Evolution isn’t libertarian

Larry Arnhart wrote a strange article in which he tried to claim Darwin and evolution for libertarianism, or as they prefer to call it nowadays, “Classical liberalism”. I was invited to give a reply, along with a few other people, but I can give the gist of my reaction here: no one gets to claim a biological justification for their political philosophy. Evolution does not endorse libertarianism, socialism, communism, or capitalism, and even if it did nudge one way or the other, that does not mean that we shouldn’t oppose the brutal short-term expediency of natural processes.

Make love, not war

Who remembers Robert Ardrey? I must shamefully confess that I was a fan back in the 1970s, when the ‘killer ape’ hypothesis was in the air. This was the idea that one of the things that made humans different and drove the evolution of the human brain was aggression and competition, specifically that big brains evolved as a weapon in a multi-million year intra-specific arms race. Arms races are cool concepts that, when first introduced to natural selection, seem like powerful mechanisms to drive the evolution of elaborate features.

I outgrew Ardrey, have no fear. As I learned more biology, I came to mistrust those umbrella hypotheses that appeared to explain everything with one simple premise — biology is complicated, and rarely fits into those simple categories. I also began to get suspicious of poorly credentialed popularizers who too often seemed most adept at twisting research to fit whatever hobby horse they were riding at the time (see also Elaine Morgan).

But mostly, it didn’t fit what we see in the real world. Think about your interactions with other human beings: probably, unless you’re in the military, the most ferociously antagonistic conflicts you encounter involve commenting on Pharyngula. The internet has a reputation for being contentious, but get real: it’s slinging words back and forth, feelings might get hurt, but the consequences to your survival and mating prospects are very, very low. You could even argue that most of the jostling isn’t about destroying our enemies, but about increasing in-group solidarity.

It’s even more true outside the abstract world of the internet. Most of our interactions with other people are regulated by deep-down protocols that we’re socialized into — if someone cuts into a queue ahead of you, we don’t pull out a stone axe and take care of the problem, we either roll our eyes and acquiesce or we complain verbally and get other people to shame the interloper. It’s relatively harmless. We go to work, and maybe you share an office with annoying jerks (of course you do, we all do), but we don’t go on a rampage and fight the boss for dominance, so we can purge the tribe of the ones we detest, who borrow our stapler and don’t give it back — no, we grumble and accommodate and cope somehow, and maybe try to work our way into a better position with social networking.

It’s what we are. We are social animals. In the history of our species, I think the most important signature of our evolutionary history is the construction of cohesive social units, groups larger than the individual, that allow us to survive better together than alone. We aren’t warring animals, we’re cooperative animals.

War is a byproduct. We’ve evolved and enculturated mechanisms that allow groups of increasingly larger size to persevere — a paleolithic tribe of 30 people is one thing, a nation of hundreds of millions or billions is another — and war occurs when these groups bump into one another. War is not the central activity of the human species, though, but a fringe event, a side-effect of processes that reinforce group cohesion and secondarily create friction when diverse social units encounter one another and demand responses that aren’t so strongly reinforced within our groups.

Anyway, that long ramble is an introduction to an interesting article on the history of war in primates. It’s just not that common in our closest relatives, the chimpanzees, and recent accounts of coordinated gang attacks may be unusual responses to high environmental stresses. This is not a good time to be a chimpanzee.

There are known examples of death by lethal tools in the human archaeological record, and this isn’t an argument that everyone since the dawn of time has been living in peaceful coexistence, but the documentable evidence of war is very thin. People are lovers, not killers.

Archaeologist Jonathan Haas of the Field Museum in Chicago concurs: “There is a very tiny handful of incidences of conflict and possible warfare before 10,000 years ago. And those are very much the exception.” In an interview with me he attributed the emergence of warfare in prehistory to growing population density, diminished food sources and the separation of people into culturally distinct groups. “It is only after the cultural foundations have been laid for distinguishing ‘us’ from ‘them,'” Haas says, “that raiding, killing and burning appear as a complex response to the external stress of environmental problems.”

On the other hand, Haas adds, “groups that are at war in one era or generation may be at peace in the next.” War’s recent emergence, and its sporadic pattern, contradict the assertion of Wrangham and others that war springs from innate male tendencies, he argues. “If war is deeply rooted in our biology, then it’s going to be there all the time. And it’s just not,” he says. War is certainly not as innate as language, a trait possessed by all known human societies at all times.

That’s the good news: warfare is a pathological condition for our species, brought on by external stress. We are not biologically committed to fighting one another.

The bad news is that external stresses are growing, with increasing demands for oil and water and food, with looming climate change likely to disrupt environmental stability, and with overpopulation increasing the friction within and between groups. Brace yourselves.

I might suggest, though, that the greatest human successes have arisen from developing tools to strengthen social unity and encourage competition — killing your neighbors is a sign of failure.

Radial tree of life

I use a very pretty radial tree of life diagram fairly often — the last time was in my talk on Friday — and every time I do, people ask where I got it. Here it is: it’s from the David Hillis lab, with this description:

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This file can be printed as a wall poster. Printing at least 54″ wide is recommended.
(If you would prefer a simplified version with common names, please see below.)
Blueprint shops and other places with large format printers can print this file for you.
You are welcome to use it for non-commercial educational purposes.
Please cite the source as David M. Hillis, Derrick Zwickl, and Robin Gutell, University of Texas.
About this Tree: This tree is from an analysis of small subunit rRNA sequences sampled
from about 3,000 species from throughout the Tree of Life. The species were chosen based
on their availability, but we attempted to include most of the major groups, sampled
very roughly in proportion to the number of known species in each group (although many
groups remain over- or under-represented). The number of species
represented is approximately the square-root of the number of species thought to exist on Earth
(i.e., three thousand out of an estimated nine million species), or about 0.18% of the 1.7 million
species that have been formally described and named. This tree has been used
in many museum displays and other educational exhibits, and its use for educational purposes
is welcomed.

There’s also a simplified version:

i-c45f00d8b68f5ff488017d61358744dc-simple_tree_of_life.jpeg

Both of those are available as scalable pdfs, so you can zoom in and out to get just the right view, which is very handy.

More creationist misconceptions about the eye

Jonathan Sarfati, a particularly silly creationist, is quite thrilled — he’s crowing about how he has caught Richard Dawkins in a fundamental error. The eye did not evolve, says Sarfati, because it is perfectly designed for its function, and Dawkins’ suggestion that there might be something imperfect about it is wrong, wrong, wrong. He quotes Dawkins on the eye.

But I haven’t mentioned the most glaring example of imperfection in the optics. The retina is back to front.

Imagine a latter-day Helmholtz presented by an engineer with a digital camera, with its screen of tiny photocells, set up to capture images projected directly on to the surface of the screen. That makes good sense, and obviously each photocell has a wire connecting it to a computing device of some kind where images are collated. Makes sense again. Helmholtz wouldn’t send it back.

But now, suppose I tell you that the eye’s ‘photocells’ are pointing backwards, away from the scene being looked at. The ‘wires’ connecting the photocells to the brain run over all the surface of the retina, so the light rays have to pass through a carpet of massed wires before they hit the photocells. That doesn’t make sense…

What Dawkins wrote is quite correct, and nowhere in his refutation does Sarfati show that he is wrong. Instead, Sarfati bumbles about to argue against an argument that no biologist makes, that the eye is a poor instrument for detecting patterns of light. The argument is never that eyes do their job poorly; it’s that they do their job well, by a peculiar pattern of kludgy patches to increase functionality that bear all the hallmarks of a long accumulation of refinements. Sarfati is actually supporting the evolutionary story by summarizing a long collection of compromises and odd fixes to improve the functionality of the eye.

There’s a fundamental question here: why does the vertebrate eye have its receptors facing backwards in the first place? It is not the best arrangement optically; Sarfati is stretching the facts to claim that God designed it that way because it was superior. It ain’t. The reason lies in the way our eye is formed, as an outpocketing of the cortex of the brain. It retains the layered structure of the cortex, even; it’s the way it is because of how it was assembled, not because its origins are rooted in optical optimality. You might argue that it’s based on a developmental optimum, that this was the easiest, simplest way to turn a light-sensitive patch into a cup-shaped retina.

Evolution has subsequently shaped this patch of tissue for better acuity and sensitivity in certain lineages. That, as I said, is a product of compromises, not pre-planned design. Sarfati brings up a series of odd tweaks that make my case for me.

  1. The vertebrate photoreceptors are nourished and protected by an opaque layer called the retinal pigmented epithelium (RPE). Obviously, you couldn’t put the RPE in front of the visual receptors, so the retina had to be reversed to allow it to work. This is a beautiful example of compromise: physiology is improved at the expense of optical clarity. This is exactly what the biologists have been saying! Vertebrates have made a trade-off of better nutrient supplies to the retina for a slight loss of optical clarity.

  2. Sarfati makes the completely nonsensical claim that the presence of blood vessels, cells, etc. in the light path do not compromise vision at all because resolution is limited by diffraction at the pupil, so “improvements of the retina would make no difference to the eye’s performance”. This is clearly not true. The fovea of the vertebrate eye represents an optimization of a small spot on the retina for better optical properties vs. poorer circulation: blood vessels are excluded from the fovea, which also has a greater density of photoreceptors. Obviously, improvements to the retina do make a difference.

    It’s also not a condition that is universal in all vertebrates. Most birds, for instance, do not have a vascularized retina — there is no snaky pattern of blood vessels wending their way across the photoreceptors. Birds do have greater acuity than we do, as well. What birds have instead is a strange structure inside their eye called the pecten oculi, which looks kind of like an old steam radiator dangling into the vitreous humor, which seems to be a metabolic specialization to secrete oxygen and nutrients into the vitreous to supply by diffusion the retina.

  3. Sarfati also plays rhetorical games. This is a subtly dishonest argument:

    In fact, cephalopods don’t see as well as humans, e.g. no colour vision, and the octopus eye structure is totally different and much simpler. It’s more like ‘a compound eye with a single lens’.

    First, there’s a stereotype he’s playing to: he’s trying to set up a hierarchy of superior vision, and he wants our god-designed eyes at the top, so he tells us that most cephalopods have poorer vision than we do. He doesn’t bother to mention that humans don’t have particularly good vision ourselves; birds have better eyes. So, is God avian?

    That business about the cephalopod being like a compound eye is BS; if it’s got a single lens, it isn’t a compound eye, now is it? It’s also again pandering to a bias that our eyes must be better than mere compound eyes, since bugs and other lowly vermin have those. Cephalopods have rhabdomeric eyes, meaning that their photoreceptors have a particular structure and use a particular set of biomolecules in signal transduction, but that does not in any way imply that they are inferior. In fact, they have some superior properties: the cephalopod retina is tightly organized and patterned, with individual rhabdomeres ganged together into units called rhabdomes that work together to process light. Their ordered structure means that cephalopods can detect the polarity of light, something we can’t do at all. This is a different kind of complexity, not a lesser one. They can’t see color, which is true, but we can’t sense the plane of polarity of light in our environment.

    I must also note that the functions of acting as a light guide (more below) and using pigment to shield photoreceptors are also present in the cephalopod eye…only by shifting pigments in supporting cells that surround the rhabdome, rather than in a solid RPE. Same functions, different solutions, the cephalopod has merely stumbled across a solution that does not simultaneously impede the passage of light.

    Color vision, by the way, is a red herring here. Color is another compromise that has nothing to do with the optical properties of the arrangement of the retina, but is instead a consequence of biochemical properties of the photoreceptors and deeper processing in the brain. If anything, color vision reduces resolution (because individual photoreceptors are tuned to different wavelengths) and always reduces sensitivity (you don’t use color receptors at night, you may have noticed, relying instead on rods that are far less specific about wavelength). But if he insists, many teleosts have a greater diversity of photopigments and can see colors we can’t even imagine…so humans are once again also-rans in the color vision department.

  4. Sarfati is much taken with the discovery that some of the glial cells of the eye, the Müller cells, act as light guides to help pipe light through the tangle of retinal processing cells direct to the photoreceptors. This is a wonderful innovation, and it is entirely true that in principle this could improve the sensitivity of the photoreceptors. But again, this would not perturb any biologist at all — this is what we expect from evolution, the addition of new features to overcome shortcomings of original organization. If we had a camera that clumsily had the non-optical parts interposed between the lens and the light sensor, we might be impressed with the blind, clumsy intricacy of a solution that involved using an array of fiber optics to shunt light around the opaque junk, but it wouldn’t suggest that the original design was particularly good. It would indicate short-term, problem-by-problem debugging rather than clean long-term planning.

  5. Sarfati cannot comprehend why the blind spot would be a sign of poor design, either. He repeats himself: why, it’s because the eye needs a blood supply. Yes, it does, and the solution implemented in our eyes is one that compromises resolution. I will again point out that the cephalopod retina also needs a blood supply, and they have a much more elegant solution; the avian eye also needs a blood supply, but is not invested with blood vessels. He gets very circular here. The argument is not that the vertebrate eye lacks a solution to this problem, but that there are many different ways to solve the problem of organizing the retina with its multiple demands, and that the vertebrate eye was clearly not made by assembling the very best solutions.

Sarfati really needs to crawl out of his little sealed box of creationist dogma and discover what scientists actually say about these matters, and not impose his bizarre creationist interpretations on the words of people like Dawkins and Miller. What any comparative biologist can see by looking at eyes across multiple taxa is that they all work well enough for their particular functions, but they all also have clear signs of assembly by a historical process, like evolution and quite unlike creation, and that there is also evidence of shortcomings that have acquired workarounds, some of which are wonderfully and surprisingly useful. What we don’t see are signs that the best solutions from each clade have been extracted and placed together in one creature at the pinnacle of creation. And in particular — and this has to be particularly grating to the Genesis-worshipping creationists of Sarfati’s ilk, since he studiously avoids the issue — Homo sapiens is not standing alone at that pinnacle of visual excellence. We’re kinda straggling partway down the peak, trying to compensate for some relics of our ancestry, like the fact that we’re descended from nocturnal mammals that let the refinement of their vision slide for a hundred million years or thereabouts, while the birds kept on optimizing for daylight acuity and sensitivity.

Now we’ve got some big numbers to throw around, too

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Only ours are methodologically valid. It’s a common creationist tactic to fling around big numbers to ‘disprove’ evolution: for instance, I’ve had this mysterious Borel’s Law (that anything with odds worse than 1 in 1050 can never happen) thrown in my face many times, followed by the declaration that the odds of the simplest organism forming by chance are 1 in 10340,000,000. It’s complete nonsense, of course — their calculations all ignore the reality of the actual events, assuming that everything must form spontaneously and all at once, which is exactly the opposite of how probability plays a role in evolution. It’s annoying and inane, and the creationists never seem to learn…perhaps because the rubes they pander to are easily dazzled by even bogus mathematics, so they keep doing it.

We’re going to have to start firing back. Doug Theobald, a long-time contributor to Talk.Origins and the Panda’s Thumb, has written a very nice paper testing the likelihood that all life on earth is not related by common descent, and he comes up with some numbers of many digits to support evolutionary theory. Nick Matzke has a summary, and the story has been written up for National Geographic.

Basically, the idea is this: take a small set of known, conserved proteins that are shared in all organisms, not restricting ourselves to one kingdom or one phylum, but grabbing them all. In this paper, that data set consists of 23 proteins from 12 taxa in the Big Three domains: Bacteria, Archaea, and Eukarya. Then set up many different models to explain the relationships of these species. For instance, you could organize them into the classic single tree, where all are related, or you could model them as three independent origins, for each of Bacteria, Archaea, or Eukarya, or you could postulate other combinations, such as that Bacteria arose independently of Archaea and Eukarya, which share a common ancestor. Finally, you tell your computer to do a lot of statistics on the models, asking how likely it is that two independent groups would each arrive at similar sequences, rating each of the models for parsimony and accuracy against the evidence.

And the winner is…common ancestry, with one branching tree! This is what we expected, of course, and what Theobald has done is to test our assumptions, always a good thing to do.

More complicated permutations of these models were also tried. What if there were a significant amount of horizontal gene transfer? Would that make multiple origins of modern life more likely? He was testing models like the ones below, where the dotted lines represent genes that leap across taxa to confuse the issue.

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The answer here is that they don’t. These models can also be evaluated by statistical methods, and the best fit is again the one on the right, with a single ancestral root. People might recall the infamous “Darwin was wrong” cover from New Scientist—well, these results say that New Scientist was wrong, the existence of extensive horizontal gene transfer does not negate the fact of common descent.

So what’s the big number? There are lots of them in the paper, since it evolves many comparisons, but Theobald distills it down to just the odds that bacteria have an independent origin from Archaea and eukaryotes:

But, based on the new analysis, the odds of that are “just astronomically enormous,” he said. “The number’s so big, it’s kind of silly to say it”–1 in 10 to the 2,680th power, or 10 followed by 2,680 zeros.

One in 102680? Hey, aren’t those odds a little worse than Borel’s criterion of one in 1050?

Stay tuned to the Panda’s Thumb. Apparently, once he finishes up the trifling business of wrapping up a semester’s teaching, Theobald will be putting up a synopsis of his own and answering questions online.

Theobald D (2010) A formal test of the theory of universal common ancestry. Nature 465(13):219-222.

Neandertal!

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You don’t have to tell me, I know I’m late to the party: the news about the draft Neandertal genome sequence was announced last week, and here I am getting around to it just now. In my defense, I did hastily rewrite one of my presentation to include a long section on the new genome information, so at least I was talking about it to a few people. Besides, there is coverage from a genuine expert on Neandertals, John Hawks, and of course Carl Zimmer wrote an excellent summary. All I’m going to do now is fuss over a few things on the edge that interested me.

This was an impressive technical feat. The DNA was extracted from a few bone fragments, and it was grossly degraded: the average size of a piece of DNA was less than 200 base pairs, much of that was chemically degraded, and 95-99% of the DNA extracted was from bacteria, not Neandertal. An immense amount of work was required to filter noise from the signal, to reconstruct and reassemble, and to avoid contamination from modern human DNA. These poor Neandertals had died, had rotted thoroughly, and the bacteria had worked their way into almost every crevice of the bone to chew up the remains. All that was left were a few dead cells in isolated lacunae of the bone; their DNA had been chopped up by their own enzymes, and death and chemistry had come to slowly break them down further.

Don’t hold your breath waiting for the draft genome of Homo erectus. Time is unkind.

We have to appreciate the age of these people, too. The oldest Neandertal fossils are approximately 400,000 years old, and the species went extinct about 30,000 years ago. That’s a good run; as measured by species longevity, Homo sapiens neandertalensis is more successful than Homo sapiens sapiens. We’re going to have to hang in there for another 200,000 years to top them.

The samples taken were from bones found in a cave in Vindija, Croatia. Full sequences were derived from these three individuals, and in addition, some partial sequences were taken from other specimens, including the original type specimen found in the Neander Valley in 1856.

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Samples and sites from which DNA was retrieved. (A) The three bones from Vindija from which Neandertal DNA was sequenced. (B) Map showing the four archaeological sites from which bones were used and their approximate dates (years B.P.).

The three bones used for sequencing were directly dated to 38.1, 44.5, and 44.5 thousand years ago, which puts them on the near end of the Neandertal timeline, and after the likely time of contact between modern humans and Neandertals, which probably occurred about 80,000 years ago, in the Middle East.

Just for reference: these samples are 6-7 times older than the entire earth, as dated by young earth creationists. The span of time just between the youngest and oldest bones used is more than six thousand years old, again, about the same length of time as the YEC universe. Imagine that: we see these bone fragments now as part of a jumble of debris from one site, but they represent differences as great as those between a modern American and an ancient Sumerian. I repeat once again: the religious imagination is paltry and petty compared to the awesome reality.

A significant revelation from this work is the discovery of the signature of interbreeding between modern humans and Neandertals. When those humans first wandered out of the homeland of Africa into the Middle East, they encountered Neandertals already occupying the land…people they would eventually displace, but at least early on there was some sexual activity going on between the two groups, and a small number of human-Neandertal hybrids would have been incorporated into the expanding human population—at least, in that subset that was leaving Africa. Modern European, Asian, and South Pacific populations now contain 1-4% Neandertal DNA. This is really cool; I’m proud to think that I had as a many-times-great grandparent a muscular, beetle-browed big game hunter who trod Ice Age Europe, bringing down mighty mammoths with his spears.

However, it is a small contribution from the Neandertals to our lineage, and it’s not likely that these particular Neandertal genes made a particularly dramatic effect on our ancestors. They didn’t exactly sweep rapidly and decisively through the population; it’s most likely that they are neutral hitch-hikers that surfed the wave of human expansion. Any early matings between an expanding human subpopulation and a receding Neandertal population would have left a few traces in our gene pool that would have been passively hauled up into higher numbers by time and the mere growth of human populations. In a complementary fashion, any human genes injected into the Neandertal pool would have been placed into the bleeding edge of a receding population, and would not have persevered. No uniquely human genes were found in the Neandertals examined, but we can’t judge the preferred direction of the sexual exchanges in these encounters, though, because any hybrids in Neandertal tribes were facing early doom, while hybrids in human tribes were in for a long ride.

Here’s the interesting part of these gene exchanges, though. We can now estimate the ancestral gene sequence, that is, the sequences of genes in the last common ancestor of humans and Neandertals, and we can ask if there are any ‘primitive’ genes that have been completely replaced in modern human populations by a different variant, but Neandertal still retained the ancestral pattern (see the red star in the diagram below). These genes could be a hint to what innovations made us uniquely human and different from Neandertals.

i-eacb5bc2f9cc81fa2e29370680c5e1c5-neander_sweep.jpeg
Selective sweep screen. Schematic illustration of the rationale for the selective sweep screen. For many regions of the genome, the variation within current humans 0 is old enough to include Neandertals (left). Thus, for SNPs in present-day humans, Neandertals often carry the derived -1 allele (blue). However, in genomic regions where an advantageous mutation arises (right, red star) and sweeps to high frequency or fixation in present-day humans, Neandertals will be devoid of derived alleles.

There’s good news and bad news. The bad news is that there aren’t very many of them: a grand total of 78 genes were identified that have a novel form and that have been fixed in the modern human population. That’s not very many, so if you’re an exceptionalist looking for justification of your superiority to our ancestors, you haven’t got much to go on. The good news, though, is that there are only 78 genes! This is a manageable number, and represent some useful hints to genes that would be worth studying in more detail.

One other qualification, though: these are 78 genes that have changes in their coding sequence. There are also several hundred other non-coding, presumably regulatory, sequences that are unique to humans and are fixed throughout our population. To the evo-devo mind, these might actually be the more interesting changes, eventually…but right now, there are some tantalizing prospects in the coding genes to look at.

Some of the genes with novel sequences in humans are DYRK1A, a gene that is present in three copies in Down syndrome individuals and is suspected of playing a role in their mental deficits; NRG3, a gene associated with schizophrenia, and CADPS2 and AUTS2, two genes associated with autism. These are exciting prospects for further study because they have alleles unique and universal to humans and not Neandertals, and also affect the functioning of the brain. However, let’s not get confused about what that means for Neandertals. These are genes that, when broken or modified in modern humans, have consequences on the brain. Neandertals had these same genes, but different forms or alleles of them, which are also different from the mutant forms that cause problems in modern humans. Neandertals did not necessarily have autism, schizophrenia, or the minds of people with Down syndrome! The diseases are just indications that these genes are involved in the nervous system, and the differences in the Neandertal forms almost certainly caused much more subtle effects.

Another gene that has some provocative potential is RUNX2. That’s short for Runt-related transcription factor 2, which should make all the developmental biologists sit up and pay attention. It’s a transcription factor, so it’s a regulator of many other genes, and it’s related to Runt, a well known gene in flies that is important in segmentation. In humans, RUNX2 is a regulator of bone growth, and is a master control switch for patterning bone. In modern humans, defects in this gene lead to a syndrome called cleidocranial dysplasia, in which bones of the skull fuse late, leading to anomalies in the shape of the head, and also causes characteristic defects in the shape of the collar bones and shoulder articulations. These, again, are places where Neandertal and modern humans differ significantly in morphology (and again, Neandertals did not have cleidocranial dysplasia — they had forms of the RUNX2 gene that would have contributed to the specific arrangements of their healthy, normal anatomy).

These are tantalizing hints to how human/Neandertal differences could have arisen—by small changes in a few genes that would have had a fairly extensive scope of effect. Don’t view the many subtle differences between the two as each a consequence of a specific genetic change; a variation in a gene like RUNX2 can lead to coordinated, integrated changes to multiple aspects of the phenotype, in this case, affecting the shape of the skull, the chest, and the shoulders.

This is a marvelous insight into our history, and represents some powerful knowledge we can bring to bear on our understanding of human evolution. The only frustrating thing is that this amazing work has been done in a species on which we can’t, for ethical reasons, do the obvious experiments of creating artificial revertants of sets of genes to the ancestral state — we don’t get to resurrect a Neandertal. With the tools that Pääbo and colleagues have developed, though, perhaps we can start considering some paleogenomics projects to get not just the genomic sequences of modern forms, but of their ancestors as well. I’d like to see the genomic differences between elephants and mastodons, and tigers and sabre-toothed cats…and maybe someday we can think about rebuilding a few extinct species.

Green RE, Krause J, Briggs AW, Maricic T, Stenzel U, Kircher M, Patterson N, Li H, Zhai W, Fritz MH, Hansen NF, Durand EY, Malaspinas AS, Jensen JD, Marques-Bonet T, Alkan C, Prüfer K, Meyer M, Burbano HA, Good JM, Schultz R, Aximu-Petri A, Butthof A, Höber B, Höffner B, Siegemund M, Weihmann A, Nusbaum C, Lander ES, Russ C, Novod N, Affourtit J, Egholm M, Verna C, Rudan P, Brajkovic D, Kucan Z, Gusic I, Doronichev VB, Golovanova LV, Lalueza-Fox C, de la Rasilla M, Fortea J, Rosas A, Schmitz RW, Johnson PL, Eichler EE, Falush D, Birney E, Mullikin JC, Slatkin M, Nielsen R, Kelso J, Lachmann M, Reich D, Pääbo S. (2010) A draft sequence of the Neandertal genome. Science 328(5979):710-22.

The secret life of babies

Years ago, when the Trophy Wife™ was a psychology grad student, she participated in research on what babies think. It was interesting stuff because it was methodologically tricky — they can’t talk, they barely respond in comprehensible way to the world, but as it turns out you can get surprisingly consistent, robust results from techniques like tracking their gaze, observing how long they stare at something, or even the rate at which they suck on a pacifier (Maggie, on The Simpsons, is known to communicate quite a bit with simple pauses in sucking.)

There is a fascinating article in the NY Time magazine on infant morality. Set babies to watching puppet shows with nonverbal moral messages acted out, and their responses afterward indicate a preference for helpful agents and an avoidance of hindering agents, and they can express surprise and puzzlement when puppet actors make bad or unexpected choices. There are rudiments of moral foundations churning about in infant brains, things like empathy and likes and dislikes, and they acquire these abilities untaught.

This, of course, plays into a common argument from morality for religion. It’s unfortunate that the article cites deranged dullard Dinesh D’Souza as a source — is there no more credible proponent of this idea? That would say volumes right there — but at least the author is tearing him down.

A few years ago, in his book “What’s So Great About Christianity,” the social and cultural critic Dinesh D’Souza revived this argument [that a godly force must intervene to create morality]. He conceded that evolution can explain our niceness in instances like kindness to kin, where the niceness has a clear genetic payoff, but he drew the line at “high altruism,” acts of entirely disinterested kindness. For D’Souza, “there is no Darwinian rationale” for why you would give up your seat for an old lady on a bus, an act of nice-guyness that does nothing for your genes. And what about those who donate blood to strangers or sacrifice their lives for a worthy cause? D’Souza reasoned that these stirrings of conscience are best explained not by evolution or psychology but by “the voice of God within our souls.”

The evolutionary psychologist has a quick response to this: To say that a biological trait evolves for a purpose doesn’t mean that it always functions, in the here and now, for that purpose. Sexual arousal, for instance, presumably evolved because of its connection to making babies; but of course we can get aroused in all sorts of situations in which baby-making just isn’t an option — for instance, while looking at pornography. Similarly, our impulse to help others has likely evolved because of the reproductive benefit that it gives us in certain contexts — and it’s not a problem for this argument that some acts of niceness that people perform don’t provide this sort of benefit. (And for what it’s worth, giving up a bus seat for an old lady, although the motives might be psychologically pure, turns out to be a coldbloodedly smart move from a Darwinian standpoint, an easy way to show off yourself as an attractively good person.)

So far, so good. I think this next bit gives far too much credit to Alfred Russel Wallace and D’Souza, though, but don’t worry — he’ll eventually get around to showing how they’re wrong again.

The general argument that critics like Wallace and D’Souza put forward, however, still needs to be taken seriously. The morality of contemporary humans really does outstrip what evolution could possibly have endowed us with; moral actions are often of a sort that have no plausible relation to our reproductive success and don’t appear to be accidental byproducts of evolved adaptations. Many of us care about strangers in faraway lands, sometimes to the extent that we give up resources that could be used for our friends and family; many of us care about the fates of nonhuman animals, so much so that we deprive ourselves of pleasures like rib-eye steak and veal scaloppine. We possess abstract moral notions of equality and freedom for all; we see racism and sexism as evil; we reject slavery and genocide; we try to love our enemies. Of course, our actions typically fall short, often far short, of our moral principles, but these principles do shape, in a substantial way, the world that we live in. It makes sense then to marvel at the extent of our moral insight and to reject the notion that it can be explained in the language of natural selection. If this higher morality or higher altruism were found in babies, the case for divine creation would get just a bit stronger.

No, I disagree with the rationale here. It is not a problem for evolution at all to find that humans exhibit an excessive altruism. Chance plays a role; our ancestors did not necessarily get a choice of a fine-tuned altruism that works exclusively to the benefit of our kin — we may well have acquired a sloppy and indiscriminate innate tendency towards altruism because that’s all chance variation in a protein or two can give us. There’s no reason to suppose that a mutation could even exist that would enable us to feel empathy for cousins but completely abolish empathy by Americans for Lithuanians, for instance, or that is neatly coupled to kin recognition modules in the brain. It could be that a broad genetic predisposition to be nice to fellow human beings could have been good enough to favored by selection, even if its execution caused benefits to splash onto other individuals who did not contribute to the well-being of the possessor.

But that idea may be entirely moot, because there is some evidence that babies are born (or soon become) bigoted little bastards who do quickly cobble up a kind of biased preferential morality. Evolution has granted us a general “Be nice!” brain, and also that we acquire capacities that put up boundaries and foster a kind of primitive tribalism.

But it is not present in babies. In fact, our initial moral sense appears to be biased toward our own kind. There’s plenty of research showing that babies have within-group preferences: 3-month-olds prefer the faces of the race that is most familiar to them to those of other races; 11-month-olds prefer individuals who share their own taste in food and expect these individuals to be nicer than those with different tastes; 12-month-olds prefer to learn from someone who speaks their own language over someone who speaks a foreign language. And studies with young children have found that once they are segregated into different groups — even under the most arbitrary of schemes, like wearing different colored T-shirts — they eagerly favor their own groups in their attitudes and their actions.

That’s kind of cool, if horrifying. It also, though, points out that you can’t separate culture from biological predispositions. Babies can’t learn who their own kind is without some kind of socialization first, so part of this is all about learned identity. And also, we can understand why people become vegetarians as adults, or join the Peace Corps to help strangers in far away lands — it’s because human beings have a capacity for rational thought that they can use to override the more selfish, piggy biases of our infancy.

Again, no gods or spirits or souls are required to understand how any of this works.

Although, if they did a study in which babies were given crackers and the little Catholic babies all made the sign of the cross before eating them, while all the little Lutheran babies would crawl off to make coffee and babble about the weather, then I might reconsider whether we’re born religious. I don’t expect that result, though.

Everything old is new again

If you’ve ever invited me out to give a science talk, you know that what I generally talk about is this concept of deep homology: the discovery that features that we often consider the hallmarks of complex metazoan life often have at their core a network of genetic circuitry that was first pioneered in bacteria. What life has done is taken useful functional elements that were worked out in the teeming, diverse gene pools of the dominant single-celled forms of life on earth and repurposed it in novel ways. The really interesting big bang of life occurred long before the Cambrian, as organisms evolved useful tools for signaling, adhesion, regulation, and so forth — all stuff that was incredibly useful for a single cell negotiating through space and time in a complex external environment, and which could be coopted for building multicellular organisms.

But if you don’t feel like flying me out to tell you all about it, Carl Zimmer has an excellent article on deep homology in the NYT, and he uses a new example I’ll have to steal: a genetic module that we use to regulate blood vessel growth that can also be found in yeast cells, where it is used to maintain cell walls.