Category: evidence for evolution

Misconceptions about evolution

June 14, 2023 • 9:35 am

Over the 14 years (can it be that long?) that I’ve been writing this website, I’ve put up several lists of misconceptions about or misrepresentations of evolution, but they’ve all been compiled by other people (for example, see here, here, and here). Some of them aren’t really misconceptions, such as the second link, which lists “misrepresentations” that are really pieces of advice about how to teach evolution.  Those are generally good, though I can’t say I agree fully with this one: ““Avoid giving the impression that evolution is atheistic, or that evolutionists must be atheists.”

The way I teach evolution, starting with two sessions on why we accept evolution (these lectures were turned into Why Evolution is True), involves a certain amount of creationism-bashing. That’s because I use the rejection of creationism in favor of evolution in the late 18th century as an example of the way science proceeds: theories are discarded when they become increasingly incompatible with the evidence, while the alternative theory (evolution in this case) is able to explain facts that stymie creationism. The fossil record, anomalies of development, vestigial organs, and (my favorite) biogeography are all areas in which evolution explains phenomena that can’t be explained by Biblical creationism.

Now it wasn’t I who made this argument, but Darwin. If you read On the Origin of Species, which Darwin himself characterized as “one long argument,” you’ll see that he’s constantly opposing creationism with evolution without going too hard after Christian creationism (Britain wasn’t full of fundamentalists like America is now). Describing the imbalance of organisms on oceanic islands, for instance, was a very clever way that Darwin showed how evolution could explain phenomena that baffled creationists. In fact, I’ve never seen a good creationist explanation of biogeography, especially of the “unbalanced” nature of life on oceanic islands: the lack of endemic mammals, amphibians, and freshwater fish while there are plenty of endemic insects, plants, and birds.

But teaching this way offended a few of my religious students, who called me out for “creation-bashing” in my evaluations. I reject that criticism, for, after all, creationism was THE going explanation for life and its patterns before Darwin, and within a decade his compelling arguments had vanquished that explanation. Teaching this way, I think, is a good object lesson in how science is done (yes, creationism was a scientific hypothesis before Darwin), as well as educating the students on why nearly all scientists accept the fact of evolution.  And I took this approach in Why Evolution is True. The usefulness of opposing two theories and adjudicating them with evidence is supported by the success of that book—far greater than I expected.

I don’t say anything about atheism in my classes, for that’s not part of my job, but most students do get the idea that the Bible should not be taken literally as a theory of biology. And if they ask me my views about gods straight out, I will be honest with them.  Further, if they ask me, according to the guidance in bold above, whether religion and evolution (or science in general) are compatible, I will explain to them (privately, because the explanation is long) that while one can be religious and accept evolution, they are incompatible in a fundamental way: one accepts religious “truths” based only on authority, dogma, or scripture, while science accepts empirical truths based on evidence and the consensus of scientists.  (Yes, religions do make truth claims.) That is why I wrote Faith Versus Fact.  But I’ve never had a student complain that I’ve said that either evolution or science are atheistic, for I have never claimed that in lecture. It is of course true in an important way, for a practicing scientist rejects the idea that what he/she is investigating could have divine explanations.  You leave your faith at the door of the lab. (I won’t reiterate my incompatibility claims here; read FvF if you want to see my argument.)

In that sense, then, science is atheistic, for it rejects belief in gods. Let me emphasize that, as I say in FvF, that this rejection is not by a priori agreement: scientists didn’t get together in some smoke-filled room and agree to reject gods, despite some creationists who claim that.   Indeed, there were times in science, like early astronomy or when Biblical creationism reigned, that divine explanations were part of science.  But since they haven’t proven useful in explaining anything, we now reject them as being useless.  The best expression of this idea is the conversation that supposedly took place between the Emperor Napoleon and the French polymath Pierre-Simon Laplace in 1802, after Napoleon had been given Laplace’s five-volume work on celestial mechanics.  There are many versions of this conversation,  which may never have taken place, but here’s one from British mathematicial Walter Ball, published in 1888:

“Laplace went in state to Napoleon to accept a copy of his work, and the following account of the interview is well authenticated, and so characteristic of all the parties concerned that I quote it in full. Someone had told Napoleon that the book contained no mention of the name of God; Napoleon, who was fond of putting embarrassing questions, received it with the remark, ‘M. Laplace, they tell me you have written this large book on the system of the universe, and have never even mentioned its Creator.’ Laplace, who, though the most supple of politicians, was as stiff as a martyr on every point of his philosophy, drew himself up and answered bluntly, ‘Je n’avais pas besoin de cette hypothèse-là.’ [‘I had no need of that hypothesis.’]

Even if the conversation never happened, the anecdote explains why science is atheistic in practice: we have no need of that hypothesis.

But I digress. In August I’m lecturing to people on a cruise to the Galápagos Islands, which of course were visited by Darwin on the Beagle.  I’m giving two lectures on that trip, “Darwin on the Galápagos” and “Why evolution is true”, as well as a Q&A session with two five-minute mini-lectures.  But first let me point out two widespread misconceptions about Darwin and the Galápagos islands, which I won’t go into here but will do on the voyage:

  1. Darwin did not have an “aha moment” in the Galápagos islands when suddenly evolution and natural selection became clear to him.
  2. The famous “Darwin’s finches”, while they did play some role in Darwin’s thinking that led to The Origin, did not play a major role. He doesn’t even mention the finches in that book, and barely mentions the Galápagos (only 16 times). Other data and ideas were more important to the revolution in thought wrought by Darwin.  If you want to read about his adventures on the islands, read Chapter XVII of  the earlier The Voyage of the Beagle, “Galapagos Archipelago.”  It’s free online at the link.

But I digress again. I have 5-10 minutes to explain to the guests what the biggest misconceptions about evolution are, so of course I have to leave some out. But the list is designed to inspire discussion, so here it is:

  1. Evolution is “only a theory”
  2. In evolution, everything happens by accident
  3. Natural selection transforms individuals over time (in reality, individuals don’t change, but populations and species)
  4. Evolution operates “for the good of the species”
  5. Evolution is inherently progressive
  6. Evolution equips organisms to face challenges that arise in the future
  7. Humans are no longer evolving

I could of course give more, but these are the seven I’ve chosen to explain, and I hope I can do it in no more than ten minutes. (I’m leaving out details and hope that they’ll come out in audience discussion.)

I may give summaries of my other minitalks here later (on the ship I’ll ask people which one(s) they want to hear), which include “What evidence would disprove evolution?”, “What IS the theory of evolution?”, and “Why do so many Americans reject evolution?”.

**********

Here’s a first-edition of On the Origin of Species in a presentation copy. (I’m not sure what that is for the handwriting is surely not Darwin’s.) Only 1250 copies were printed, and this one goes for $950,000:

Is there more evidence for Jesus’s Resurrection than for biological evolution?

March 20, 2023 • 9:15 am

I love it when I wake up to an email like this, showing me that there’s still work to be done among the neuronally deprived. Unfortunately, readers like “Henry” are unlikely to be persuaded since they instantiate the very definition of faith discussed below. 

At his friend’s behest, Henry started reading my 2016 post, “Peter Boghossian accused of hate speech for correctly defining ‘faith’.” (By the way, Peter’s definition of “faith” was “pretending to know things that you don’t know” and “belief without evidence”.) Peter’s definition angered Christian apologist named James Bishop, who wrote a long article attacking Boghossian and his claim (it’s no longer online). Bishop’s response was the subject of my piece: was there was anything more to “faith” than Boghossian’s simple definition? Note that Bishop played the “hate speech” card way back in 2016:

I consider Boghossian’s view to be bordering on hate speech. It’s not simply Boghossian’s redefinition of a word that appears hateful but it is the implications it has when it comes to human people – since many religious people do in fact match Boghossian’s  definition of faith. In other words, history well tells us that it is an incredibly dangerous thing to single out a people or a group in such a way as to ostracize and demonize them. That is what it would appear Boghossian is doing here.

Note that there are 120 comments on the post, but that was back in the day when people actually made comments. Now I weep in frustration. . .

At any rate, reader “Henry” was directed by his pal to the piece above, and decided he had to comment on it now; his comment responded not just to my post, but also to a comment made by reader Sastra.

Instead of posting Henry’s comment in the original thread, which nobody will read since it’s seven years old, I’ll put it here because it’s not only bizarre, but shows the mindset of those marinated in faith: how readily they reject a ton of evidence so that they can believe what makes them feel good.  So much for those who claim that there’s no conflict between science and religion!

Here’s Henry’s comment:

I’m only commenting on this because a friend sent me the link.I started reading the above article with the intention of finishing. However, after progressing to roughly the middle of it I concluded the rest wasn’t worth reading. The author would do well to get a grasp on what constitutes “evidence”. The evidence so far supporting evolution as ‘fact’ as opposed to the convoluted diatribe used by atheists towards Christianity (you know, that irritating value system which underpins western civilisation) is somewhat scant. In contrast the evidence for the existence of Jesus as an historical character is fairly comprehensive.The issue is whether or not he rose from the dead.If Jesus was not raised from the dead then the house of cards collapses. The bible as a book, is a collection of books & writings assembled in antiquity with the authors (& eye witness) being much closer to the event than we are today. If you can believe that historical characters like, Julius Caesar existed then why do atheists get upset when Jesus is mentioned ??? I suspect the answer to that lies in psychology. Bad behaviour by organised religion has ruined many lives & generated much (deserved) anger & damaged the credibility of institutions who profess a faith which they themselves have abused. Distinguishing ‘saint’ from ‘sinner’ has become blurred to the point irrelevance in the minds of those who hold a genuine well founded grudge.

Note the absolutely ridiculous claim that we have more evidence that Jesus rose from the dead than we do for biological evolution, despite the fact that evidence for evolution appears in many books and papers, with more coming out daily, while the Resurrection appears in only one book and there’s no more evidence since the Old Testament appeared. (There could be—if Jesus came back again!)

Note as well that Henry’s “evidence” that Jesus rose from the dead goes beyond just what the New Testament says: he considers it “evidence” that if the Resurrection isn’t true, then Christianity collapses. This is of a piece that if a religion persists for a long time, then its truth claims must be accurate. So much for all those many dead religions that flourished for a long time!

Finally, note that Henry really instantiates Boghossian’s claim: Henry’s a guy who rejects one claim in favor of another, even though there’s a gazillion times more evidence for the former (evolution) than the latter (Resurrection).

But of course the validity of evidence has nothing to do with the existence or duration of social structures based on that evidence.  Does the presence of 17 million Mormons in the world mean that Joseph Smith did indeed find that now-disappeared set of Golden Plates discovered in 1820.  After all, the evidence for that is not just a sacred book (The Book of Mormon, of course), but the fact that the book is prefaced by the sworn testimony of eleven people (in the 19th century, not 50-100 A.D.) who said that they had actually seen  the golden plates. Doesn’t that make the evidence for Mormonism stronger than that for Christianity?

But I digress. It’s a bit cheeky of Henry to tell me about the relative weight of evidence for evolution vs. the Resurrection when I not only wrote the book about the former, but have also read read a lot about the latter. There is no comparison. It would be great if reader Peter Nothnagle sent me one of his patented New-Testament-debunking pieces to forward on to Henry.

If I wanted to refute “Henry” further, I’d go into the lack of evidence for Jesus’s miracles (and perhaps his very existence), including his vow to return before some of his contemporaries had died (but he didn’t show), that prayers don’t work, nor does a trip to Lourdes restore missing eyes and limbs, and that there’s been a disturbing lack of evidence for Jesus in the past two thousand years. It’s as if after he was Resurrected, he decided to vanish forever.

But I’ll leave any rebuttal up to the readers. Address your comments to Henry (or take on this topic) below, and I’ll forward him the link tomorrow.

Evidence for evolution: Hairless animals have dead genes for a full coat of hair

January 15, 2023 • 9:30 am

In Why Evolution is True, one of the most telling pieces of evidence I adduce for evolution is the existence of dead (nonfunctional or “vestigial”) genes found in the DNA in living species. For example, mammals like us carry three dead genes for making egg yolk. Evolution has rendered them nonfunctional, as mammalian embryos are nourished through the placenta, but they’re still there in the genome, rendered useless by mutations.

The genome of nearly all animals we know is a veritable graveyard of dead genes. These, like our egg-yolk genes, constitute irrefutable evidence for evolution. They’re still there because we inherited them from a common ancestor, but evolution usually inactivates unneeded genes not by snipping them out of the genome, but by allowing “inactivation” mutations to kill the genes’s production of protein. (Alternatively, inactivation can occur by killing off a promoter gene that causes a gene to be transcribed.) The genes just sit there, “silent signs of history.”

Both types of dead genes were found in this new eLife paper, and they are genes normally promoting the growth hair in the relatives of species that have lost most of their hair. That the genes are still there, but are nonfunctional, simply can’t be explained by anything other than common ancestry. That’s why creationists, like the chowderhead I’ll highlight in the next post, ignore them. (Similarly, they ignore the evidence for biogeography of oceanic islands—also explained in Why Evolution is True—because there’s no creationist explanation save “Well, God wanted things to look like they’d evolved.”)

This is a long and complicated paper from eLife, but the popular version in Science Alert, shown below that, is not sufficiently detailed. I’ll try to simplify the eLife paper but give more information than the popular precis.

The pdf for the eLife paper is here, and the reference is at the bottom.

The short take: the authors sequence a handful of relatively hairless species that descended from ancestors that had hair, looking for genes in common to these set that a. were likely involved in producing hair, but b. had been inactivated in these species by “relaxation of selection”. That is, there was no longer natural selection in these species to maintain a coat of hair (and good reason not to), and so mutations inactivating the genes–and their controlling elements–accumulated.  Further, natural selection can accelerate this trend by favoring gene variants that reduce hair, either because regular genes that make hair use up metabolic energy that isn’t needed and, more likely, that hair is an impediment to their lifestyle.

The interesting thing about the paper is that, by sequencing the DNA of relatively hairless species, they found sets of genes in common among the hairless species, implying that there were common evolutionary-genetic pathways for hair reduction. This is what’s called convergent evolution, which usually refers to similar appearances of organisms that have similar lifestyles but aren’t closely related—like the marsupial mole and the placental mole—but in this case it’s convergence at the level of genes.

Here are the species they looked at:

rhinoceros
elephant
naked mole rat
human
pig
armadillo
walrus
manatee
dolphin
orca

. . and a subset of all species studied showing their evolutionary relatedness. I love the example they use for humans:

(from the paper): Hairless species show an enrichment of hair-related genes and noncoding elements whose evolutionary rates are significantly associated with phenotype evolution. (A) Phylogenetic tree showing a subset of the 62 mammal species used for analyses. Note that all 62 species were included in analyses and only a subset are shown here for visualization purposes. Foreground branches representing the hairless phenotype are depicted in orange alongside photographs of the species.

Most of these animals have some hair, but the authors conjecture, with reason, that their ancestors were much hairier. This is likely to be true, though the elephant and manatee had a recent common ancestor and it’s not clear whether their hairlessness evolved twice. The authors support this by adducing the existence of the hairy mammoths as animals more closely related to the modern elephant, implying that the ancestral pachyderm was hairy. But hairy elephants could have represented the re-evolution of hair in a relatively hairless ancestor. Likewise with the dolphins and orcas; I’m not sure how these two, which are fairly closely related marine mammals, could be taken as independent losses of hair. (On the other hand, the walrus, less closely related, could have lost its hair independently).

They also looked at 52 other species, for you need a comparison of DNA sequences in hairy animals. The figure above shows some of the hairy species whose DNA was sequenced (they looked at a lot of genome: nearly 20,000 coding genes and 350,000 regulatory regions).

Surprisingly, they found a fair number of genes that lost function (or had “relaxed selection”) in all of the hairless species. Not all of the genes had a known function, but most were associated with hairs themselves, the hair follicles,or the dermal papillae, the crucial structures that allow hair to grow.  Here’s a list of five genes and a table of the likelihood that they would have changed so rapidly in all the species. The colors show where the genes act.

(From the paper): Diagram of hair shaft and follicle with shading representing region-specific enrichment for coding and noncoding sequence. Both coding and noncoding sequence demonstrate accelerated evolution of elements related to hair shaft (cortex, cuticle, and medulla). Noncoding regions demonstrate accelerated evolution of matrix and dermal papilla elements not observed in coding sequence. All compartment genesets were compiled from Mouse Genome Informatics (MGI) annotations that contained the name of the compartment except the arrector pili geneset (Santos et al., 2015).

Note that both coding (genes) and noncoding (controlling-element) DNA was involved; in fact, among all the genes identified as likely contributors to hairlessness, there were more noncoding changes than coding changes, which is often what we find when either new structures evolve or old structures are lost. I used to think—and wrote a controversial paper about this with Hopi Hoekstra—that structural (coding) genes were more important in evolutionary change, but the data show that it might be the other way around. In other words, Hopi and I may have been wrong.

Now the paper is long and complicated, and bits of it are beyond my pay grade, but I do have a few comments. First, the significance levels they use to ascertain common evolution of genes among the set of relatively hairless species are not that small. They even highlight genes, as you can see above, with adjusted probability values above 0.05; conventionally these would be considered “nonsignificant”. I’m not sure why they did that. However, as you can see from the table above, some of the adjusted probabilities were very, very small: the p value for noncoding sequences in the hair cortex is, for instance, 0.000003. I’m confident that they did at least find some genes that changed rapidly in the entire group of hairless species.

Second, they’re not sure in some cases that the rapid gene evolution was indeed associated with loss of gene function. You can tell this for coding genes because there will be a “stop codon” or a “nonsense codon” in the DNA sequence that will code for mRNA that makes a nonfunctional protein.  They don’t talk about this in detail, but simply use “rapid evolution” as an index of nonfunctionality. (I may have missed something.)

Finally, for pairs like the elephant and manatee on one hand and the dolphin and orca on the other, I don’t have a lot of confidence that their loss of hair occurred independently.

Nevertheless, we can have confidence, given the low probability values, that some structural and controlling DNA has evolved independently in a group of hairless species, causing them to lose hair. That’s a case of convergent evolution of genes that is quite novel.

Oh, I forgot to mention why these species lost hair. In our species, it probably happened to promote easier cooling of our bodies via sweating as we evolved into upright creatures on the savanna. This probably also holds for rhinos and elephants, especially because elephantine species in northern climes, like mammoths, were hairy. In marine mammals it’s obvious: hair is useless for insulation, and is just an impediment to swimming. As for armadillos and pigs, it’s anybody’s guess. Wild pigs are pretty hairy (at least the ones I’ve seen), but armadillos have shells, and that serves to insulate the animal (they do have hair on their bellies, but it’s sparse).

An armadillo’s belly from Flickr:

 

THE UPSHOT:  These are likely cases of “vestigial genes,” though the cases would become textbook examples if they knew exactly what the genes did and, importantly, could show without doubt that they have been inactivated in the hairless species. Those data will come some day, but in the meantime I prefer to cite the broken egg-yolk genes in mammals: remnants of genes that produced nutrients for the embryos in our reptilian, fishy, and amphibian ancestors. That is a very solid case.

You can read the “popular” take below:

h/t: Barry

______________

Kowalczyk, A., M. Chikina, and N. Clark. 2022.  Complementary evolution of coding and noncoding sequence underlies mammalian hairlessness. eLife 11:e76911.  https://doi.org/10.7554/eLife.76911

My interview about evolution with Ray the Producer

September 4, 2022 • 1:35 pm

Yesterday I had an interview with “Ray the Producer” (his YouTube channel, “Allah Who?” is here, and he tends to interview people who are critical of Islam. I was invited on to talk about evolution, a theory that is widely rejected by Muslims, especially those who are Qur’anic literalists. And so the 1.5 hour conversation is about the evidence for evolution and why people reject it. (Ray is an ex-Muslim atheist.)

Here’s the video, and remember that I had about three hours of sleep when I did it yesterday morning. As always, I haven’t listened to it as I cannot abide seeing myself on video. If you can, and want to, here it is for your delectation.

Lactase persistence in populations that drink milk: a classic story of human evolution re-evaluated

July 29, 2022 • 9:15 am

The classic tale of “gene-culture coevolution” in humans—the notion that cultural changes in behavior changed the selection pressures that impinged on us—is the evolution of “lactase persistence” (LP) over the past four thousand years.  LP is a trait that allows you to consume, as an adult, lots of milk or dairy products without suffering the side effects of indigestion, flatulence, or diarrhea.

Young children are able to tolerate milk while nursing, of course, but after weaning many of them no longer tolerate milk—they are lactose intolerant (LI). The ability to digest lactose goes away after weaning because the gene producing the necessary enzyme gets turned off.

The gain of LP, which enables you to drink milk and eat dairy products into adulthood without ill effect, rests on single mutations in the control region of the gene producing lactase, an enzyme that breaks down the milk sugar lactose.  These mutations have arisen independently several times, but only after humans began “pastoral” activities: drinking milk from domesticated sheep, goats, and cows. And the mutations act to keep lactase turned on even after weaning. (Why humans turn off the gene after weaning isn’t known, but presumably involved the metabolic cost of producing an enzyme that wasn’t used in our ancestors, who didn’t drink milk after weaning until about about 10,000 years ago—when farming and animal domestication began.)

Based on analysis of fossil DNA, the LP mutations began spreading through Europe (starting from what is now Turkey) about 4000 years ago. And so the classic story—one that I taught my evolution classes—is that humans began drinking milk from captive herds, and that gave an advantage to retaining the ability to digest milk even after weaning. Ergo, natural selection for the nutritional benefits of milk led to the spread of LP mutations, as their carriers may have had better health (ergo more offspring) than individuals who turn off the enzyme at weaning).

This leads to the “coevolution” that is the classic evolutionary tale: a change in human behavior (raising animals for milk) led to selection for the persistence of the milk-digesting enzyme, and thus to genetic evolution. The “coevolution” part is the speculation that being able to digest milk without side effects would cause humans to raise even more dairy animals and drink even more milk, intensifying the selection for LP, and so the gene for LP would keep increasing in frequency.

A new paper in Nature, which is being touted all over social media, argues against this classic story, suggesting that it’s more complex than previously envisioned.  Although the new results are touted as overturning the earlier story, they really don’t. There is still human genetic evolution promoted by a change in culture, and there’s still a reproductive advantage in drinking milk.

The new part of the story is simply that that reproductive advantage comes not constantly (as previously envisioned), but only during times of famine and disease, when those who couldn’t digest lactose were at a severe disadvantage because the diarrhea caused by lactose intolerance would contribute to the death of diseased or malnourished individuals. This is a twist on the main story, but doesn’t overturn it completely. There’s still the connection between culture and human evolution, and there’s still a reproductive advantage to LP that leads to natural selection and genetic evolution of our species.  What’s different is how and when the selection acts (see “the upshot” at the bottom).

Click the title screenshot below to read, or you can download the pdf here. The full reference is at the bottom, and Nature deemed this worthy of two News and Views pieces in the same issue: (here and here).

First, the authors show the spread of dairy use in the figure below (the redder the color, the more milk usage over time in Eurasia. This was estimated from looking at the frequency of pot shards that had milk residue (click to enlarge). By 1500 BC, milk use was widespread.

Caption (from Nature): Interpolated time slices of the frequency of dairy fat residues in potsherds (colour hue) and confidence in the estimate (colour saturation) using two-dimensional kernel density estimation. Bandwidth and saturation parameters were optimized using cross-validation. Circles indicate the observed frequencies at site-phase locations. The broad southeast to northeast cline of colour saturation at the beginning of the Neolithic period illustrates a sampling bias towards earliest evidence of milk use. Substantial heterogeneity in milk exploitation is evident across mainland Europe. By contrast, the British Isles and western France maintain a gradual decline across 7,000 years after first evidence of milk about 5500 BC. Note that interpolation can colour some areas (particularly islands) for which no data are present.

One reason the authors doubt the classical story is that while dairying and milk-drinking by adults began about 10,000 years ago, the gene for LP (determined from sequencing “fossil DNA”) didn’t spread widely until about 4,000 years ago.  Why is that? The mutation for LP is dominant, which means it could have spread widely very quickly, as even carriers of one copy would have a reproductive advantage. This temporal disparity is what led the authors to propose their alternative hypotheses for the spread of the LP alleles (there are several).

Further, when the authors tried to correlate the frequencies of the LP allele with the frequency of milk use (the classical explanation), they found no correlation—that pattern was indistinguishable from a general rise in frequency over Europe regardless of milk use.

One other set of data led to the new hypothesis. That is the observation that LI people in both Britain and China can still drink lots of milk without suffering any measurable health or reproductive effects (milk drinking has recently proliferated in China).  Of course, things are different now from 4000 years ago, but one of the differences led to the authors’ two hypotheses: the spread of the LP allele was promoted especially strongly in prehistoric times by the prevalence of famine and of disease—with the latter coming often from animals, either domesticated or those that hang around settlements. (As the authors note: “about 61% of known and about 75% of emerging human infectious disease today come from animals”).

So the authors erected two hypotheses, the crisis mechanism and the chronic mechanism. I’ll let them describe the hypotheses that they tested (my emphases)

Given the widespread prehistoric exploitation of milk shown here and its relatively benign effects in healthy LNP individuals today, we propose two related mechanisms for the evolution of LP. First, as postulated in ref. 24, the detrimental health consequences of high-lactose food consumption by LNP individuals would be acutely manifested during famines, leading to high but episodic selection favouring LP. This is because lactose-induced diarrhoea can shift from an inconvenient to a fatal condition in severely malnourished individuals and high-lactose (unfermented) milk products are more likely to be consumed when other food sources have been exhausted. This we name the ‘crisis mechanism’, which predicts that LP selection pressures would have been greater during times of subsistence instability. A second mechanism relates to the increased pathogen loads—especially zoonoses—associated with farming and increased population density and mobility. Mortality and morbidity due to pathogen exposure would have been amplified by the otherwise minor health effects of LNP in individuals consuming milk—particularly diarrhoea—due to fluid loss and other gut disturbances, leading to enhanced selection for LP We name this the ‘chronic mechanism’, which predicts that LP selection pressures would have increased with greater pathogen exposure.

In other words, the reproductive advantage of having the LP allele came from the reproductive disadvantage (through death) of lactose-intolerant people during times of famine and disease.

They tested the two hypotheses by correlating indices of famine and of disease deduced from archeological and paleontological evidence:

Crisis mechanism: “Subsistence instability”, or famine, was assessed by prehistoric fluctuations in population size, which, the authors say, is correlated with the likelihood of famine (they provide no evidence for the latter supposition). But the correlation gives a significantly better fit to the pattern of LP allele frequency than just assuming uniform selection over time and space.

Chronic mechanism:  The authors hypothesized that the frequency of disease would correlate with the likelihood of “zoonoses” (diseases caught from animals), which itself would correlate with temporal variation in settlement densities.  These data, which to me would be correlated with “prehistoric fluctuations in population size” above, also explained LP allele frequencies better than an assumption of uniform selection.

Of course, there’s no reason (and the authors say this) that both mechanisms couldn’t operate together. Curiously, though, indices of the density of domestic animals did not support the “chronic mechanism” though measurements of the proportion of wild animals around humans did.  This implies that, if the “chronic mechanism” is correct, people were getting sick not from their horses, dogs, cattle, or sheep, but from wild animals (perhaps from eating them).

Other hypotheses that the authors mention but didn’t test include “drinking milk as a relatively pathogen-free fluid”, allowing “earlier weaning and thus increased fertility.” I would add that if diseases are causal here, they could come not from being around animals, but having drunk contaminated water, giving an advantage to those who prefer milk. But there’s no way of assessing that from the archaeological record.

The upshot: On the last page of the paper the authors say that they’ve debunked the prevailing narrative:

The prevailing narrative for the coevolution of dairying and LP has been a virtuous circle mechanism in which LP frequency increased through the nutritional benefits and avoidance of negative health costs of milk consumption, facilitating an increasing reliance on milk that further drove LP selection. Our findings suggest a different picture. Milk consumption did not gradually grow throughout the European Neolithic period from initially low levels but rather was widespread at the outset in an almost entirely LNP population. We show that the scale of prehistoric milk use does not help to explain European LP allele frequency trajectories and thus it also cannot account for selection intensities. Furthermore, we show that LP status has little impact on modern milk consumption, mortality or fecundity and milk consumption has little or no detrimental health impact on contemporary healthy LNP individuals.

Instead, they say that they find support for the increase of LP alleles through both famine or pathogen exposure.

Well, the data are the data, and their indices comport better with those data than does the classical hypothesis—the “prevailing narrative.” I’m still not convinced that their proxies for famine or disease are actually correlated with famine and disease themselves, but other researchers will undoubtedly dig into that.

What I want to emphasize is that if the work of Evershed et al. is accurate, it still does not overturn the story of gene-culture “coevolution”.  The “coevolution” is still there, the fact that a change in human culture influenced our evolution is still there, and the fact that drinking milk conferred higher reproductive fitness is still there. What has changed is only the nature of selection. Granted, that’s a significant expansion in understanding the story, but to listen to the media—social or otherwise—you’d think that the “classical narrative” is completely wrong. It isn’t. It’s still correct in the main, but the way selection acted may be different from what we used to think. The media love “evolution scenarios are wrong” tales, and that seems to be the cast of at least some stuff I’ve seen in the news and on social media.

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Reference: Evershed, R.P., Davey Smith, G., Roffet-Salque, M. et al. 2022. Dairying, diseases and the evolution of lactase persistence in Europe. Nature. https://doi.org/10.1038/s41586-022-05010-7

Vox’s evidence for evolution from vestigial traits in humans

June 14, 2022 • 2:00 pm

Here’s an old video from Vox that shows morphological evidence for evolution in the human body based on vestigial organs and traits. Most of these can be found in Why Evolution is True, but it’s good to see them in video like this.

This takes the website back to its original aim: giving the readers evidence for why evolution is true.

A vestigial trait of birds that may have been functional in ancestors: remote-sensing of vibrations in the bill (still active in the kiwi)

December 11, 2020 • 10:00 am

A new scientific paper from the Proceedings of the Royal Society Series B (first screenshot below) tells a rather complex story that I’ll deliberately simplify to save space. The paper is behind a paywall, but a pdf may be found via judicious inquiry, and the reference is at the bottom.

The article above is aptly summarized by Veronique Greenwood in the New York Times‘s “Trilobite” column

Three groups of birds have evolved a remarkable feature: the ability to remotely sense prey (i.e., detecting prey without touching them) by sticking their bills in the ground and sensing vibrations. These groups are the kiwis, the ibises, and some shorebirds. The detection can occur either through the direct sensing of vibrations of prey movement, or the reflection of sound waves off hard-shelled prey as the bird sticks its beak into the ground. This feature is called “remote touch.”

It turns out that the bill tips of “remote touch” birds are pitted with small depressions that contain cells called “Herbst corpuscles”, which are the motion-detecting organs. aThese birds also have an expanded area of the brain that is used to process the extremely important touch signals.

Other species have different ways of using their bills to detect prey by touch. Ducks and geese have a bony organ at the tip of their bills that also have pits with Herbst corpuscles, but they are organized differently, with mechanoreceptors beside them. These are what ducks use in “dabbling”—turning their butts up and sticking their beak into the dirt or sediments to forage. Finally, parrots have a different kind of bill-tip organ with receptors not located in the bone.

Below are photos from the paper showing the different types of bill tips. The authors also examined skulls of hundreds of living species and dissected beak tissue from many to see if there were Herbst cells associated with the bill pits.

First, a bird without remote sensing, as with most birds. It’s a kelp gull (Larus dominicus). There are a few pits at the tip of the bill, but soft tissue analysis showed no receptor cells. It does not forage by touch.

Here are two birds with remote sensing. First, the hadeda ibis (Bostrychia hagedash). Note the highly pitted bill tip organ (enlarged). It also has the Herbst cells as well as an enlarged bit of the brain for detecting touch. (This bird, like all other birds save the ratites and tinamous, falls into the large group of species called neognaths.)

Ditto for the kiwi, which falls into the other group of birds, the paleognaths, a small group that contains only the large flightless birds or ratites (emus, ostriches, etc.) plus the tinamous, which can fly, but not well. Its remote sensing organ with Herbst cells is located at the very tip of its long bill. Indeed, the ratio of bill length to skull size is one of several keys to diagnosing whether these birds have remote sensing.

Finally, the tinamou, a paleognath that= has a remote-sensing organ containing the pits but no Herbst corpuscles in them. But this species doesn’t feed by probing the ground. Other ratites, like the ostrich and emu, also have a pit-studded bill, but no vibration-detecting cells. The pits seem to be a leftover from an ancestor which had pits that were useful because they contained vibration-detecting cells. In other words, they’re a vestigial trait.

The other ratites also lack the expanded brain regions for processing information from the touch receptors. This makes sense, for while it may not cost much to retain some pits in the bill when you don’t need them, brain tissue is metabolically expensive, and if you’re not using it it would pay to divert those resources to other functions that would help you reproduce.

As I said, the presence of the pits in birds that don’t use them suggest that this trait is a vestigial trait carried over from an ancestor.  One can distinguish the remote-touch birds from other species by a combination of bill length/skull size ratio, number of pits, and spacing between the pits.

But which ancestor? It turns out that we have fossil skulls of ancient extinct birds, the lithornithids, which are very early paleognaths. Although soft tissue wasn’t available for these birds, some of the species show the mechano-sensing organ—as evidenced from the number and spacing of the pits, as well as the bill/skull ratios characterized by remote foragers. Here’s a photo of the two lithornithid skulls; captions under the photos are from the paper (click to enlarge photo).

Cranial fossils of two species of lithornithids, showing high degree of pitting on the surfaces of their beaks, similar to all extant palaeognathous birds, potentially indicative of a bony bill-tip organ. (e) Lithornis promiscuus: (i) skull and attached maxilla (USNM 391983) showing the shape of the beak relative to the skull; (ii) distal portions of maxilla and mandible (USNM 336535). ( f ) Paracathartes howardae: maxilla (USNM 404758) and distal portion of mandible (USNM 361437).

The conclusion is that putative ancestors of the paleognaths were remote-touch-sensing species. The fact that living paleognaths like emus and tinamous still retain the pits suggests that this nonfunctional “organ” is a useless remnant of a trait inherited by all paleognaths from a lithornithid ancestor.  Indeed, the authors think that the ancestor of all birds might have been a remote-sensing prober (my emphasis):

Our analyses corroborate that the basal palaeognaths, the small, volant lithornithids, had a tactile bony bill-tip organ enabling them to use remote touch to locate buried invertebrate prey items. This finding, combined with our understanding of the evolution of the lithornithids, suggests a Cretaceous origin of the remote-touch sensory system in modern birds before the palaeognath–neognath split.

As for why among living paleognaths only the kiwi has a functional touch organ when it was present in an extinct ancestor, that could be explained by either of two scenarios. The first involves, the organ’s loss in a more recent ancestral species and then the re-acquisition of the organ in just the kiwi lineage. The second possibility is that the kiwi kept an ancestral remote-probing organ while all the other paleognaths lost it. The authors are unable to distinguish between these two scenarios.

What about the neognaths that have remote-sensing organs, like the ibis or shorebirds? Did they retain the ancestral touch organ while all other neognaths—the vast majority of living birds—lost it? Probably not; as the authors say, this is an independent case of evolution.

What is even more fascinating is the possibility that this ability to detect prey remotely may have been present in the reptilian ancestors of birds, which may scientists think are the theropod dinosaurs:

Interestingly, there is increasing evidence that some non-avian theropods had specialized sensory structures located on the distal portion of their rostra, based on a high degree of external foramina/pitting preserved on their mandibles. We speculate that perhaps such sensitive snouts in non-avian theropods may have been precursors to the evolution of remote touch in their avian relatives.

It’s interesting to note that alligators and crocodiles also have touch-sensitive “dome receptors” in their upper jaws, also associated with pitting in the bones.  The archosaurs are a group of early reptiles ancestral to both birds and crocodilians, and maybe the receptors we see in crocs and gators are related, in some way, to the pits in the beak of the kiwi.

This is all speculative, but what seems pretty solid is that the bill pitting and useless “touch organs” in non-kiwi ratites and tinamous are vestigial remnants of a functional organ in an ancient ancestor. And that’s evidence for evolution.

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Toit, C. J. d., A. Chinsamy, and S. J. Cunningham. 2020. Cretaceous origins of the vibrotactile bill-tip organ in birds. Proceedings of the Royal Society B: Biological Sciences 287:20202322.

An atavistic claw in a duckling?

June 2, 2020 • 12:30 pm

The other day I took a picture of this juvenile mallard—one of Honey’s babies—and a friend noticed it had what appeared to be an atavistic claw on its wing. At least I think it’s on its wing; it could be on a  foot tucked behind the bird. But I doubt it.

Here I’ve circled it:

And enlarged it:

The question is whether this is an atavistic claw: the remnant of the claw that was on the reptilian forelimb, and was also prominent in early birds (ignore the labeling of Archaeopteryx as “the earliest known bird”.

Birds also have “spurs“, which are outgrowths of bone that aren’t developmentally homologous to a true claw. But the duckling above seems to have a true claw; it doesn’t look like a bone spur, but is recurved and apparently made of keratin.

Real bird claws, as in the hoatzin,  grow from the digit that’s in the bird wing; in this case it would be the “thumb”. Here’s a “normal” bird.

 

But birds like hoatzins have true claws, especially in the chicks, which use them to climb back into trees when they fall in the water. I’ve put an Attenborough video of this behavior below the picture, and what it shows is that the claim that a “vestigial” character has to be nonfunctional to be considered vestigial is incorrect. Vestigial traits are simply remnants of traits that evolved earlier but have been coopted for a different function (“exaptations”, Steve Gould might call them). The hoatzin’s claw, very useful for the bird, is certainly a vestigial trait, and is just as much evidence for evolution (of birds from reptiles) as if it were completely nonfunctional.

Some species of waterfowl are known to have these claws (see here and here), but I can’t find something explicitly on mallards.

So we have a mystery here, and I’ve asked a few experts to weigh in. This is either a true atavistic claw in the wing, or one of the claws (nails) in the duck’s rear foot, which could be tucked behind it. You can weigh in, or wait for an answer. Stay tuned.

h/t: Nicole, Greg

 

My talk in Tallahassee in late March

February 25, 2020 • 12:00 pm

In almost exactly one month, I’m speaking to the Tallahassee Scientific Society in Tallahassee, Florida. My talk is on Thursday, March 26, and I think the time and venue are the same as those for the previous speaker: 7 p.m. at Tallahassee Community College’s Center for Innovation on Kleman Plaza. The topic is “Why Evolution is Still True”, and I’ll give a brief rundown of the evidence for evolution (updated in light of new discoveries), followed by discussion of why Americans remain so resistant to this scientific truth.

I’ll give one more announcement in mid-March or so, and all are welcome to come. I believe they’ll also have my two trade books on sale, which I’ll be glad to autograph. And, if you tell me the genus and species of any felid besides the house cat, I’ll draw a cat in it.

Here’s a photo I sent them to use for advertising the talk; the picture is from Wikipedia so it’s in the public domain. Toes, teeth, and size!

40bd9fb2-c3b2-4206-a1fa-4d888b06006f-Coyne_Evolution
Photo credit: H. Zell (from Wikimedia Commons; CC license CC BY_SA 3.0).

 

More evidence for evolution: Horse embryos start forming five toes, and four primordia disappear

February 10, 2020 • 9:00 am

When I started this website in 2009, my intention was just to publicize my new book, Why Evolution is True. On the advice of my publishers, I created a site with the idea of occasionally posting new evidence for evolution to complement what was in the book. I expected to post about once a month or so.  Well, what a monster this has become!

But today I’m writing about some new work that fits perfectly with the original aim of this site. It’s a paper in the Proceedings of the Royal Society by Kathryn Kavanagh et al. that gives developmental evidence for the five-toed ancestry of modern one-toed horses. You can read the paper by clicking on the screenshot below or reading the pdf here ; a full reference is at the bottom. If you want a short but less informative piece, the New York Times has a report. 

Lots of organisms show developmental evidence for their evolution from very different ancestors; I describe some of this in chapter 3 of Why Evolution is True.  Embryonic dolphins, for example, develop hindlimb buds, which in their four-legged ancestors went on to become legs, but in the dolphin the buds regress before birth, leaving newborns with no hind limbs. We humans, like all terrestrial vertebrates, begin development by forming what go on to become gill slits in our fishy ancestors. In reptiles, amphibians, and mammals, though, those gill slits are transformed into other stuctures, like our esophagus.

In my evolution class I talk about the lanugo: the thick coat of hair that human fetuses develop at about six months after conception. It’s shed before birth—but not in chimps, our closest relatives, who are born hairy (remember: we are the “naked ape”). The transitory formation of that coat of hair in our species, which is of no use to the embryo, can be explained only by our descent from a primate with hair.

So if these transitory features disappear, why do we see them at all? We’re not sure, but their appearance may be necessary to provide developmental “cues” for the appearance of features that do remain. Remember, development is a very complex process which requires a nexus of coordinated features appearing at the right times. In the dolphin, for instance, the hind limb buds may provide cues for the development of other skeletal structures, and then disappear because they are no longer needed, for natural selection would remove them because they’re cumbersome, a waste of resources, and unnecessary in a marine mammal.

Horses are another example. We know from the fossil record that modern horses evolved from five-toed ancestors, but what we have left, the lower leg and hoof, are the remnants of only the middle toe. The other four toes disappeared over time (we can see this in the fossil record), though the two toes flanking the middle one remain as vestigial “splint bones” on the horse’s leg. The outer two toes are gone completely. Here’s a drawing of one of the vestigial toes in a modern horse: a splint bone (lateral view; there’s one on the other side, too):

Source: Atlanta Equine Clinic

But you can see all five toes if you look closely during development, as reported in this new paper. If you get horse embryos at the right early stage of development, you can see the primordia for all five toes forming, with the outer ones fusing and shrinking to leave only the middle toe, which becomes the lower leg and hoof. Previously, nobody had been able to see this evidence of ancestry in embryos, but Kavanagh et al. managed to get the right material.

The authors procured (don’t ask me how) horse embryos from artificially inseminated mares, and analyzed four of them by making tissue sections of embryos between days 29 and 35 after copulation. (There is a very narrow window of time to see the primordia for all five digits, as shrinkage and disappearance of the four superfluous ones is fast.)

First, here’s a diagram of what the primordia look like. On the right side you see the evolutionary progression of horse ancestors (also shown below), starting with five, then four, and then three, with the two side toes gradually being reduced to the splint bones. We’re not sure why this happened, but a likely explanation is that at the time these horses were evolving—and they evolved in what is now North America—the climate was drying up and the forests of the West were giving way to grasslands. While toes are good for running fast around trees and vegetation, if you’re escaping predators in a featureless grassland, you want a hoof to run fast and straight.

On the left side, in blue, are the toe primordia in four embryos; those blue bits are regions where cartilage would normally condense and then bone would form. (“FL is “foreleg” and “HL” is “hindleg”). You can see that two of the embryos have five primordia early on, with the central one, which becomes the lower leg, being the largest, as it’s the toe that will become the hoof. The other two embryos have three primordia, with the central one the largest.

Figure 1. (a) Illustration of arrangement and relative sizes of pre-cartilaginous condensations in developing Equus FL and HL digits based on reconstructions of histological sections of 30–35 dpc embryos from this study. (b) Fossil transition series of adult horse FL digits (isometrically scaled) showing the sequence of reduction of anterior and posterior digits and increasing dominance of central digit III. (i) Phenacodus (AMNH 4369), (ii) Hyracotherium (AMNH 4832), (iii) Mesohippus (AMNH 39480 and AMNH 1477), (iv) Hypohippus (AMNH 9407), (v) Hipparion (AMNH 109625), (vi) Dinohippus (AMNH 17224). Illustration from Solounias et al. [6]. (Online version in colour.)
Here’s a photo of the two embryos showing five toe primordia at different points along the legs. You can see five shadowy primordia, with the largest in the middle in (b) of embryo 1 and (g) of embryo 2. (“Proximal” is toward the body and “distal” is toward the future hoof.) In later embryos studied by other people, the big primordium in the middle goes on to develop into the lower leg and hoof, and the others disappear.

 

Now of course we don’t need this kind of evidence to show evolution, or even to show evolution of toe loss in horses, as we have an excellent fossil record of horses and a good idea of their “family tree”. Here’s a figure from the Encyclopedia Brittanica:

But the developmental evidence is a nice confirmation of what the fossils tell us, and add the information that the evolutionary sequence of toe loss is mirrored in the developmental sequence of modern one-toed horses. This is a version of the “biogenetic law” stating that “ontogeny recapitulates phylogeny” (i.e., development mimics evolutionary history). That law has many exceptions, for sometimes the ancestral stages are competely lost in embryos, but it does hold for horse toes. First five, then three, then one—in both development and in the fossil record.

By the way, sometimes the side toes don’t disappear, but, probably through a screwup in development, form rudimentary adult toes, producing polydactylous horses like this one:

Similarly, sometimes the dolphin’s hind limbs don’t disappear and we get dolphins with little legs sticking out of its rear, like this one that I show in my “evidence for evolution” talk:

UPDATE: I forgot to include the authors’ point that many vertebrates have lost toes from the ancestral five, and that these species are ripe for embryological investigations of the type shown here. They give a table of some of these animals. Would embryos of the camel or the three-toed jerboa, for instances, show five toe primordia that are then lost? We don’t know if this is the case, and the absence of five primordia wouldn’t disprove evolution, for the retention of toe primordia is a lucky (for us) feature of development, but isn’t expected in every case.

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Kavanagh, K. D., C. S. Bailey, and K. E. Sears. 2020. Evidence of five digits in embryonic horses and developmental stabilization of tetrapod digit number. Proceedings of the Royal Society B: Biological Sciences 287:20192756.