during one of these phases (although it could happen at other times).

For example, a gene in a male might have male-typical epigenetic marks. But what happens if that male has a daughter? Well, normally, those marks would be removed during one of the reprogramming phases, and then female-typical epigenetic marks would be established at the site early in his daughter’s development.

The idea here is that sometimes this reprogramming does not happen. So, maybe the daughter inherits an allele with male-typical epigenetic marks. If the gene influences sexual orientation by modulating androgen sensitivity, then maybe the daughter develops the (male-typical) sexual preference for females. Similarly, a mother might pass on female-typical epigenetic marks to her son, and these might lead to his developing a (female-typical) sexual preference for males.

So, basically, in this model, homosexuality is a side effect of the epigenetic canalization of sex differences. Homosexuality itself is assumed to impose a fitness cost, but this cost is outweighed by the benefit of locking in sexual preference in those cases where reprogramming is successful (or unnecessary).

Sociological Concerns

Okay, if you ever took a gender-studies class, or anything like that, this study may be raising a red flag for you. After all, the model here is basically that some men are super manly, and sometimes their manliness leaks over into their daughters. This masculinizes them, which makes them lesbians. Likewise, gay men are gay because they were feminized by their mothers.

That might sound a bit fishy, like it is invoking stereotype-based reasoning, but I don’t think that would be a fair criticism. Nor do I think it raises any substantial concerns about the paper in terms of its methodology or its interpretation. (Of course, I could be wrong. If you have specific concerns, I would love to hear about them in the comments.) The whole idea behind the paper is to treat chromosomal sex, gonadal sex, and sexual orientation as separate traits that are empirically highly (but not perfectly) correlated. The aim is to understand the magnitude and nature of that empirical correlation.

The other issue that this raises is the possibility of determining the sexual orientation of your children, either by selecting gametes based on their epigenetics, or by reprogramming the epigenetic state of gametes or early embryos. This technology does not exist at the moment, but it is not unreasonable to imagine that it might exist within a generation. If this model is correct in its strongest form (in that the proposed mechanism fully accounts for variation in sexual preference), you could effectively choose the sexual orientation of each of your children.

Image: Brainless Tales.

This, of course, is not a criticism of the paper. The biology is what it is. It does raise certain ethical questions that we will have to grapple with at some point. (Programming of sexual orientation will be the subject of the next installment of the Genetical Book Review.)

Plausibility/Testability Check

The question one wants to ask of a paper like this is whether it is 1) biologically plausible, and 2) empirically testable. Basically, my read is yes and yes. The case for the existence of mechanisms of epigenetic canalization of sex differentiation seems quite strong. We know that some epigenetic marks seem to propagate across generations, evading the broad epigenetic reprogramming. We don’t understand this escape very well at the moment, but the assumptions here are certainly consistent with the current state of our knowledge. And, assuming some rate of escape, the model seems to work for plausible-sounding parameter values.

Testing is actually pretty straightforward (conceptually, if not technically). Ideally, empirical studies would look for sex-specific epigenetic modifications, and for variation in these modifications that correlate with variation in sexual preference. The authors note that one test that could be done in the short term would be to do comparative epigenetic profiling of the sperm of men with and without homosexual daughters.

As Opposed to What?

The conclusions reached by models in evolution are most strongly shaped by the set of alternatives that are considered in the model. That is, a model might find that a particular trait will be selectively favored, but this always needs to be interpreted in the context of that set of alternatives. Most importantly, one needs to ask if there are likely to be other evolutionarily accessible traits that have been excluded from the model, but would have changed the conclusions of the model if they had been included.

The big question here is the inherent leakiness of epigenetic reprogramming. A back-of-the-envelope calculation in the paper suggests that for this model to fully explain the occurrence of homosexuality (with a single gene controlling sexual preference), the rate of leakage would have to be quite high.

An apparent implication of the model is that there would then be strong selection to reduce the rate at which these epigenetic marks are passed from one generation to the next. In order for the model to work in its present form, there would need to be something preventing natural selection from finding this solution.

Possibilities for this something include some sort of mechanistic constraint (it’s just hard to build something that reprograms more efficiently than what we have) or some sort of time constraint (evolution has not had enough time to fix this). The authors seem to favor this second possibility, as they argue that the basis of sexual orientation in humans may be quite different from that in our closest relatives.

On the other hand this explanation could form a part of the explanation for homosexuality with much lower leakage rates.

What Happened with the Press?

So, how do we go from what was a really good paper to a slew of really bad articles? Well, I suspect that the culprit was this paragraph from the press release from NIMBios:

The study solves the evolutionary riddle of homosexuality, finding that “sexually antagonistic” epi-marks, which normally protect parents from natural variation in sex hormone levels during fetal development, sometimes carryover across generations and cause homosexuality in opposite-sex offspring. The mathematical modeling demonstrates that genes coding for these epi-marks can easily spread in the population because they always increase the fitness of the parent but only rarely escape erasure and reduce fitness in offspring.

If you know that this is a pure theory paper, this is maybe not misleading. Maybe. But phrases like “solves the evolutionary riddle of homosexuality” and “finding that . . . epi-marks . . . cause homosexuality in opposite-sex offspring,” when interpreted in the standard way that I think an English speaker would interpret them, pretty strongly imply things about the paper that are just not true.

Rice, W., Friberg, U., & Gavrilets, S. (2012). Homosexuality as a Consequence of Epigenetically Canalized Sexual Development The Quarterly Review of Biology, 87 (4), 343-368 DOI: 10.1086/668167

Update: Also see this excellent post on the subject by Jeremy Yoder over at Nothing in Biology Makes Sense.

Two new characters at Darwin Eats Cake

So, if you’re a regular reader of Darwin Eats Cake, you’ll already know that two new characters have been introduced to the strip: R A Fisher’s Pipe and J B S Haldane’s Moustache.

If you’re not a regular reader, you should be, because it will make me happy (and it is, after all, the holiday season), and also because Robert Gonzales once called it “my [meaning Robert’s] new favorite webcomic” over at io9.

For those of you who are not population geneticists, or at least evolutionary biologists, Fisher and Haldane are two of the major figures of the “modern synthesis” in evolution in the first part of the twentieth century. This was basically the integration of the Mendelian idea of the gene with the Darwinian idea of gradual change via natural selection. Fisher, in addition, created a whole lot of modern statistics, which have found applications far outside of evolutionary biology.

R. A. Fisher smoking his pipe. Not a euphemism.
J. B. S. Haldane, um, I guess, having his mustache. Note the lack of “o” in the American spelling of mustache.

Fisher loved himself a good smoke. In fact, late in his life, he publicly challenged research purporting to show a causal link between smoking and lung cancer. Oops.

Haldane once chased my former officemate and his mother down the street in a rainstorm in Calcutta to offer them an umbrella.

These two anecdotes provide all the information you need to accurately reconstruct the political views of each.

Fisher passed away in 1962, and Haldane in 1964. Fortunately, one of the most salient features of each was preserved in a jar for posterity. And now, half a century later, the two have reunited to bring you their genetically inspired comedy stylings.

Here’s what you’ve missed so far:

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Legitimate rape, seminal priming, and preeclampsia

So, as you are well aware, a couple of days ago, human-shaped pile of garbage Todd Akin articulated his belief that “legitimate rape” rarely leads to pregnancy, due to the magical uterine “shutting that whole thing down” properties of the uterus. Here at Lost in Transcription, we discussed the fact that there are some species that do, in fact, exhibit the capacity for “post-copulatory female choice.” However, humans are not one of these species, unless you count the set of medical interventions that Akin is trying to outlaw (along with Romney, Ryan, and the official Republican party platform).

If you’re interested, Kate Clancy wrote up an excellent summary of the actual science on the topic of pregnancy and rape.

Jesse Bering (an evolutionary psychologist who has been featured on this blog previously) also weighed in on the science, using twitter to point to an article that had recently written on “Darwin’s Morning After Pill.” In the article, Bering outlines an argument for the adaptive value of preeclampsia. The argument features “seminal priming theory,” which Bering calls “criminally unread,” and which has been promoted by Gordon Gallup (who, like a certain goat I know, has an adaptationist story for just about everything).

Roughly, the argument is this. Women don’t want to let a man get them pregnant unless they are certain that the man is going to stick around for the long haul. So, you want to have a biological mechanism that prevents pregnancy from one-night stands, but encourages pregnancy when you are in a committed relationship. Preeclampsia is a convenient (if life threatening) way for mother nature to terminate your pregnancy when it would be better not to have a baby. Therefore, preeclampsia should be more common for pregnancies resulting from sex with an unfamiliar male. Preeclampsia should be less common when it is the product of a long-term sexual relationship.

The proposed mechanism is that exposure to a male’s semen sort of habituates the female to the biochemistry of that particular male. Preeclampsia is associated with certain inflammatory features that share some similarities with an immune response. In that sense, preeclampsia is sometimes thought of as the mother rejecting the foreign body of the fetus, sort of like how one might reject a transplanted organ. The idea, then, is that through exposure to the male’s semen, the female ratchets down this response, thereby allowing the pregnancy to move forward.

One way of thinking about preeclampsia is as the rejection of an alien body by the mother

Jeremy Yoder has written a nice piece detailing how, even if we accept all of this, it is ridiculous to think of this mechanism as an adaptation. In particular, even under the most generous set of assumptions, natural selection acting on such a mechanism would be vanishingly small. And, of course, even to get there, you have to buy the typical evolutionary psychology assumption of an “environment of evolutionary adaptation” that looks an awful lot like the normative middle-class, suburban values of 1950s television America.

There are a few lines of evidence that are cited (by Bering, and in general) in support of the idea. The bulk of the evidence hinges on the observation that changing partners increases a woman’s probability of preeclampsia. For example, if your second pregnancy has the same father as your first pregnancy, you are less likely to develop preeclampsia than if the two pregnancies have different fathers. This is a finding that has been replicated a number of times, and with very large samples, so that’s pretty solid, right?

Actually, no. While the association between paternity switch and preeclampsia is true, it probably doesn’t mean what Bering and Gallup think it means, and the relevant data doesn’t actually support the seminal priming theory.

The problem is that a change in paternity correlates with time between pregnancies. So, if your two kids have different fathers, it is more likely that the two pregnancies were spaced farther apart. My reading of the literature is this: in every case where there is an association between paternity switching and preeclampsia, the study has not separately controlled for time between pregnancies. In each study where time between pregnancy is explicitly controlled for, the association with paternity switching vanishes. (See, e.g., this or this.)

In fact, controlling for time between pregnancies, if you have preeclampsia in your first pregnancy, switching partners actually makes you less likely to have preeclampsia in your second one. Don’t get too excited though. The converse is also true. If you don’t get preeclampsia in one pregnancy, switching partners makes you more likely to get it in the next one.

What that suggests (to me, anyway), is that some fathers are more likely to produce preeclampsia than others (or, alternatively, that the probability of preeclampsia depends on some interaction between the maternal and paternal genotypes). According to this explanation, if you don’t get preeclampsia, it means that you and your partner are at low risk. If you switch partners, though, you go back into the standard risk pool. (This interpretation is also consistent with this study, which followed fathers.)

There are a few other lines of evidence, which are cleaner in their implications. One study on artificial insemination finds preeclampsia more often in cases where the woman was inseminated with a stranger’s sperm than in cases where she was inseminated with her partner’s. There is also a study that finds that frequent oral sex correlates with a reduced risk of preeclampsia. (That’s her performing oral sex on him, not the other way round.) Does the frequency of oral sex correlate with the spacing between kids? I don’t know. I’m hoping that some of you will weigh in on that in the comments.

Males ingesting female gametes also has well documented health benefits.

The problem with these studies is that, unlike the partner-switching studies, we’re looking at small numbers. Whether or not they will hold up under more extensive analysis it not yet clear.

My read on the whole thing? At the moment, the data just isn’t there. All that exists in support of the seminal priming theory is an adaptationist fairy tale and a couple of small studies that have yet to be reproduced.

Oh, and also a whole bunch of studies that, if you cherry pick from among them, and ignore all of the studies that contradict them, support the theory. Of course, that’s pretty much true of any theory, which is exactly why evolutionary psychology continues to be such a booming field.

Post-copulatory female choice in crickets and Missouri

So, maybe you’ve seen the news today about Representative Todd Akin. He’s the republican nominee for Senate in Missouri, running this year against Claire McCaskill. In an interview he said that he opposed abortion in all circumstances, with no exception for rape, because rape does not lead to pregnancy, see, because, “If it’s a legitimate rape, the female body has ways to try to shut that whole thing down.” (Quotes on Jezebel, video here.)

After realizing that he sounded like a complete shithead, even for a contemporary Republican (and probably after receiving a scolding from national Republicans), he issued a statement in which he claims that he “misspoke,” which is politician speak for, “I accidentally said what I actually thought, and then discovered that it will negatively impact my election chances, so I’m going to lie now. No backsies!”

Although, to be fair to Akin, nowhere in his statement did he back down from the position that abortion should be outlawed without exception, merely that he would advocate for “justice.” Also, jobs!

Setting aside for the moment the woeful state of politics, is it true, or even possible, that the female body could have “ways to try to shut that whole thing down”?

Actually, in a lot of non-human animals, something sort of like that does exist.

In species where polyandry (where females mate with multiple males) is common, there is often competition for reproductive access both before and after copulation, where one male may participate in a larger share of a female’s reproduction. In many cases, this is going to be something like sperm competition, where differential reproductive success depends on traits associated with the sperm, and by extension, with the competing males. This is not really what we’re talking about, though.

In a few cases, you can actually get “post-copulatory female choice,” where it is clearly the female deciding whether or not to allow fertilization. One such set of cases occurs in some spiders and crickets, where the male transfers a spermatophore to the female. This is basically a bag full of sperm that is attached to the female during copulation. She may then modulate the success of the sperm through the amount of time she permits it to remain attached to her.

For example, here‘s a paper on field crickets that shows not only that females modulate spermatophore retention time in response to male song quality, but that this modulation is contingent on the female’s prior experience. This is important because it emphasizes the aspect of female choice.

But what about humans? Well, actually, yes. Human females have the capacity to engage in post-copulatory female choice, such that they do not necessarily have to give birth to their rapist’s child. It’s called safe, legal abortion. It still exists in this country, but if too many more Todd Akins get elected, the American female body will no longer have “ways to try to shut that whole thing down.”

Rebar, D., Zuk, M., & Bailey, N. W. (2011). Mating experience in field crickets modifies pre- and postcopulatory female choice in parallel Behavioral Ecology, 22, 303-309

The selfish herd

So, one of the most interesting questions in evolutionary biology is the origin of collective behaviors. This can be the complex division of labor that we see in social insects and human societies, flocking behavior in migratory birds, or microbial formation of biofilms. It can be predators engaging in collective hunting, or prey engaging in collective being hunted. It’s this last one that we’re going to be talking about today.

As with many questions in evolutionary biology, there are a couple of dimensions that people are interested in untangling: proximal and ultimate causation. Proximal explanations focus on the “how” part of the solution, as in, “what are the molecular, genetic, etc. mechanisms and environmental cues that result in this behavior?” Ultimate explanations focus on “why,” in the evolutionary sense of “what were the selective pressures that led to the evolution of this behavior?”

Herding or flocking behavior is a classic case. For example, why do sheep hang out in a big group, in contrast to say, leopards, which tend to be pretty solitary? There are a number of possible (and not mutually exclusive) ultimate explanations, but the most talked about one is probably defense against predators.

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Back in the mid-twentieth century, it was common for biologists to talk in fairly loose terms about collective behaviors having evolved as a result of their benefits to the group. Then, in 1966, G. C. Williams published Adaptation and Natural Selection, which dropped a lot of truth into the community. In particular, it emphasized the gene-centered view of natural selection that hit the public consciousness with Richard Dawkins’s 1976 book, The Selfish Gene, and which has remained the dominant paradigm in evolutionary biology ever since.

Williams demonstrated that group selection, while possible, will generally be a much weaker force than selection acting on the individual. Therefore, it is good practice to look for evolutionary explanations at this lower level. Given plausible adaptive stories at the individual and group levels, one should favor the individual-level story. While the two stories might not be mutually exclusive, individual-level selective pressures are more likely to have played an important role in  the evolution of any particular trait than group-level selective pressures (all else being equal, of course).

In 1971, W. D. Hamilton published a theoretical analysis that brought this individual-level perspective to herding behavior. Hamilton argued that all you need is for animals to be trying to evade predators as individuals. If there are other individuals of their type around, they just need to try to position themselves between other individuals. Here’s how Hamilton draws it:

This frog wants to position itself between the two frogs on the right. That way, when the sea snake comes up, it will eat one of the frogs at the edge, and the one in the middle will be safe.

All you need is for everyone to follow one simple rule: when a predator comes, position yourself between two other individuals. What you get then is a tight cluster of individuals.

You can actually try this at home. You probably need about eight or ten people. So, most of you might not be able to try this at home, but you could maybe try it at school or work. Have each person pick two other people in the group (but don’t tell who your picks are). Then, everyone tries to get between the two people they picked. What you’ll get is something a lot like a cluster of frogs climbing all over each other to get away from a sea snake.

Frogs maneuvering to get between other frogs results in the formation of a clusterf**k of frogs. I know, right? I was surprised, too, but my herpetologist friends assure me that “clusterf**k” is the official collective noun for a group of frogs. Don’t even ask about sea snakes. You don’t want to know.

Bonus activity: after you’ve disentangled yourselves from the frogpile, try this one. Each person picks two people again, labeling them “A” and “B” (in your head). Again, no one needs to say whom they picked. Now, each person should position themselves so that their “A” person is between them and their “B” person. If it helps, imagine that “A” is Mitt Romney, that “B” is the American People, and you are Mitt’s tax returns. Your job is to position yourself so that Mitt keeps the American People from seeing you. I won’t spoil how it comes out.

So, Hamilton’s model provides a nice, simple model that can produce the observed behavior. The model is attractive because (1) it requires selection only at the level of the individual, and (2) it requires each individual only to follow a very simple behavioral rule. The collective behavior is an emergent property requiring no coordination at the group level.

Now, there’s a new paper out that is attempting to look at this empirically, in sheep. The study involves strapping adorable GPS backpacks on a bunch of sheep (Figure 1c, below) and then letting a sheepdog chase them around.

You can look at the movies here. It’s only a brief communication, and does not really nail anything down, but the authors interpret their results as broadly consistent with the selfish herd model. In particular, they are able to see that individual sheep seem to be trying to get to the center of the flock.

The cool thing is more the potential for this type of experiment. Yes, Hamilton’s model is attractive and parsimonious, but if we want to understand the rules that actually govern the behavior of sheep when they are faced with a predator (or, in this case, an annoyator), we will need to get good quantitative data on individual behaviors in a variety of contexts.

Plus, look at that little GPS backpack!

I’ll leave you with this.

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King AJ, Wilson AM, Wilshin SD, Lowe J, Haddadi H, Hailes S, & Morton AJ (2012). Selfish-herd behaviour of sheep under threat. Current biology : CB, 22 (14) PMID: 22835787

Hamilton, W. D. (1971). Geometry for the Selfish Herd Journal of Theoretical Biology, 31, 295-311 DOI: 10.1016/0022-5193(71)90189-5

How to pronounce "Muller’s Ratchet"

So, how would you pronounce the name “Muller”? According to the standard pronunciation rules of American English, it should sound like a word that means “one who mulls,” with the “u” pronounced like the “u” in mullet. Curiously, however, when evolutionary biologists talk about “Muller’s ratchet,” more often than not they will pronounce the name so that it rhymes with “Bueller,” as in “Hermann Mueller’s Day Off.”

[Aside: Muller’s ratchet refers to a model in which deleterious mutations arise in a population, but there are no beneficial mutations. An individual’s fitness is a decreasing function of the number of deleterious mutations they possess. These deleterious mutations are held in check by purifying selection, such that there is a steady-state distribution of the population into fitness classes. The “ratchet” part refers to the fact that, in a finite population, stochastic fluctuations will eventually lead to the loss of the highest fitness class. The whole distribution then shifts down. This progresses in a ratchet-like fashion, and the fitness of the whole population declines over time. The take-home point is that purifying selection alone is not sufficient to preserve adaptation indefinitely. You also need some number of beneficial mutations to maintain fitness in the long run. Recombination can reconstitute higher fitness classes, reversing the ratchet in the short term, but still leaves the system susceptible to the stochastic fixation of deleterious mutations.]

If you ask one of these evolutionary biologists why they pronounce “Muller” like “Mueller,” they will often point you towards the umlaut on the u (or, somewhat equivalently, the e following the u). The thing is, there is no umalut, nor is there an e. Sometimes they will point to the fact that Muller was German, and that therefore, you know, it should sound more German. Except for the fact that Muller was not German. He was born in New York City. His parents were also born in the United States.

Now, according to Wikipedia:

H. J. Muller and science fiction writer Ursula Le Guin were second cousins; his father (Hermann J. Muller Sr.) and her father’s mother (Johanna Muller Kroeber) were siblings, the children of Nicholas Müller who immigrated to the United States in 1848.

That’s sort of cool about Ursula Le Guin. It also suggests that Muller’s grandfather was, in fact, named “Müller,” which would not really be pronounced the way that people say “Mewler,” but that would at least be the more standard Americanization of the name. What it looks like is that Muller’s grandfather changed his name (either by choice, or by orthographical fiat, as was often the case at Ellis Island). It would not surprise me if he pronounced it in the German fashion, but that the name became fully Anglicized over the course of the next couple of generations.

Of course, with names, I figure the rule is that the correct pronunciation is always how the person themselves pronounces (or, in this case, pronounced) it. On that point, all I can do is point to a seminar by Matt Meselson that I once attended. At the end of his talk, someone from the audience asked a question about “mewler’s ratchet.” Before answering, Meselson made the point that he had known Muller, and the Muller had pronounced it “Muller.” I have attempted to contact Muller’s surviving daughter for more direct confirmation, but have not heard anything back yet. If and when I do, I’ll post an update.

In the meantime, here’s a little mnemonic I’ve whipped up for you

There was once a professor named Muller
whose breakfast could not have been duller.
As his fitness crept down
with a ratcheting sound,
he said, “Man, I could go for a cruller!”

NB: I have also found no evidence that Muller ever lived in Nantucket.

FDA Recommends more Judicious use of Antibiotics in Agriculture

So, the FDA recently put out its report recommending that the agriculture industry reduce its use of antibiotics. Specifically, they urge that the use of antibiotics that are also used to treat humans be used more “judiciously.”

There are two specific widespread practices that the FDA aims to discourage: 1) the use of antibiotics to make animals gain weight faster, and 2) prophylactic use of antibiotics to prevent the outbreak of a disease, even in the absence of any indication that such an outbreak is likely. Both of these are commonly achieved by feeding animals a constant, low dose of antibiotics in their feed or water. This constant-low-dose scheme is, of course, optimal, assuming that your goal is to maximize the rate at which bacteria acquire antibiotic resistance.

As per the FDA’s website, the plan is this: “implementing a voluntary strategy to promote the judicious use in food-producing animals of antibiotics that are important in treating humans,” which basically means leaving it up to the food producers themselves. So, you can fully expect that absolutely nothing will happen, and that you will still die a very slow, painful death from a virulent antibiotic-resistant bacterial infection.

Nature Reviews Microbiology has just published an editorial on the topic in which they point out that these steps by the FDA are not nearly enough, and they provide this depressing tidbit:

In 1977 the FDA began a process which could have resulted in a similar ban to that seen in the EU, by issuing notice of their intention to hold hearings into the withdrawal of approval for the use of penicillin and tetracycline in animals. However, these hearings never took place, and in December 2011 the agency announced that these notices had been formally withdrawn. 

Really, FDA? Are you really that incompetent and corrupt? Don’t answer that, it was a rhetorical question.

Anyway, here’s a strip that appeared last year at Darwin Eats Cake, where Andy and Eleonora debate the use of antibiotics in agriculture. It’s from back before I increased the font size, so it is easier to read on the original site.

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Blue-eyed-people-are-all-related zombie news

So, you know how sometimes at night you’re lying in bed when you burp, but then the burp turns out to actually be you throwing up into your mouth just a little bit, and it tastes like a combination of whatever you ate for dinner and evil? Well, this is sort of like that.

Four years ago, a group of researchers from the University of Copenhagen published a nice paper on the genetics of blue eye color. In that paper they look at a bunch of Danish families in which some people have blue eyes and some have brown eyes (or, combination blue-brown eyes, which, for purposes of this study, are treated as non-blue). They also look at a small sample of non-Danish blue-eyed folks: five from Turkey and two from Jordan.

The paper makes a compelling case that the pure blue eyes phenotype depends on a particular nucleotide substitution that alters regulation of the gene OCA2. Furthermore, there is an extended haplotype around the key mutation that is shared by everyone in their sample (a few people have additional nucleotide substitutions that most likely post-date the key functional mutation). This suggests that, while there are many genes that contribute to eye color variation and to pigmentation in general, there may be a single critical mutation responsible for all of the blue eyes out there. Which is pretty cool.

For reasons that I still don’t understand, this study has popped back into the news recently. In particular, an article that looks to have been written back in 2008 in USA Today was “updated” in February, and has resurfaced on AOL, which describes it as a “study from USA Today,” and warns people with blue eyes about the dangers of falling in love with another blue-eyed beauty. Presumably because of incest (also shown is a clip from HLN — the artist formerly known as CNN Headline News — featuring the anchor doing a whole “ick” thing).

In worst-of-media-coverage-of-science fashion the reports that I have found (both from 2008 and from 2012), coverage focuses on stuff from the paper that is tangential, irrelevant, or wrong.

First, “all blue-eyed people are related.” Where to start. The researchers suggest that the mutation might have arisen 6000-10000 years ago in the Black Sea region, prior to the Neolithic agricultural expansion into Europe. If we assume a generation time of, say, 25 years, that is 240-400 generations. If we look back that far in the past, even just to the 6000 year mark, each of us has 2^240 ancestors. That’s 1.7 x 10^72, which, you will notice, is not just much larger than 7 x 10^9 (the current population of the whole world), but is close to the ballpark of the total number of atoms in the universe.

The fact is, once you go back more than a few hundred years, each of us has a list of ancestors that features the same people over and over again. Not only are we all related, we are all related over and over and over again. While your brother may not be your cousin, your tenth cousin is quite likely to be your seventh cousin as well.

So, yes, all blue-eyed people are related, but there is not really anything here to suggest that they are significantly more closely related than any two people.

Second, both the 6000-10000 year timeframe and the Black Sea origin of the mutation — both of which featured heavily in press coverage of the paper — are completely unsupported by anything in the data. What the authors actually say is this:

The mutations responsible for the blue eye color most likely originate from the neareast area or northwest part of the Black Sea region, where the great agriculture migration to the northern part of Europe took place in the Neolithic periods about 6–10,000 years ago (Cavalli-Sforza et al.1994).

The high frequency of blue-eyed individuals in the Scandinavia and Baltic areas indicates a positive selection for this phenotype (Cavalli-Sforza et al. 1994; Myant et al. 1997). Several theories has been suggested to explain the evolutionary selection for pigmentation traits which include UV expositor causing skin cancer, vitamin D deficiency, and also sexual selection has been mentioned. Natural selection as suggested here makes it difficult to calculate the age of the mutation.

That is, we don’t know how old the mutation is, and have not tried to perform any sort of analysis to ask the question. That’s fine, because what the paper actually does is provide us with a basis for asking these sorts of questions, although that will require more extensive sampling.

The supposition here is based solely on the fact that there was this expansion of agriculture (along with, to a not-fully-characterized extent, an expansion of the genes of the people who developed that early agricultural technology), and that stuff in Europe probably came with that.

The actual way to ask the question would be to go and sequence the DNA of a bunch of folks from all across Europe. To first approximation, we might assume that the mutation first arose in the region where the blue-eyes haplotype shows the greatest within-haplotype genetic diversity. For example, if the mutation first arose near the Black Sea, we should see more genetic variation right around the key mutation among blue-eyed people near the Black Sea. If the allele arrived more recently in Sweden, blue-eyed Swedes would be more genetically similar to each other in the same genomic region, simply because there would have been less time for differences to accumulate.

All else being equal, we might expect the geographical origin of a particular mutation to be at the central point of its range, or near the place where the mutation has reached its highest frequency. That supposition would place the origin somewhere near the Baltic (rather than the Black) Sea. But, there is good reason to believe that this mutation may have been subject to selection. The blue-eyes allele also affects other aspects of pigmentation, and lighter coloring is thought to have been favored at higher latitudes due to the reduced incidence of sunlight.

The fact that we think that natural selection would have pushed the mutation northward means that that its origin was probably somewhere to the South of its current center. Exactly how far depends on a bunch of details, like the strength of selection, and how that strength of selection changes as you move from South to North.

The problem is that, to do it right, you would have to build a model that explicitly incorporates the agricultural expansion and natural selection acting on OCA2, with the strength of selection favoring lighter pigmentation depending on latitude. Maybe also the fact that there are other genes affecting pigmentation. It is something that is doable, especially now that we have a specific gene to focus on, but at this point what we have is a bunch of speculation.

So, to recap, 1) Cool paper. 2) Sex between blue-eyed people is not incest. 3) We have no idea when or where this mutation came from, but it is now conceivable that we could ask the question. 4) Embarrassingly bad science reporting spontaneously rises from the grave four years later and tries to eat your brain.

Eiberg, H., Troelsen, J., Nielsen, M., Mikkelsen, A., Mengel-From, J., Kjaer, K., & Hansen, L. (2008). Blue eye color in humans may be caused by a perfectly associated founder mutation in a regulatory element located within the HERC2 gene inhibiting OCA2 expression Human Genetics, 123 (2), 177-187 DOI: 10.1007/s00439-007-0460-x