Category: evidence for evolution

Caturday felids trifecta: kitten rescued after tornado; brave cat spooks bear; why cats can’t taste sweetness; and lagniappe

June 20, 2026 • 9:45 am

On May 9, the AP’s odd news site recounted a kitten rescue (click on screenshot to read):

An excerpt:

As storm chaser Ashton Lemley picked his way through a tornado-ravaged Mississippi trailer park, he heard the unmistakable meow of a kitten pierce the predawn darkness.

The homes were flattened just hours earlier as storms spawned at least three tornadoes across the bottom half of Mississippi, injuring a dozen at the trailer park in the rural community of Bogue Chitto.

Lemley had no idea where the kitten was, but he was determined to find it. After a few minutes, the meowing stopped, and Lemley feared the worst.

Then, five minutes later, he heard it again.

“I said, ‘Oh, he’s still alive!’” Lemley told The Associated Press on Thursday.

Lemley quickly dug under insulation from a flattened wall until his flashlight beam found the kitten — wet, scared and hiding between two wooden posts.

Lemley captured the moment on video: “Oh my goodness, I found him!” he says to the camera. “Are you OK? Come here – it’s OK. … We’ll get you cleaned up, baby. Don’t you worry.”

Lemley held the kitten in his arms for a few minutes before handing it off to the commander of the United Cajun Navy, a volunteer disaster-response group, who dried it off and took it to safety. Lemley marveled that it didn’t appear to be injured.“I’ve been in these situations so many times,” said Lemley, who has been chasing storms since 2010. “I don’t try to get overly emotional. But it is very heartbreaking to see any type of animal or human go through something like that.”

Lemley says there’s already a lot of interest from people who want to adopt the kitten if its owners are not located. Some, he said, want to name it Tornado.

It won’t be coming home with him, though: Lemley is allergic to cats.

Here’s a short video of the rescue. Look at that sodden little moggy! But it will be okay.

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From PetHelpful, we have a Tik Tok video and the video notes (indented below).

Little Bear Visits My Bedroom Window

An unexpected guest can make for a delightful surprise, and nothing illustrates this better than when I found a little black bear gazing curiously through my bedroom window. This moment was not only adorable but also a wonderful reminder of the beauty of wildlife right at our doorstep.

Bears are fascinating creatures known for their intelligence and curiosity. When a bear approaches residential areas, it often piques curiosity and concern among homeowners. Observing animals in their natural habitat can lead to valuable insights about their behavior. In this case, Little Bear seemed intrigued by what was happening inside the house, highlighting the need for a peaceful coexistence with wildlife..It’s important to remember that while these encounters can be entertaining, maintaining a safe distance from wild animals is essential for both human and animal safety. Living close to nature offers unique experiences, but it also requires responsibility. If you find yourself in a similar situation, enjoy the moment, take pictures if safe, but avoid feeding or trying to interact directly with wild animals.

In closing, this little bear visiting my window was a charming experience that reminded me of the vibrant wildlife that surrounds us. Have you had any wildlife encounters in your area? Share your stories or tips on safely observing animals in nature!

Here’s a very short video of the cat, safely inside, lashing out with its paw at the bear. Bear heads for the hills!

@missashleyrubes

I was reading in bed when I looked over to Little Bear looking into my window 🪟🐻 #bear #blackbear #animal #nature #wildlife

♬ Curious Animals – Eitan Epstein Music

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If you own a cat, you probably know that they can’t taste sweetness in food. This article from Space Daily (click on screenshot) explains why. Well, it’s not rocket science: cats don’t have the rcceptors to taste sweetness. Or rather, they have the genes that allowed their ancestors (and their living mammalian relatives) to taste sweetness, but the genes are broken. (This is, of course, proof of evolution: why else would a cat have genes that function in its relatives, but that are broken in felids?

An excerpt:

Cats are notoriously indifferent to sweet things. Pour syrup near a dog and the dog will investigate. Pour syrup near a cat and the cat will ignore it. Veterinarians and cat-food companies have long noted that cats show no preference for sugar in feeding tests, no matter how much sugar is presented. The reason is not a behavioural quirk or a learned aversion. It is genetic, and it traces back tens of millions of years to the point at which the ancestors of modern cats became obligate carnivores, eating only meat. The gene that produces a working sweet receptor on the tongue, called Tas1r2, has been broken in cats for so long that it no longer functions at all. A cat looking at a sugar cube is in the same sensory position as a human looking at an ultraviolet light source: the signal exists, but the receptor that would detect it does not.

The molecular discovery came in 2005 from a team led by Xia Li and Joseph Brand at the Monell Chemical Senses Center in Philadelphia, in collaboration with colleagues at the Waltham Centre for Pet Nutrition in the United Kingdom. Their paper in PLOS Genetics, titled “Pseudogenization of a Sweet-Receptor Gene Accounts for Cats’ Indifference toward Sugar,” established that the cat sweet receptor is not just inefficient. It is, at the genetic level, non-functional.

. . . The animals affected included the California sea lion, the southern fur seal, the Pacific harbor seal, the Asian small-clawed otter, the spotted hyena, the fossa (Madagascar’s largest carnivore), and the banded linsang. Crucially, the disabling mutations in each of these species occurred in different places within the Tas1r2 gene, indicating that the losses happened independently in each lineage, not via inheritance from a common ancestor. The same evolutionary pressure that turned off the gene in cats turned it off, separately, in at least seven other carnivorous lineages over the same broad timeframe. Behavioural testing of two of the genotyped species — the Asian small-clawed otter (broken Tas1r2) and the spectacled bear (intact Tas1r2, and predominantly herbivorous despite its order) — confirmed the pattern. The otter showed no preference for sweet compounds. The bear preferred sugars and even some non-caloric sweeteners.

. . . The animals affected included the California sea lion, the southern fur seal, the Pacific harbor seal, the Asian small-clawed otter, the spotted hyena, the fossa (Madagascar’s largest carnivore), and the banded linsang. Crucially, the disabling mutations in each of these species occurred in different places within the Tas1r2 gene, indicating that the losses happened independently in each lineage, not via inheritance from a common ancestor. The same evolutionary pressure that turned off the gene in cats turned it off, separately, in at least seven other carnivorous lineages over the same broad timeframe. Behavioural testing of two of the genotyped species — the Asian small-clawed otter (broken Tas1r2) and the spectacled bear (intact Tas1r2, and predominantly herbivorous despite its order) — confirmed the pattern. The otter showed no preference for sweet compounds. The bear preferred sugars and even some non-caloric sweeteners.

And since people here should know some science, you’ll be able to understand this from the paper’s abstract:

Because the mammalian sweet-taste receptor is formed by the dimerization of two proteins (T1R2 and T1R3; gene symbols Tas1r2 and Tas1r3), we identified and sequenced both genes in the cat by screening a feline genomic BAC library and by performing PCR with degenerate primers on cat genomic DNA. Gene expression was assessed by RT-PCR of taste tissue, in situ hybridization, and immunohistochemistry. The cat Tas1r3 gene shows high sequence similarity with functional Tas1r3 genes of other species. Message from Tas1r3 was detected by RT-PCR of taste tissue. In situ hybridization and immunohistochemical studies demonstrate that Tas1r3 is expressed, as expected, in taste buds. However, the cat Tas1r2 gene shows a 247-base pair microdeletion in exon 3 and stop codons in exons 4 and 6. There was no evidence of detectable mRNA from cat Tas1r2 by RT-PCR or in situ hybridization, and no evidence of protein expression by immunohistochemistry. Tas1r2 in tiger and cheetah and in six healthy adult domestic cats all show the similar deletion and stop codons. We conclude that cat Tas1r3 is an apparently functional and expressed receptor but that cat Tas1r2 is an unexpressed pseudogene. A functional sweet-taste receptor heteromer cannot form, and thus the cat lacks the receptor likely necessary for detection of sweet stimuli. This molecular change was very likely an important event in the evolution of the cat’s carnivorous behavior.

The upshot: tasting sweetness in mammals requires a protein that is a dimer made from the product of two genes. In house cats (and some other carnivores), one of the genes is expressed normally but the other is nonfunctional because of a large deletion of the DNA sequence, so that the dimer itself isn’t formed. Ergo cats can’t detect sweetness, and thus you shouldn’t expect your cats to like sweets (they shouldn’t get them anyway). If your cat licks ice cream, it is tasting not the sweetness but the dairy-ness: fats and proteins.  Cheetahs and tigers also lack the dimeric protein.

Why do dogs taste sweetness and cats don’t? Because dogs produce the dimer and cats don’t.  Somewhere in the ancestor of all felids, the gene for Tastr2 experienced a deletion.  Because all cats are obligate carnivores, and don’t eat stuff like berries, they have no “need” to taste sweetness, so a deleted gene is not a deleterious gene. It just continued to mutate, staying in the DNA but doing nothing.

I suppose d*g ancestors, and mammals like bears and hedgehogs, do benefit from sugar in their diet and so have retained the genes to detect it. (We do, too: sugars were valuable components of the diet in us and our primate relatives, and so our taste chemistry evolved to not only detect sweetness, but also find it pleasurable so that we seek out a needed nutrient. Unfortunately, sugars are much more common now than in the millions of years of our ancestry since we diverged from the chimp/bonobo lineage; and so we eat too many of them and get cavities and grow obese.)

The alternative theory is that God decided to make cats obligate meat-eaters, and so he left out their ability to detect sugar. But that doesn’t work because why would God give cats genes that are very similar to those of their sweetness-tasting relatives, but don’t work?  The creation-by-God theory fails, and we’re left only with common ancestry, i.e., evolution.

We have a similar broken gene, as I describe in Why Evolution is True:

The most famous human pseudogene is GLO, so called because in other species it produces an enzyme called L-gulono-γ-lactone oxidase. This enzyme is used in making vitamin C (ascorbic acid) from the simple sugar glucose. Vitamin C is essential for proper metabolism, and virtually all mammals have the pathway to make it—all, that is, except for primates, fruit bats, and guinea pigs. In these species, vitamin C is obtained directly from their food, and normal diets usually have enough. If we don’t ingest enough vitamin C, we get sick: scurvy was common among fruit-deprived seamen of the nineteenth century.

The reason why primates and these few other mammals don’t make their own vitamin C is because they don’t need to. Yet DNA sequencing tells us that primates still carry most of the genetic information needed to make the vitamin.

It turns out that the pathway for making vitamin C from glucose involves a sequence of four steps, each promoted by the product of a different gene. Primates and guinea pigs still have active genes for the first three steps, but the last step, which requires the GLO enzyme, doesn’t take place: GLO has been inactivated by a mutation. It has become a pseudogene, called ¯ψGLO” (ψ is the Greek letter psi, standing for “pseudo”). ψGLO doesn’t work because a single nucleotide in the gene’s DNA sequence is missing. And it’s exactly the same nucleotide that is missing in other primates. This shows that the mutation that destroyed our ability to make vitamin C was present in the ancestor of all primates, and was passed on to its descendants. The inactivation of GLO in guinea pigs happened independently, since it involves different mutations. It’s highly likely that since fruit bats, guinea pigs, and primates got plenty of vitamin C in their diet, there was no penalty for inactivating the pathway that made it. This could even have been beneficial since it eliminated a protein that might have been costly to produce.

A dead gene in one species that is active in its relatives is evidence for evolution, but there’s more. When you look at ψGLO in living primates, you find out that its sequence is more similar between close relatives than between more distant ones. The sequences of human and chimp ψGLO, for example, resemble each other closely, but differ more from the ψGLO of orangutans, which are more distant relatives. What’s more, the sequence of guinea pig ψGLO is very different from that of all primates.

Only evolution and common ancestry can explain these facts.

Inactive pseudogenes that are functional in relatives constitute some of the strongest evidence for evolution, as there is no alternative theory that explains them. The article above alludes to the gene loss being a product of evolution, but doesn’t mention something that I see as crucial given Americans’ reluctance to accept evolution: the nature of the gene loss and the sequence similarity among pseudogenes is strong evidence for evolution.

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Lagniappe:  From an Archaeology and Art Facebook post:  Draw a cat using only straight lines.  Here you go:

And extra lagniappe (is that redundant?). Only in Turkey will there be spectators!

h/t: Ginger K.,

Convincing evidence for human evolution

November 2, 2023 • 11:30 am

I occasionally get questions like this one: “What do you consider the most convincing evidence for evolution?”  My answer is usually “the fossil record combined with dating methods,” but I often add that “the evidence from biogeography is so convincing that I’ve never seen a creationist even try to rebut it.” (You can see some of the biogeographic evidence in chapter 4 of Why Evolution is True, and I give the fossil evidence in Chapter 2.)

And if someone asks me, “What’s the most convincing evidence for human evolution?”, I’d also give the first answer above. That’s because the temporally ordered record of human evolution shows a fairly clear progression from the morphology of an ape somewhat like a chimp (i.e., our common ancestor with the chimp and bonobo that lived about 6.4 million years ago).  It’s not a straight line pathway, and we don’t know all the details, for human evolution, like all evolution, is a branching bush, and some branches went extinct.

When I was on a BBC Three show, “Conspiracy Road Trip,” with each of us assigned to convince a group of British creationists of the truth of one bit of evolution (mine was to dispel Noah’s Ark and the great flood scenario), the most convincing evidence to the creationists was the presentation of an evolutionary series of hominin skulls by Tim at White at Berkeley. That bit begins at 42:26 in the video below (I appear earlier).

This week I got a note from an upset parent whose child attended a religious school where the kid was told that humans could not possibly have descended from apes. I responded that humans were apes, and we descended from a common ancestor with chimps (and from other ancestors with other primates)—an ancestor that, I suspect, looked rather chimplike. (It is of course a misconception that we descended from living chimps.)

I tried to help the parent by giving him evidence for human evolution, and that included this photo from the Smithsonian, posted on Talk Origins, Doug Theobald’s site), showing (with the exception of the skull at the top left corner), various hominin skulls laid out in temporal order.  

The key:

Figure 1.4.4. Fossil hominid skulls. Some of the figures have been modified for ease of comparison (only left-right mirroring or removal of a jawbone). (Images © 2000 Smithsonian Institution.)

Note that the skull at upper left is the skull of a modern chimp, so it doesn’t really belong with the others. It’s just there for comparison. But look how things change over time: the face gets pulled back, the teeth get smaller, the brow ridges shrink, and most evident, the braincase gets larger.

Creationists have big trouble with this because they don’t know where to draw the line between “apes” and “humans”. Some maintain that every fossil earlier than some arbitrary one (say a Homo habilis) is an “ape”, while everything after that is simply a human (they might even say “a malformed human”!) But that tactic is so arbitrary and capricious that it’s not convincing even to some of the British creationists above.

I like the photo simply because it’s a wonderful piece of evidence for human evolution, with the skulls laid out in temporal order. (Now they’ve eliminated the “robust” hominins, and that would confuse things a bit though it would be more accurate, for the robust hominins are still hominins. It also leaves out more recently discovered fossils such as Homo floresiensis, the tiny “hobbit” hominin that went extinct about 50,000 years ago.

Also, we don’t know that this is the line of evolution to modern humans (and it probably isn’t), but it does show gradual change over time that’s undoubtedly genetic, and that is what evolution means.  We do not see fossils resembling modern humans 3 million years ago, but we see them now. The earliest hominin skulls we see resemble the skulls of early apes, and gradually evolve into skulls that look like those those of modern humans.  What better evidence of human evolution could we wish for? I’m always amazed that fossils really exist, and also that human fossils are especially rare—yet there are enough of them to provide convincing evidence that our species evolved from a common ancestor with other apes.

Putting the chimp skull in the figure does cause some confusion, as described at Anthropology.net  by Kambiz Kamrani:

I have some slight problems with this image, though. The biggest problem, and a common misconception I see in regards to understanding human evolution, is the whole we descended from chimpanzees train of thought. This image compounds it. The lineage of primates that have become the chimpanzees have been evolving independently of the human lineage. And because the non-human primate fossil record is rather spotty — it is hard to see these types of trends and transitions that we see in the above image happen along in chimpanzees.

Working on that note, this composition implies that our ancestral form was a chimp and once the chimp and human lines diverged then humans went through many natural selection events while chimps just remained stagnant as chimps. That’s wrong. Chimps and humans share a common ape ancestor.

But if you point out that the modern chimp skull is simply there for comparison, and that in all likelihood is fairly similar to the skull of our common ancestor with modern chimps, the problem disappears. Still, many people think that we evolved from modern chimps, and it takes some doing to dispel that idea by explaining the branching pattern of evolution and the idea of common ancestry. Those are a bit harder.

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?”.

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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

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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