I like this hypothesis

But we have to be clear that it is only a hypothesis at this point. I was reading about domestication syndrome (DS) — selecting animals for domestication has a whole collection of secondary traits that come along for the ride, in addition to tameness. We are selecting for animals that tolerate the presence of humans, but in addition, we get these other traits, like floppy ears, patchy coat color, shortened faces, etc.; the best known work in this area is by Belyaev (YouTube documentary to get you up to speed) who selected silver foxes for domesticity, and got friendly foxes who also had all these other differences from their wilder brethren. Similar changes have been seen in rats and mink, so it seems to be a mammalian characteristic that all these differences are somehow linked. Here’s a handy list of the changes in domestication syndrome.

List of traits modified in the “domestication syndrome” in mammals

Trait Animal species Location/source
Depigmentation (especially white patches, brown regions) Mouse, rat, guinea pig, rabbit, dog, cat, fox, mink, ferret, pig, reindeer, sheep, goat, cattle, horse, camel, alpaca, and
Cranial and trunk
Floppy ears Rabbit, dog, fox, pig, sheep, goat, cattle, and donkey Cranial
Reduced ears Rat, dog, cat, ferret, camel, alpaca, and guanaco Cranial
Shorter muzzles Mouse, dog, cat, fox, pig, sheep, goat, and cattle Cranial
Smaller teeth Mouse, dog, and pig Cranial
Docility All domesticated species Cranial
Smaller brain or cranial capacity Rat, guinea pig, gerbil, rabbit, pig, sheep, goat, cattle, yak, llama, camel, horse, donkey, ferret, cat, dog, and mink Cranial
Reproductive cycles (more frequent estrous cycles) Mouse, rat, gerbil, dog, cat, fox, goat, and guanaco Cranial and trunk (HPG axis)
Neotenous (juvenile) behavior Mouse, dog, fox, and bonobo Cranial
Curly tails Dog, fox, and pig Trunk

(Hah, reduced brain size. I have a cat, I believe it.)

We have a very good idea of the proximate cause of tameness: the animals have reduced adrenal glands, which means their stress response is reduced, they’re generally less fearful, and they are more open, in early life at least, to socialization. But why can’t genetic mutations that reduce the size of the adrenal gland occur without also changing the floppiness of the ears? There isn’t an obvious physiological link between the two, or other traits in that list.

One idea is that there is a Genetic Regulatory Network (GRN). A GRN is a set of genes that mutually regulate each other’s expression, and may be controlled by the same set of signals. Imagine a lazily wired house in which the lights in the kitchen and the living room are on the same circuit, so you use one switch to turn them both on and off. Or perhaps you’ve cleverly wired in a simple motion sensor, so that when you trip the living room light, the changing shadows concidentally trigger the kitchen light too. Everything is tangled together in interacting patterns of connectivity, so you often get unexpected results from single inputs. The mammalian GRN works, though, so it’s been easier to keep it for a few tens of millions of years, rather than rewiring everything and risking breaking something.

More evidence that there’s a network involved is the fact that these domestication changes can happen incredibly rapidly — Belyaev was getting distinctive behaviors with only decades of selective breeding. What that means is that we’re not dealing with the sudden emergence of mutations of large effect, but with many subtle variations of multiple genes that are being brought together by recombination. This also makes sense. Rather than gross changes that change the entire GRN, what you are doing is tapping into small differences in a number of genes that individually have little or no effect, but together modify the target organ. So in order to change the size of an adrenal gland, you gather together an existing mutation that makes a tiny change in the size while also making ears floppier, and another one that also makes a tiny change in size while also shortening the snout, and another that makes a tiny change while modifying pigment cells.

That’s a very nice general explanation, but in order to advance our understanding we need something a little more specific. What genes? What links all these traits together?

Wilkins and his colleagues have suggested an obvious starting point: it’s all neural crest. Neural crest cells (NCCs) are an early population of migrating cells that infiltrate many tissues in the embryo — they form pigment cells, contribute to craniofacial cartilages, supporting cells for the nervous system, and just generally are found in precisely the places where we see the effects of domestication. So one reasonable hypothesis is that when you’re selecting for domestication, you’re actually selecting for reduced adrenal glands, which is most easily achieved by selecting for retarded or reduced or misdirected NCC migration or increased NCC apoptosis (multiple possible causes!), which has multiple effects.


In a nutshell, we suggest that initial selection for tameness leads to reduction of neural-crest-derived tissues of behavioral relevance, via multiple preexisting genetic variants that affect neural crest cell numbers at the final sites, and that this neural crest hypofunction produces, as an unselected byproduct, the morphological changes in pigmentation, jaws, teeth, ears, etc. exhibited in the DS. The hypothesized neural crest cell deficits in the DS could be produced via three routes: reduced numbers of original NCC formed, lesser migratory capabilities of NCC and consequently lower numbers at the final sites, or decreased proliferation of these cells at those sites. We suspect, however, that migration defects are particularly important. In this view, the characteristic DS phenotypes shown in parts of the body that are relatively distant from the sites of NCC origination, such as the face, limb extremities, tail, and belly midline, reflect lower probabilities of NCC reaching those sites in the requisite numbers. The stochastic, individual-to-individual variability in these pigmentation patterns is consistent with this idea.

They document all the phenotypic changes associated with domestication, and strongly correlate them with neural crest mechanisms. It’s a mostly convincing case … my major reservation is that because NCCs are ubiquitous and contribute to so many tissues, it’s a little bit like pointing at a dog and predicting that its features are a product of cells. It’s a very general hypothesis. But then they also discuss experiments, such as neural crest ablations or genetic neurocristopathies that directly modify the same processes involved in domestication syndrome. So it is a bit helpful to narrow the field from “all cells” to “this unique set of cells”.

I have a similar reservation about their list of genes that are candidates for the GRN — they list a lot of very familiar genes (PAX and SOX families, GDNF, RTKs) that are all broadly influential transcription factors and signaling molecules. Again, it helps to have a list of candidates, it’s a starting point, but in an interacting network, I’d be more interested in a summary of connections between them than in scattered points in the genome.

You need a diagram to summarize this hypothesis, and here it is, featuring the important distinction between selected and unselected traits.


I do have one question that wasn’t discussed in the paper, and would be interesting to answer with better genetic data. We talk about domestication syndrome as if it all goes one way: wild predator becomes more tolerant of humans. But it seems to me that it’s a two-way process of selection, and humans also had to be less stressed out and tolerant of sharing a space with an animal that would like to eat them, or compete with them for resources. Are humans self-domesticated apes? Were we selected for reduced neural crest input? If we figured out the changes in genes involved in domestication, it would be cool to look at dogs and cats and foxes, and then turn the lens around and ask if we experienced similar changes in our evolution.

Wilkins AS, Wrangham, RW and Fitch WT (2014) The “Domestication Syndrome” in Mammals: A Unified Explanation Based on Neural Crest Cell Behavior and Genetics. Genetics 197(3):795-808.

They don’t understand allometry!

I think the engineers are just trying to wind me up, again. Joe Felsenstein tackles a paper published in an applied physics journal that redefines evolution and tries to claim that changes in aircraft design are a good model for evolution. It’s a terrible premise, but also, the execution is awful.

But permit me a curmudgeonly point: This paper would have been rejected in any evolutionary biology journal. Most of its central citations to biological allometry are to 1980s papers on allometry that failed to take the the phylogeny of the organisms into account. The points plotted in those old papers are thus not independently sampled, a requirement of the statistics used. (More precisely, their error residuals are correlated). Furthermore, cultural artifacts such as airplanes do not necessarily have a phylogeny, as they can borrow features from each other in massive “horizontal meme transfer”. In either case, phylogeny or genealogical network, statistical analysis requires us to understand whether the points plotted are independent.

The paper has impressive graphs that seem to show trends. But looking more closely we notice that neither axis is actually time. If I interpreted the graphs as trends, I would conclude that birds are getting bigger and bigger, and that nobody is introducing new models of small airplanes.

And they really do redefine evolution.

Evolution means a flow organization (design) that changes over time.

I’m going to redefine bridge construction as gluing together lots of matchsticks. Hire me, everyone, to help fix your infrastructure problems! I can probably underbid everyone!

But it’s just kind of amazing that they’ve defined evolution without any mention of populations or shifting allele frequencies or any of the processes (which don’t include design) that lead to changes in genotype, or even a recognition of how these processes derive from a core unity and lead to diversity. Design done did it.

My big gripe is that they got this paper published that is all about allometry with scarcely any understanding of the concept. Here’s the abstract of The evolution of airplanes.

The prevailing view is that we cannot witness biological evolution because it occurred on a time scale immensely greater than our lifetime. Here, we show that we can witness evolution in our lifetime by watching the evolution of the flying human-and-machine species: the airplane. We document this evolution, and we also predict it based on a physics principle: the constructal law. We show that the airplanes must obey theoretical allometric rules that unite them with the birds and other animals. For example, the larger airplanes are faster, more efficient as vehicles, and have greater range. The engine mass is proportional to the body size: this scaling is analogous to animal design, where the mass of the motive organs (muscle, heart, lung) is proportional to the body size. Large or small, airplanes exhibit a proportionality between wing span and fuselage length, and between fuel load and body size. The animal-design counterparts of these features are evident. The view that emerges is that the evolution phenomenon is broader than biological evolution. The evolution of technology, river basins, and animal design is one phenomenon, and it belongs in physics.

Isn’t it cute how they claim biology as a small subset of physics? Blech.

But they only address a very narrow part of allometry. There is a functional constraint on form: you won’t survive if you have a human-sized body and a mouse-sized heart; if you scale the diameter of your legs linearly with your height, you won’t be able to walk; for a given metabolic rate and mass, you need a certain amount of respiratory surface area. That’s interesting stuff to a physiologist, but it’s also purely defined by necessity.

A developmental biologist might be more interested in how the relative sizes of different body parts change over time. Again, relative growth rates of different parts of your body are not linearly related; imagine being six feet tall with the same proportions as a baby. There are regulatory constraints on development that impose different rates in different areas.

But these guys are talking about evolution and allometry…and they treat it as a simple function of physics, where you need an engine of size X to propel a plane of size Y. Then how come every animal of the same size don’t look identical? Why doesn’t every passenger plane that carries a certain number of customers look the same (well, they do kind of blur together for me, but I’m sure any aerospace aficionado can tell me about all the differences between Boeing and Airbus. But many of these differences in animals are a result of inherited patterns, and phylogeny is essential to understand them.

For example, here’s a plot of brain mass relative to body mass (yeah, ugh, “lower” and “higher” vertebrates; let’s call them anamniotes and amniotes instead).


Notice that there are two lines drawn. Both show an upward trend, with a slope that’s proportional to the 2/3 power of the body size (that N2/3 shows up a lot in allometric growth plots). But given a fish (an anamniote, or “lower” vertebrate) and a mammal (an amniote, or “higher”) of exactly the same body mass, the mammal will have a relatively and absolutely much larger brain.

Explain that, engineer, with nothing but algebra and no concern about phylogenetic relationships. It takes more to understand evolution than physics alone, and you have to take into account history, environment, inherited properties, selection, and chance as important parameters.

Oh, well, I’ve learned that physics must be really simple. I can design a plane from the ground up if I simply postulate a spherical 747. Ha ha, all those fools getting engineering degrees when they could just bring in a clever biologist to solve all their trivial little problems.

Quote-mined by Casey Luskin!

Once again, Casey Luskin demonstrates that he’s a biological ignoramus. He is much buoyed by a science report that chloroquinone resistance in the malaria parasite requires two mutations, claims that Michael Behe has been vindicated because that’s exactly what he said, and demands an apology from all of Behe’s critics.

Will Ken Miller, Jerry Coyne, Paul Gross, Nick Matzke, Sean Carroll, Richard Dawkins, and PZ Myers Now Apologize to Michael Behe?


Here’s what his critics actually said. We have no problem with the idea that a particular functional phenotype requires a couple of mutations; I can think of lots of examples of that, such as the work of Joe Thornton on corticosteroid receptors. That the malaria parasite needs two mutations was never a point of contention, nor was it particularly worrisome. What was wrong with Behe’s work is that he naively claimed that the two mutations had to occur simultanously in the same individual organism, so that the probability that could happen was the product of multiplying the two individual probabilities. That’s ridiculous.

As Sean Carroll explained:

Behe’s main argument rests on the assertion that two or more simultaneous mutations are required for increases in biochemical complexity and that such changes are, except in rare circumstances, beyond the limit of evolution. .. Examples of cumulative selection changing multiple sites in evolving proteins include … pyrimethamine resistance in malarial parasites (6) — a notable omission given Behe’s extensive discussion of malarial drug resistance.

To show that the activity required two mutations, as the new paper says, is not an issue; it would have to claim that two simultaneous mutations were required, and that the cumulative accumulation of mutations in the population does not happen. And Behe goes further and declares on the basis of his bogus calculations that no evolution, beyond minor changes in a species or genus, occur at all.

So it’s weird to see Luskin announce that I’ve already conceded Behe’s point. No, I have not.

What we’ll probably get is nothing more than PZ Myers’s concession, offered in the context of the rant quoted above:

Fair enough; if you demand a very specific pair of amino acid changes in specific places in a specific protein, I agree, the odds are going to be very long on theoretical considerations alone, and the empirical evidence supports the claim of improbability for that specific combination.

Well, that’s more or less what’s required to generate chloroquine resistance. We’ll gladly take this — i.e., simply being proven right — in lieu of an apology.

Yet if you actually read the post in question, you’ll see that I’m not conceding that Behe is right — I’m explaining that a low probability is not a barrier to evolution.

Yet his argument for this dramatic conclusion is not only weak, it’s wrong. I could, for instance, correctly argue that the odds of getting a straight flush dealt to you in a 5 card poker hand is about 1 in 6×104; we could calculate this with probability theory, and we could also deal lots of poker hands and determine it empirically. No one’s going to argue with that part of the math.

But now, if I were to define a Straight Flush Complexity Cluster (SFCC) parameter and wave it around and claim that “no hand of the same complexity as a straight flush has been dealt by chance in the last ten years of poker games here in town,” that players can only possibly win one hand in 60,000, or worse, that no one has won a poker hand without cheating and stacking the deck, you’d know I was crazy. But that is basically Behe’s entire argument — he claims to have found the “edge of evolution,” and that it is much sharper and steeper and more impassable than anyone but a creationist could believe.

I’m flattered that Luskin thinks a concession from me would be so significant, but he ought to wait until I’ve actually made one before declaring victory.

Ken Miller wrote to second my comments:

With respect to the malaria mutations, your rebuttal is exactly correct. I’m attaching my review of Behe’s book in Nature. The portion of that review that directly deals with Behe’s contention about two mutations is this:

Behe, incredibly, thinks he has determined
the odds of a mutation “of the same complexity”
occurring in the human line. He hasn’t. What
he has actually done is to determine the odds of
these two exact mutations occurring simultaneously
at precisely the same position in exactly
the same gene in a single individual. He then
leads his unsuspecting readers to believe that
this spurious calculation is a hard and fast statistical
barrier to the accumulation of enough
variation to drive darwinian evolution.
It would be difficult to imagine a more
breathtaking abuse of statistical genetics.

Then, later on, I wrote:

“Behe obtains his probabilities by considering
each mutation as an independent event, ruling
out any role for cumulative selection, and
requiring evolution to achieve an exact, predetermined
result. Not only are each of these
conditions unrealistic, but they do not apply
even in the case of his chosen example. First,
he overlooks the existence of chloroquine resistant
strains of malaria lacking one of the
mutations he claims to be essential (at position
220). This matters, because it shows that there
are several mutational routes to effective drug
resistance. Second, and more importantly, Behe
waves away evidence suggesting that chloroquine
resistance may be the result of sequential,
not simultaneous, mutations (Science 298,
74–75; 2002), boosted by the so-called ARMD
(accelerated resistance to multiple drugs)
phenotype, which is itself drug induced.”

I hope these quotes are useful to you and your readers. As usual, Luskin is playing the “pretend” game of taking a new scientific paper and telling folks that it presents a “problem” for evolution. Ain’t life grand?

Best Wishes,


The difference between astronomers and biologists

The debate about intelligent, extra-terrestrial aliens goes on, with the usual divide: astronomers insisting that the galaxy must be swarming with alien intelligences, which is popular with the media, and the biologists saying no, it’s not likely, there are probably swarms of single-celled organisms, but big multicellular intelligences like ours are probably rare. And the media ignores us, because that answer simply is not sufficiently sensational.

But we will fight back! Here’s an interesting review of the alien argument. There is actually a historical and conceptual reason why astronomers think the way they do.

In response [to a paper arguing that SETI was a waste of time], Sagan co-wrote a paper with William Newman “The Solipsist Approach to Extraterrestrial Intelligence” which right from the title attacks Tipler for believing Earth to be unique. Sagan is of course citing the Copernican Principle, which roughly states the Earth is NOT the center of the heavens. The Copernican Principle is the modern foundation for Astronomy, Cosmology and Relativistic Physics. Sagan thought anyone claiming the Earth to be special must be doing bad science. Here’s a typical quote: Despite the utter mediocrity of our position in space and time, it is occasionally asserted, with no sense of irony, that our intelligence and technology are unparalleled in the history of the cosmos. It seems to us more likely that this is merely the latest in the long series of anthropocentric and self-congratulatory pronouncements on scientific issues that dates back to well before the time of Claudius Ptolemy.

It’s all about our perception of the rules. Astronomers see a universe with uniform laws that set up similar patterns everywhere: stars, rocks, gas. Life is lumped in with rocks as a phenomenon that just pops up everywhere, and with their limited idea of biology, just see all life as life like ours. Biologists also see universal laws, but we know from our experience that those laws generate endless diversity — there are millions of species on this planet, and each one is unique.

Now unlike Astronomy, the discipline of Biology takes a highly favorable view of uniqueness. Evolution constantly discovers quirky and highly contingent historical paths. Biology takes it for granted that everybody is a special snowflake. In fact the third sentence of Tipler’s 1980 paper calls this out:

The contemporary advocates for the existence of such [extraterrestrial intelligent] beings seem to be primarily astronomers and physicists, such as Sagan (2), Drake (3), and Morrison (4), while most leading experts in evolutionary biology, such as Dobzhansky (5), Simpson (6) Francois (7), Ayala et al. (8) and Mayr (9) contend that the Earth is probably unique in harbouring intelligence, at least amongst the planets of our Galaxy.

And as quoted in Mark A. Sheirdan’s book, we have eminent Evolutionary Biologist Theodosius Dobzhansky (“Nothing in Biology Makes Sense Except in the Light of Evolution“) joining the fray:

In his article Dobzhanksy turned Sagan’s argument on its head. Dobzhansky cited the fact that of the more than two million species living on Earth only one had evolved language, extragenetically transmitted culture, and awareness of self and death, as proof that it is “fatuous” to hold “the opinion that if life exists anywhere else it must eventually give rise to rational beings.”

And here’s a nice, short table to summarize the differences.


I have to add that it is probably another of those universal laws that Darwinian replicators will expand to fill an empty ecosystem, but that there are many ways to do that. It’s also a rule that the replicators are exploiting short term advantages to supplant competitors — there is no teleological imperative that says Strategy X is a good one, because while it slows our species down for the next billion years, there’s a chance we might build spaceships two billion years from now. Spaceship building is never going to be a selectively advantageous feature — it’s only going to emerge as a spandrel, which might lead to a species that can occupy a novel niche. And that means that spaceship builders are only going to arise as a product of chance, which will mean they’re going to be very rare.

On the other hand, a species that does successfully exploit space as an ecosystem is going to have a phenomenally fascinating future history of radiating forms. Think of the first space colonizers as equivalent to the first cells that evolved a metabolism that allowed them to exist outside the coddled, energy-rich environment of a deep-sea vent. It’s only the first step in a long evolutionary process that’s going to produce endless forms most beautiful…and also unexpected variations. It’s silly to expect that the successful, thriving interstellar life forms will be bipeds adapted to life on a planetary surface, living in large metal shells as autonomous agents crewing a spaceship. The real thing would be alien, and probably terrifyingly incomprehensible.

So that’s what chemistry is good for…

Stinky stuff! This fits perfectly with my biased preconceptions. So here are two examples of chemistry used to analyze things you’d normally run away from.

The oldest traces of human poop have been dug out of a cave in Spain — and it’s Neandertal poop. It’s about 50,000 years old, and it’s been reduced to a compressed, thin smear of organic compounds, so I guess it isn’t actually so stinky anymore, but there was enough of it to analyze chromatographically. In case you’ve wondered your whole life about what Neandertal poop would look like, here you go.

Microphotographs of a slightly burned coprolite of putative human origin identified in El Salt Stratigraphic Unit X (sample SALT-08-13). The images under plane polarized light show the pale brown color and massive structure of the coprolite, as well as the common presence of inclusions, which are possibly parasitic nematode eggs or spores.

Microphotographs of a slightly burned coprolite of putative human origin identified in El Salt Stratigraphic Unit X (sample SALT-08-13). The images under plane polarized light show the pale brown color and massive structure of the coprolite, as well as the common presence of inclusions, which are possibly parasitic nematode eggs or spores.

Dead for 50 millennia, and what we know about this dead person is that they took a massive dump that was full of parasites. TMI.

I thought the paper was preliminary and rather general — they don’t or can’t make very specific conclusions, but then, I imagine they were excited to be the first to get any discussion of Neandertal feces into the scientific literature. We do know a couple of things: Neandertals ate both their meat and their vegetables, and they had gut bacteria with similar physiological properties to our own.

Taken together, these data suggest that the Neanderthals from El Salt consumed both meat and vegetables, in agreement with recent hypotheses based on indirect evidence. Future studies in Middle Palaeolithic sites using the faecal biomarker approach will help clarify the nature, role and proportion of the plant component in the Neanderthal diet, and allow us to assess whether our results reflect occasional consumption or can be representative of their staple diet. Also, this data represents the oldest positive identification of human faecal matter, in a molecular level, using organic geochemical methods.

Besides having corroborated our method and obtained the first evidence of an omnivorous Neanderthal diet from faeces, our results also have implications regarding digestive systems and gut microbiota evolution. Approaching the evolution of the human digestive system is difficult because there is no fossil record indicating soft tissue preservation. Our results show that Neanderthals, like anatomically modern humans, have a high rate of conversion of cholesterol to coprostanol due to the presence of bacteria capable of doing so in their guts. Further research will allow us explore this issue in the context of human evolution.

I said I had two unpleasant examples of useful chemistry, and here’s the second: using the characteristic odors of different stages of decay to quantify the time of death.

An international research team used two-dimensional gas chromatography time-of-flight mass spectrometry to characterise the odours that create this smell of death:  volatile organic compounds (VOCs).  By measuring the VOCs released from pig carcasses the team identified a cocktail of several different families of molecules, including carboxylic acids, aromatics, sulfurs, alcohols, nitro compounds, as well as aldehydes and ketones. The combination and quantities of these VOCs change as a function of time as a cadaver goes through different stages of decomposition.

I think I’m getting a sense of the difference between chemistry and biology. I prefer the bodily fluids in my subjects to be fresh, preferably spurting; chemists seem to favor observing the degradation and volatilization of fluids from dead things. Chemists may offer their repudiations of my sentiments in the comments.

Deconstructing metaphors

Oh, that’s right — that’s what philosophers are good for. They’re really good at questioning models. John Wilkins has been busily dismantling the cheap and easy metaphors we use to describe molecular biological concepts in a series of posts, taking on genes as language, other popular gene myths and metaphors, and explaining why genes aren’t information. The problem is that when we explain stuff we know well to students, we use metaphors and analogies to get across the initial ideas, and unfortunately, because scientists are human, the metaphors take on a life of their own and sometimes become the dominant paradigm for understanding the reality. And that can be hazardous.

I’ve lived through the era in which everyone started thinking of the genome as an elaborate computer program — we still have lots of people thinking that way, and in some ways it’s gotten worse as bioinformatics has brought in a synergy with computer science. But it’s not! It’s nothing like a series of instructions! This model has become a serious impediment to getting the new generation of advanced students to understand the biology, and worse, they try to shoehorn the biology into how they think a sophisticated computer program ought to work.

We’ve also got the problem of naive idiots thinking the metaphor is the thing and drawing false conclusions. The genome is a recipe, and every recipe needs a cook, therefore God, etc., etc., etc., ad nauseam.

Genes and DNA are one important component of a complex of compartmentalized biochemical reactions, in which every reaction product interacts with and influences the state of the whole. We’re seeing an excessive reductionism borne of the last 50 years of success in molecular biology, and it’s about time the pendulum swung back to a more balanced perspective. One gene tells us very little; you need to step back and look at the interactions of networks of gene products in a complex environment to understand what’s going on in the cell, and then you have to step back further to look at patterns of interactions between cells, and then further still to see how individuals interact with one another and the environment, and then you have to step way back to see how populations interact, and then, maybe then, you’re really talking about evolution.

This is a test

It’s true — I’ve heard a lot more about student protests of commencement speakers this year. At the Twin Cities branch campus of my university, for instance, there was an eruption of student activism over inviting war criminal Condoleeza Rice to give the commencement address — although part of the protest may have been over the fact that she would have been paid $150,000 to spew a few platitudes for 20 minutes.

We may have been missing the point. Zach Weinersmith explains the situation.


He then goes on to explain the reason behind these costly displays. I give you a choice. You can go read the rest of the comic, which is the easy way out. Or you can go read this paper by Joseph Henrich (pdf), titled “The evolution of costly displays, cooperation and religion: credibility enhancing displays and their implications for cultural evolution”, which will take rather more of your time, requires slogging through a little math and logic, but will enhance your credibility because of your investment in the subject.

The paper is also a little annoying because it will require looking at a university, or any other institution, through the same lens you would a religion. I made that sacrifice, though, so that you can see my opinion as justified and worthy by virtue of my effort.

Now I have to take my wife on a walk to the coffee shop…to help her “determine how much to commit to, or believe in, a particular representation”. I can tell that thinking this way is going to lead to a rather cynical transactional view of relationships.

Multi-component, schmulti-component

I’m having a light dinner while traveling off to a visit with Humanists of Minnesota, and I thought I’d deal with a little email. I got a request to address a fairly common creationist argument–here’s the relevant part of the claim.

As a member of the Greater Manchester Humanists I was recently involved in a discussion with the Ahmadi sect of Islam with regards to evolution. They had asked me to look at a couple of chapters in a book entitled ‘Revelation, Rationality, Knowledge and Truth by their prophet Mirza Tahir Ahmad. One of those chapters was called ‘The Blind Watchmaker who is also Deaf and Dumb’ – riffing badly on Dawkins’s book, of course. Suffice it to say, there was very little of any of that in the book, but during the discussion one of their number said he did not believe in neo-Darwinism because he could not see ‘how all the supporting and connecting mult-component systems could all have evolved as, for example, the eye, as it progressed through geological time.’

He quoted the hagfish and work done by Prof Trevor Lamb to show ‘just how complex those multi-component systems are’ – but when I looked up Lamb’s work it is quite obvious that he is a supporter of evolution, and that he in no way suggests that such complexity is divine in nature….!

Yep, he’s got us. If evolution were sequential, linear, and goal-directed, this would be a serious problem. If you’re used to imagining that the only way complexity can possibly emerge is by purposeful, serial action to build an end result, rather like putting together your furniture from Ikea or building a model airplane, then gosh, it all seems so impossible.

Unfortunately for the follower of Mirza Tahir Ahmad, none of that is true, and this is just a variant of the “it’s too complicated to evolve” argument, with more sciencey sounding words and references to misinterpreted fragments of the scientific literature.

Let’s consider the major misconceptions in the question.

  • Evolution isn’s sequential. It’s massively parallel. Massively. Humans have about 20,000 genes, and all of them are evolving at once, with trial runs in about 7 billion individuals. New variants are arising all the time, and then they’re tested to destruction in multiple combinations over time. Scrap your weird idea that the pieces of a complex system must be developed one at a time — they can’t, and all of them are being constantly tinkered with. It is the most badly designed scientific experiment or engineering program ever, with no controls and every variable getting randomly tweaked at random intervals. So don’t be surprised that multiple elements are getting juggled.

  • Evolution doesn’t care how it arrives at a solution — all that matters is the final effect on the organism. In the case of the eye, the viable end result is an organ with sufficient resolution and contrast, and various special purpose detectors for things like motion or looming. The organism doesn’t know or care how that comes about — it is born with a combination of attributes, and lives or dies by their success. It may have accomplished its end by, for instance, refining the lens, or fine-tuning the receptor, or building in secondary signal processing elements…or all of the above and more. The organism doesn’t care and doesn’t have any control. And in a massively parallel system, probably every level is being tinkered with, and the final solution is going to be multi-component. It would be weird if it wasn’t.

  • Evolution is not teleological. An organ like the eye is not being assembled to a set of specific, detailed instructions — it just has to work, or the organism is at a disadvantage to other organisms with better eyes. So a hodge-podge of solutions is accumulated, and the end result has all kinds of complexity. But you don’t get to argue after the fact that the details imply some specificity of purpose.

    For example, here’s a number: 343767. It’s kind of big, you might be tempted to argue that it’s a fancier or more complex number than, say, 300000 (you’d be wrong), or you might want to argue for the significance of individual digits, or find a pattern in it. Humans tend to do that. But the reality is that I just went to a random number service and asked for a 6 digit number. Similarly, eyes wandered through a random space constrained by functional requirements and ended up at a somewhat arbitrarily complex configuration — and different lineages followed different paths.

OK, that’s my off-the-cuff explanation scribbled up while I nibble on a fruit salad at a cafe in Minneapolis. The whole multi-component problem is a red herring contrived by inadequate minds that can’t see beyond their preconceptions.

Get ‘em young

I got to meet someone in Seattle who is working on an evolution book for four year olds — this is a great idea, because I remember shopping for kids’ books and their usual idea for introducing zoology was something about Noah’s Ark. But the real story is so much more interesting!

Rough sketches of the book, Grandmother Fish, are available online; those aren’t the final drawings, and the work will be done by KE Lewis, once funding is obtained. You can see the challenges of getting a sophisticated scientific concept across to very young children, but I think the current story does the job very well.


There will be a kickstarter later this week to get the project off the ground.