The “right” species concept

June 20, 2011 • 9:02 am

In my presidential address to the Society for the Study of Evolution last night, I started off, as I had to, by defining what I meant by speciation (my talk was, after all, about speciation).  I said that I was using the “biological species concept” (BSC), which conceptualizes species as populations separated by reproductive isolating barriers: genetically based features, like mate discrimination and hybrid sterility, that prevent gene flow between different groups.  And when I put up a slide of the BSC, I said it was the “right” species definition.

That was meant to be both funny and provocative: I know that different groups of biologists have different species concepts, and in some cases they should—you can’t use the BSC in bacteria, for example, which don’t really have sexual reproduction. But in my book Speciation with Allen Orr we note that there’s no one “right” species concept: concepts are more or less useful depending on the biological problem you’re addressing.

Since my problem is addressing the origin of distinct groups that coexist in one place without much interbreeding, the BSC is the only one that makes sense. Indeed, regardless of the species concept proposed by biologists—and there are many—when biologists go about studying the process of speciation in sexually reproducing groups, all of them, nearly without exception, adhere to the BSC. That is, when they study speciation they invariably study the origin of barriers to gene flow.  So if the origin and existence of discrete groups of sexual taxa nature is the problem—why there are blackbirds and robins and crows and sparrows, all living distinctly and discretely in one place—then the BSC is the go-to concept.

I used the word “right,” of course, to make people laugh, to provoke them (after all, the meeting includes a lot of systematists, many of whom abjure the BSC), and because it’s well known that I’m a staunch advocate of using the BSC for the “species problem” described above and have been a vociferous critic of other species concepts.

So when Carl Zimmer made this (ugh) “tweet” on the evol#11 Twitter feed, he was sort of on the mark:

I wasn’t purely joking but I was partly joking.  And Carl, my good man, if you want to know what I meant, all you have to do is ask.

Evolution 2011: Darwinian medicine

June 20, 2011 • 8:12 am

The meetings so far have gone very smoothly; the organizers have done a terrific job (despite us having to live out in the middle of nowhere), and there have been few glitches.  What a great idea it was, too, to have a free happy hour from 5:30-7:30 every day after the last session, with all the drinks you can swallow and lots of people to talk to.

I want to report on one talk on evolutionary medicine.  If you’ve followed this website, you’ll know that I was once down on the practical uses of evolution: I thought of the discipline more as a way to understand the world than to improve it.  But I’ve changed my mind, largely at the instigation of Dave Hillis at the University of Texas at Austin, who has enlightened me about the real applications of evolution in medicine.

At the meeting yesterday there was an all-day symposium on “Darwinian medicine” (DM). This is the discipline that studies not only how the evolution of pathogens helps us understand disease (antibiotic resistance in bacteria is, of course, the classic example), but also how human evolution affects not only our susceptibility to disease, but explains some of our symptoms (fever, for example, may be an evolved adaptation to kill pathogens, and so you might want to hold off reducing mild fevers).

I didn’t go to all the talks, for there are many interesting talks to see on a given day, but I wanted to briefly summarize one talk on Darwinian medicine, by Randoph Nesse at the University of Michigan. Nesse, along with the late George Williams, has published extensively on Darwinian medicine and, in fact, is largely responsible for founding the discipline.

Nesse’s talk was called “What evolutionary biology and medicine offer to each other, and reflections on George Williams.”  He began simply by recounting some statistics: how few evolutionary biologists there are on medical school faculty: almost none, but that’s not much of a surprise. More surprising is how little evolutionary biology actually gets into med-school curricula, despite its importance for medicine.  Most schools teach things about antibiotic resistance, more or less because they have to, but other aspects of DM aren’t often taught in medical school: things like “adaptive” human symptoms of disease, or things that pathogens do to facilitate their own spread (the fact that malaria makes you prostrate, for instance, may actually be an adaptation of the malaria parasite to facilitate its spread; you’re more likely to be bitten by a mosquito, who transmits the parasite, if you’re laid out flat in bed).

Nesse gave six evolutionary reasons why humans are still susceptible to disease, despite the adaptive advantages of being resistant to disease:

1.  Evolutionary constraints.  We may be unable to evolve resistance to some diseases simply because to do so would entail a greater fitness cost than a fitness benefit, for there are constraints that prevent us from changing one thing without changing others, perhaps at a greater fitness cost.  Although he didn’t give any disease examples, Nesse did use the example of the human eye, which is less than optimally designed because of its evolutionary origin as an everted part of the brain. (Light has to pass through blood vessels and nerves to get to the photosensitive cells, and this reverse-wiring gives us a blind spot that isn’t present in the camera eye of the octopus, which has an independent evolutionary origin). If a reader has an example of a constraint that keeps us from evolving resistance to a disease, let me know.

2.  Mismatch between genes and environment.  Many modern genetically-based diseases may reflect genes that were neutral or even adaptive in our ancestors, but maladaptive in a modern environment to which we haven’t yet adapted.  Heart disease may result from genes that make us crave fats. Such genes may well have been adaptive in our ancestors but are now maladaptive in our fat-rich environment. Such diseases aren’t really purely “genetic diseases,” but reflect an interaction between genes and new environments.

Many “common” genes that cause disease, like those for hypertension or diabetes, may have been either neutral or adaptive in our ancestors, but are not so great to have in a modern environment. Do remember that we’ve only had about two thousand years of “modern” civilization in our 6 million years of living in small groups in Africa: modern life is thus about 0.03% of our total evolutionary history.

3.  Coevolution with pathogen transmission.  Pathogens have evolved in ways that make us susceptible to disease.  Nesse used the example of malaria that I gave above, but this isn’t really coevolution: it’s simply an adaptation in the sporozoan parasite that facilitates its own transmission.  In “coevolution,” two species each undergo evolutionary change in response to each other. I don’t really see any evolution in humans in response to malaria (except for the spread of the sickle-cell allele, which prevents malaria in heterozygotes, but that’s not what Nesse was talking about), so the point he was making here is unclear. If someone heard that talk and can explain why “coevolution” is something that explains our evolutionary susceptilibility to disease, please explain below.

4.  Tradeoffs.  Bilirubin is one product of the metabolic breakdown of hemoglobin. It’s a very toxic compound, and if you have too much of it you get jaundice (it’s responsible for not only the yellow color of jaundice, but also of urine and the yellowish tint around bruises).  About 5% of the population has elevated bilirubin, which causes Gilbert’s syndrome, which in some people has mild deleterious effects but is often asymptomatic.  Why do we get this disease? Because bilirubin, though toxic, is also beneficial in some ways: it acts as a potent antioxidant and thus can prevent the damaging effects of too much oxygen on cells, which can include heart disease.

As Nesse pointed out, people with Gilbert’s syndrome have a significantly reduced incidence of coronary artery disease because of the elevated bilirubin.  His point was that although bilirubin is a toxic compound that can cause mild (or asymptomatic) disease in a substantial number of people, that disease is a byproduct of a greater good—a tradeoff between producing a toxic compound and the net beneficial effects that that compound has on the body.

5.  Reproduction trumps health.  The currency of natural selection is not longevity or bodily well-being, but reproduction.  Nesse argued that, for example, men get sick and die more often than women simply because there’s a tradeoff between their evolved tendency to compete with other men for women, thereby spreading their genes, and the fact that this competition wears men out physiologically, making them die earlier. He cited one surprising statistic: for every 100 Oklahoma women who die at age 20, there are 300 men who die at that same age. And we all know that the tour buses of old folks you see in your city are largely women, for many of the men who would be their contemporaries died long ago.

6.  Some “disease” symptom and defenses against mortality are useful, even if costly.  Pain, fever, and vomiting may be signs of sickness, but can be useful in preventing or mitigating illness.  Pain, of course, is a way of alerting you that something is wrong: people without the ability to feel pain often suffer infected wounds and other injuries, simply because they don’t get the signal that there’s something wrong. (I think this is why sufferers of leprosy—now called Hansen’s disease—often lose noses, ears, and fingers.) Vomiting helps us purge our bodies of toxic substances.

Similarly, many of our anxieties may also reflect adaptation.  As Nesse pointed out, if our ancestors got anxious and ran away from a noise that could be a leopard, maybe 99 times out of 100 it would be nothing, and that energy and anxiety would be wasted, but it’s that one time in 100 when it’s really a leopard that the anxiety and flight reaction really pay off. It will often be useful to be fearful and anxious even without much cause, if those reactions can save your life on the rare occasion when something really is around to harm you.

It was interesting to contemplate these issues, which of course are only one part of DM, for they concern only susceptibility to disease in humans, not other aspects of human disease or evolution in the pathogens themselves.

I have only one small quibble about Nesse’s talk. He gave one example of what he considered an untenable “just-so story” about human disease: the speculation that juvenile (type I) diabetes was an adaptation for the ice ages 10,000-20,000 years ago.  Those individuals with high levels of blood glucose, so the story goes, were better able to avoid freezing to death, and so the genes producing higher glucose, i.e., those that now give us juvenile diabetes, were adaptive in our recent evolutionary past.

This does seem to be a bit of a just-so story, and Nesse is right to be wary of it. For one thing, juvenile diabetes has severe side effects that can kill you when you’re young, before you can reproduce.  The curious thing is, though, that Nesse included clinical depression on his list of one of the “diseases” that probably were adaptive in our ancestors.  Yet the evidence that depression is adaptive is even less convincing than for type I diabetes  (see my posts about this here, here, and here).

While I now think that Darwinian medicine is a useful and intriguing discipline, its practitioners must be careful not to fall into the same trap that’s snared many evolutionary psychologists: uncritical and untestable storytelling.  So far, many advocates of DM, including Nesse, seem to be largely avoiding that trap.

The gyrfalcon is a seabird and uses ancient nests

June 20, 2011 • 4:49 am

Reader Dominic has called my attention to two new reports from the BBC about the gyrfalcon (Falco rusticolis), pronounced “JER-falcon.”

First, a bit about the bird. It’s the world’s largest falcon, with some specimens reaching three pounds with a four-foot wingspan. They’re magnificent birds:


Photo by Doug Backlund; go to his page for many more great photos of the bird

Here’s the range map from Cornell’s All About Birds; they breed on the North American tundra but range widely south.  A map of its worldwide distribution, including Greenland, northern Europe and Asia can be found here.

They’re bird eaters; the Cornell site reports that they “eat mostly ptarmigan, but many other prey species have been recorded, including fulmars, gulls, jaegers, ducks, geese, Rough-legged Hawk, Short-eared Owl, sparrows, buntings, and redpolls.”   Here’s an amazing video of one taking a ptarmigan on the wing: the strike occurs at about 2:15 (I find the music annoying; you might want to turn it off).

So what’s new about the bird?  Two discoveries, both made by a team headed by Kurt Burnham, a Ph.D. student at Oxford’s Edward Grey Institute of Field Ornithology.

1.  The gyrfalcon is basically a seabird.  As the BBC reports, up to now its hunting habits during the nonbreeding season—the winter—were largely unknown.  But tracking the birds with radiocollars shows gyrfalcons to be “secret seabirds”:

Gyrfalcons living in the high Arctic overwinter out at sea, spending long periods living and hunting on pack ice.

It is the first time any falcon species has been found regularly living at sea.

The birds likely rest on the ice and hunt other seabirds such as gulls and guillemots, over what appears to be one of the largest winter ranges yet documented for any raptor.

“I was very surprised by this finding,” said ornithologist Kurt Burnham who made the discovery. “These birds are not moving between land masses, but actually using the ice floes or pack ice as winter habitat for extended periods of time.”

“Previously, all species of falcon were considered to be land-based birds.”

. . . Those on the east coast ranged far more widely, covering between 27,000-64,000 square kilometres. Some of these had no obvious winter home ranges and travelled continuously during the non-breeding period, spending up to 40 consecutive days at sea.

During the winter one juvenile female travelled more than 4,500km over 200 days, spending over half that time over the ocean between Greenland and Iceland.

2.  Some gyrfalcon nest sites are ancient. Another report, from BBC EarthNews, shows that the nesting areas used by these birds can be several thousand years old.  Like other falcons, gyrfalcons don’t build nests, but simply scrape out an area on a rock ledge.  New research shows this:

Carbon dating revealed that one nest in Kangerlussuaq in central-west Greenland is between 2,360 and 2,740 years old, the researchers report in Ibis.

Three other nests in the area are older than 1,000 years, with the youngest nest site first being occupied 520 to 650 years ago.

These ancient nests are still being regularly used by gyrfalcons.

“While I know many falcon species re-use nest sites year after year, I never imagined we would be talking about nests that have been used on and off for over 2,000 years,” says Burnham.

They also carbon-dated some gyrfalcon feathers to over 600 years old. But these aren’t the oldest continuously used nesting sites by birds, not by far:

By carbon dating solidified stomach contents, peat moss deposits and bone and feather samples from various moulting sites, researchers have in the past shown that colonies of snow petrel have returned to the same sites for 34,000 years and adelie penguins for 44,000 years.

Evolution 2011: hot research—with cats!

June 19, 2011 • 12:18 pm

I am not a big fan of Twitter, though the WEIT posts go out on it.  I hate the word “tweet,” which rankles as much as “blog,” and constant personal “tweeting” seems to me more than a tad solipsistic. But how could I not post this “tweet” from the Evolution 2011 meeting feed (#evol11):

RT @surt_lab factoid from #evol11 geographic distribution of lactose tolerance in cats parallels that in humans < would ya look @ that!

If you’ve read WEIT, you’ll know that those human populations with a history of “pastoralism” (raising cows, sheep and goats for milk) have a high frequency of genes for lactose tolerance compared to those human populations that don’t consume much milk.  Further, the allele for lactose tolerance increased in frequency only in the last 10,000 years, which parallels the time when pastoralism began. (The gene, by the way, is one that allows the enzyme lactase, which breaks down lactose into sugars, to keep being expressed into adulthood. That gene is usually turned off after childhood, when, historically, people no longer nursed.)

It’s a really good example not only of evolution in “real” (or semi-real) time, but also of gene/culture coevolution: a change in human culture—the domestication of milk-yielding mammals—has created a “natural” selective pressure that changed our genes.  This, of course, is due to the tremendous reproductive advantage of having access to such a rich food source, which you can gain only if you can digest it.  (The reproductive advantage of digesting milk in a pastoral population is a whopping 10%!).  You can read more about this system at the Understanding Evolution site.

Apparently, the same genetic changes have occurred in cats commensal with humans.  Clearly, cats have been fed milk by their pastoral owners for a considerable amount of time: cats appear to have been domesticated between 8,000 and 5,000 years ago.

Self aggrandizing note: Allen Orr and I have co-signed several copies of our book, Speciation, on sale at the Sinauer booth at these meetings.  Jointly signed copies are rare—Orr and I are rarely at the same place at the same time—so pick up one of these rarities now. (Note: there is no surcharge!)

Falconcam in Racine, Wisconsin

June 19, 2011 • 11:32 am

by Greg Mayer

For some years now,  peregrine falcons (Falco peregrinus) have been breeding on the Racine County, Wisconsin, Court House.

There was no one home when I grabbed this still, but you can see the bones of their prey scattered about the floor of the nest. Check the Falconcam for live action. The Racine County Courthouse is a great Art Deco-style building built in the 1930s and designed by the Chicago firm of Holabird and Root, and, along with the numerous buildings in the area by Frank Lloyd Wright and his school, is a must see for an architectural visit.

Auditory illusions

June 19, 2011 • 7:01 am

by Matthew Cobb

We all know about visual illusions, and the way that psychologists and neuroscientists use them to develop and test hypotheses about how the visual system works. Other kinds of sensory illusions are a bit trickier, however. ‘Phantom limb’ syndrome where amputees imagine they still have their limb (and, sadly, often feel pain in it) is an example of a touch illusion. And the ‘burning’ sensation you get from eating chili or curry is due to the fact that the pain receptors on your tongue (or your mucus membranes – ouch!) are activated by the capsaicins in the spice. It doesn’t ‘really’ hurt. Or rather, it hurts, but there is no damage being done.

This website contains 10 of the most fascinating auditory illusions. [NB – the sound files are linked to the small grey box *below* each text box describing the illusion.] Some of them are illusions that are like visual illusions. Such as number 7 (‘Falling Bells’): ‘This is a recording of a paradox where bells sound as if they are falling through space. As they fall their pitch seems to be getting lower, but in fact the pitch gets higher. If you loop this sample you will clearly see the pitch jump back down when the sample repeats. This reveals that the start pitch is obviously much lower than the finishing pitch.’

But perhaps the most striking examples are only an illusion in the way perspective is a visual illusion – you can perceive something in 3-D that’s only really in 2-D. Hear (!) you perceive something in space, when it’s just in your head. These are examples of ‘dummy head’ recording. Number 5 – ‘Virtual Barbershop’ features a session at the barber’s and is stupendous when listened to on headphones. The final seconds are great! Number 4 just features a box of matches.

If you want to know more about the science behind this, go to the web-page of Diana Deutsch, Professor of Psychology at San Diego, who developed many of these sound files.

h/t : Fellow fly-man Walton Jones.

There’s another accommodationist Biologos!

June 19, 2011 • 4:49 am

Alert reader, sleuth, and crack satirist Sigmund has discovered that the American accommodationist and pro-Adam-and-Eve organization, BioLogos, has a Doppelgänger outfit with a nearly identical name and a nearly identical aim. It’s the Finnish homeopathic institute Biologos.  Sigmund’s take on this blatant theft can be see on his website, Sneer Review.

The “Oy,” I suppose, is there to distinguish it from the purely goyische American BioLogos.

Oddly enough, the Finnish Biologos wants to show the compatibility of science and homeopathy!  Here are two of their statements (these are real, based on Google Translate):

“in some Central European countries, homeopathic drugs are compensation for a national health care system. Including Germany, France and Britain, many thousands of doctors have received training in homeopathy. There are also trained homeopath doctors.”

and

“Homeopathy is different in many respects a familiar traditional medical methods, but does not exclude the concurrent medication use.”

Note to accommodationists: if you’re going to use Francis Collins as an example of why science and faith are compatible, you have no choice but to accept that medicine and homeopathy are also compatible. After all, there are doctors who practice both traditional medicine and homeopathy!

Sigmund describes the upcoming legal proceedings about trademark infringement, and the American BioLogos‘s lame defense.  But given that both outfits are dedicated to promoting the compatibility of science and nonsense, I don’t see why they can’t find common ground. Chris Stedman, where are you?