[RUSH TRANSCRIPT BELOW]Modern biology often posits Darwinian evolution and natural selection as a settled explanation for the vast complexity of the natural world. Yet, looking closely at the nanoscale machinery inside the cell reveals molecular systems that seem to defy a gradual, evolutionary unfolding, says Michael Behe, professor of biochemistry at Lehigh University and author of “Darwin’s Black Box,” “The Edge of Evolution,” and “Darwin Devolves.”

“I was startled to see that a foundation concept of my worldview had no support; that it was all built on social considerations,” Behe says.

Importantly, Behe points out that he is not rejecting Darwinian evolution in its entirety. Minor evolutionary adaptations are well-established, he says. But can Darwin’s theory of evolution adequately explain the origin of complex biological mechanisms that require many interlocking components to function at all?

Also, what do recent discoveries in molecular genetics reveal about the boundaries of natural evolution? And why is the scientific consensus on Darwin’s theory far less unanimous than it appears?

Views expressed in this video are opinions of the host and the guest, and do not necessarily reflect the views of The Epoch Times.

RUSH TRANSCRIPT

Jan Jekielek:

Michael Behe, such a pleasure to have you on American Thought Leaders.

Michael Behe:

Thanks, Jan. It’s great to be here.

Mr. Jekielek:

So, in your decades of studying biological systems, looking deeply into the machinery, so to speak, what’s the most shocking thing you’ve come across?

Mr. Behe:

The most shocking thing happened when I first started to read about evolution, and I realized that I had been seriously misled. I was told that it was known that Darwinian processes could produce the biological systems we see in life, but I had cause to go to the library and look up papers to find the papers that explained how they happened. And there were none there. And I was startled to see that a foundational concept of my worldview had no support, that it was all built on social considerations. That’s what we were supposed to believe these days. And that’s what sent me on my road to where I am now.

Mr. Jekielek:

I’m going to get you to dig into that right away.I think, you know, you talk about this concept of irreducible complexity, okay? But when we think of evolution, Darwinian evolution, when I think of it, I immediately think of Darwin’s finches, right? This is what Darwin was looking at. And they’ve been, in fact, studied quite a bit. 

The idea is that there’s some sort of insect on a certain type of bark and it’s deeper in the bark. So some kind of finch might get a longer beak, and that will allow them to get this particular insect. And over time, those longer-beaked animals will survive and eventually will turn into a separate species of finch, right? That seems reasonable, right? But then, irreducible complexity comes in. Explain this to me.

Mr. Behe:

Okay, well, yes, Darwin’s finches, the Galapagos finches that differ a little bit from each other, they’re exactly the kind of thing that Darwin’s theory is good for. If you can change a pre-existing feature a little bit and it helps, like making a beak a little bit longer, and you can get insects inside trees and so on. Yes, that sounds reasonable. And that’s what Darwin proposed pretty much in his, On the Origin of Species, in the 19th century. But it turns out that science has progressed quite a bit from what Darwin knew back then. 

And just to give you a feeling for it, when Darwin was writing Origin, the cell, which we now know to be the foundation of life, the cell was thought to be a little glob of jelly. They called it protoplasm, and it didn’t seem like a big deal to be able to come up with a cell. As a matter of fact, some scientific associates of Darwin’s later on thought that some mud that an exploring ship had dredged up from the ocean bottom looked like a cell in their crude microscopes of the time. So they proposed that cells could just bubble up from the sea bottom. And that was later laughed off the stage by other scientists. 

But it just goes to show you that people didn’t know what the cell was back then. And molecules, which we now know to be the basis of matter, were theoretical entities. Nobody was quite sure if they even existed. And so, since then, biology has made a lot of progress. 

The brief summary is that the cell, which was thought to be so simple, has turned out to be enormously complex. It’s a nanoscale factory, and it has technology that puts human technology to shame. And importantly, it is run by literal machines, machines made out of molecules that use force to move things to do a particular job, and just like many machines in our everyday life, they need a number of different parts in order to work.

One of my examples that I give in one of my books is a mousetrap, just a simple little machine, not sophisticated like many of the machines in the cell. But even a mousetrap needs a number of parts; it needs a spring and a metal bar to snap and a bunch of others. And you need all of those for it to work. If it doesn’t have one, one of the components, the spring or the holding bar or the hammer or the platform, it’s not like it works half as well as it used to. It just doesn’t work at all. And that’s a problem for Darwin’s theory. This is where irreducible complexity comes in. 

I call things like the mousetrap irreducibly complex because they need a bunch of components to work, and if you take one away, it doesn’t work, so you can’t reduce it. It’s irreducibly complex. Darwin always insisted that his theory of evolution had to proceed gradually. You had to make tiny changes over long periods of time in numerous steps, each improving a little bit at a time, because he knew if you improve things in big leaps in a brief period of time, then it would look suspiciously as if something other than chance, random processes were involved.

As a matter of fact, he said if anything could be discovered that could not have been made by numerous successive slight modifications, his theory would not work. But then if you go back and think, what if you have a system that needs a number of components? How do you make that gradually? How do you make a mousetrap gradually? What would you start with? With just a platform? Well, that won’t catch mice. 

And each thing you add, it doesn’t catch mice until the whole thing’s together. And the relevance to actual biology is that, as I mentioned, the cell is filled with machines and they’ve got a number of components that are necessary for them to work. So it’s very difficult to see how they could be built gradually in the way Darwin envisioned.

Mr. Jekielek:

Well, let’s talk briefly about a sort of modern example where we sort of saw evolution in action, and we followed it very carefully. This is, I’m talking about, the COVID-19 pandemic, okay? Because, I mean, all of our media were talking about the new variant and so forth coming in. So we actually saw in real time a kind of Darwinian evolution happening, right, where you start off with an alpha strain, which has, you know, high mortality and relatively high mortality compared to later strains, and it spreads not as quickly. 

And you get this progression towards something which spreads extremely easily, but doesn’t kill as easily because more of that survives and gets transmitted, basically. We have an example, a recent example. Now, of course, I’m talking about a virus here that’s a lot less complicated than a cell, just to be clear. So we see it in action, right?

Mr. Behe:

Yes. So, one should immediately say that just because I argue Darwinian evolution can’t do everything, that doesn’t mean it can’t do anything. And it can explain some things that are medically and biologically important. It’s just a whole lot less than we had been told previously. 

For example, COVID, the virus changes. Yes, it does change, but it’s making little changes, small changes in pre-existing proteins. It’s got a handful of different genes in the virus, and they can mutate very, very rapidly, much, much more rapidly than cellular DNA can. 

In the whole course of the epidemic that people followed, no new proteins, no significant new changes in the basic biology of the virus were seen. And it’s interesting that it’s an RNA virus, and those things mutate about 10,000 times faster than DNA does, which is the basis of all cellular genetics. So it can change, it can alter some pre-existing system a little bit here and a little bit there.

Here is an example that might make it clearer. Suppose you had a lock and a key, and you could put the key in and turn the lock, and it worked. Now, suppose for some reason you didn’t want a thief or somebody to be able to access that lock, you could change the key a little bit and now it doesn’t fit anymore. You only have to change it a little bit, and it doesn’t fit the key anymore. It doesn’t explain the origin of the lock and the origin of the key. It’s similar with viruses.

Oftentimes, they have components that have to stick to a component of a human cell. And if the human cell changes a little bit, or the virus can change a little bit here, move this thing over here, move this thing over here, and it binds a little bit better, binds a little bit worse, and that can help it survive. You’re not even making new components of the new virus. So there are little things that Darwin’s mechanism of evolution can do, but it can’t build the complex machinery of the cell.

Mr. Jekielek:

Sometime after you looked into this irreducible complexity concept, we started getting data on malaria and its ability or inability, in fact, to create resistance to hydroxychloroquine, another drug that’s been popular in the news over the past years. But explain to me what you learned here.

Mr. Behe:

Well, okay. It turns out that one very, very important discovery we’ve made that Darwin didn’t know is that evolution is a molecular phenomenon. He and scientists of the age saw that organisms can vary. They didn’t know why. They didn’t know why changes occurred. Now we know that genetic information is carried by DNA and that it changes in DNA, and DNA carries the information to code for the machinery of the cell. So the change in DNA changes the machinery in the cell, and those are mutations. 

So, in order to understand evolution and understand the scope of Darwin’s theory, you have to look at the molecular changes that are occurring. And it turns out that the machinery of the cell is complex, so that even one gene might have a thousand units in it called nucleotides, and they code for a machine, a protein, which might then have 330 or so residues in it. This is getting into the weeds a little bit. It is really complex. 

And of those thousand nucleotides, you can change one; that would be a mutation. You could add another one; that would be another mutation. You could delete part of it; you could add more to it. But any one of those is a discrete possible event. But it turns out it takes a long time for mutations to occur because the cell is pretty faithful when it replicates DNA. It copies DNA and makes the same sequence of DNA nucleotides in a gene, except on rare, rare occasions it makes a mistake, and that’s what we call mutation. Well, it turns out if you make one change, one mutation, and that can help, that’s well within Darwin’s mechanism’s ability to explain.

Let me offer another example: the sickle cell mutation. Most people know that in Africa and South America, malaria is a very difficult problem. It kills hundreds of thousands of people every year. And over the course of the last 5,000 years or so, a number of mutations in the human genome have been selected because they give the human some resistance to malaria. And one of the most well-known mutations is the sickle cell mutation. And it turns out that’s a change in the protein called hemoglobin, which is in red blood cells of our body.

But hemoglobin has a total of hundreds of different units, amino acids. And the sickle mutation changes one, one out of those several hundred of them. And it turns out that that helps it to stick to each other.We don’t have to go into that, but that gives some resistance to malaria. And because of that, that has spread in the population in classic Darwinian fashion.

Mr. Jekielek:

But also while making a person anemic somewhat at the same time. So there’s a cost-benefit.

Mr. Behe:

Exactly. That’s an excellent point. So, yes, sickle cell by itself, if you lived in a non-malarious area of the world, it’s no good at all. As a matter of fact, it’s detrimental because it does give you some anemia. And if you’re unfortunate enough, where two parents that have just one gene for sickle hemoglobin and one of the normal genes, normal adult hemoglobin, one out of every four children of a pair like that would have two copies of the sickle gene, then you have sickle cell disease. And outside of modern medicine, that’s fatal after 10 years or so. But if you, in human history, the sickle mutation has apparently arisen only one time, maybe a couple times, and spread in the population due to this selection.

Mr. Jekielek:

And I'll just, just to be clear again to our audience, right? The argument is the reason it’s selected for is because people who have this mutation all of a sudden aren’t being killed by malaria at higher rates. These people are surviving despite being slightly anemic at a higher rate. And that would be the Darwinian mechanism. I’m just elucidating it.

Mr. Behe:

Yes, sure. That’s exactly correct. If you think of a village where a child is born with this mutation, she has resistance to malaria. Her classmates, say at school, half of them die or more from malaria. And yes, and so over the generations, that would spread in the population. One mutation in one out of the tens of thousands of proteins in our body. What if you need two mutations? Suppose the first mutation didn’t help, and only when the second one came along, then you got a beneficial effect. 

That’s what happens with chloroquine, which is actually a drug that’s used to combat malaria. And it turns out that some drugs that had been used to treat malaria before chloroquine, if you gave them to a person in a hospital, a field hospital in a malarious region of the world, they'd generally get better. But every third person, malaria, which is actually a single-celled parasite that lives in red blood cells in people after being transmitted by mosquito bite, in every third person or so, the malaria develops resistance. That older drug, every third person. With chloroquine, if you do the same thing, if you give it to people sick with malaria, only it takes a billion people before resistance to chloroquine pops up.

So you say to yourself, what’s the difference between this one, you know, it happens every third, and this other drug, it takes a billion people. And it turns out it was only in the early 2000s that the molecular basis of resistance to chloroquine was tracked down. For the earlier drugs, there only had to be one particular mutation that arose in a patient, in the malaria in a patient, to allow the malaria to survive in the presence of that drug.

But in the case of chloroquine, there had to be two specific mutations in a particular protein. Again, not a new protein, just one, two out of hundreds of amino acids, but they had to be this one and they had to be that one before resistance occurred. And because a mutation turns out happens only one every hundred million DNA replications, in the first instance, you just need a hundred million malaria cells before you get resistance to the initial drug because just by chance you'd expect to get that mutation in so many. 

And it turns out when malaria gets inside you, it replicates, you can have that many cells inside you. So there’s a good chance that you'll get it.  But to get two, you need 100 million times 100 million cells before you get just a second crummy mutation within a particular protein. And if you take three and you multiply it by 100 million, you’re getting close to the billion that we just talked about. 

So, this is a good illustration that if you need just one change, Darwin’s mechanism is what the doctor ordered. If you need just two little changes that build on each other, the first one doesn’t really help. Darwin’s mechanism starts to breathe really heavily. It’s like it’s trying to climb Mount Everest now. If you get beyond two, it’s pretty much beyond Darwin’s capacity to produce it.

In my second book, which is called The Edge of Evolution, I had previously argued that some things were beyond Darwin’s mechanism, but as a scientist, I knew that some things weren’t. So, I wanted to know, well, what’s the kind of rough dividing line between what required purposeful design or what could be explained by chance? If the conclusion is that if a feature needs multiple mutations to produce, it can’t be just one change, then you start to question whether Darwin’s mechanism can produce it. And with this machinery of the cell, you need very many mutations to produce a lot of it.

Mr. Jekielek:

So, I remember back in the day when I was studying evolutionary biology, one of the things that I considered to be a kind of a problem for a Darwinian evolutionary explanation was how do you get an eye, right? Because, you know, if you’re starting with no light sensitivity at all, then you get a light sensitivity. Maybe you can get that through Darwinian evolution. Maybe, I don’t know, maybe you would argue that’s even impossible. I'll find out, right? But eventually, you know, there are just all these complex elements in an eye, basically, that it’s hard to imagine how you could have these intermediate stages that would be, you know, fully functional and confer benefits. That the creature that had that would show up. And it seemed like there would need to be multiple mutations for each of those. 

Anyway, but then I decided to look. I asked Grok, right? Okay, well, have they figured this out? And Grok told me quite eruditely, at least it was portraying itself as being erudite, that yes, indeed, there are all these sorts of intermediate organs that have been found. And so, actually, this is not an issue anymore for Darwinian evolution. I just want you to kind of, what do you think, right? If you think about the evolution of an eye, how does that work?

Mr. Behe:

Well, I think that’s one of the icons that is trotted out to make people cower, say, I need to know a lot about biology before I. And gee whiz, this guy with a PhD is telling me why there’s a light sensitive spot and there’s a spot in the cup and there’s this. So, what’s the big problem? But it turns out, as I try to emphasize in my writings, you’ve got to look at the molecular level at all of these things because all mutations are changes in DNA and changes in the proteins that it codes for. So, you have to have gradualness at that level. 

In The Origin of Species, Darwin himself wrote about the eye, and he wrote about it in a section of The Origin called Organs of Extreme Perfection and Complication. And he specifically brought up the human eye and says, this is so complex. But then he said, well, let’s start. We know that there are some organisms, some animals that have just a light sensitive spot. And there are other ones in which that light sensitive spot is in a cup. 

If you have just a light sensitive spot, you can tell that there’s light, but you can’t tell which direction it’s coming from because any direction will just trigger it. So you can’t tell where it was from. But if it’s in a little cup, now light coming from one side will cast a shadow on the other, and you can theoretically tell which direction it’s from. And if you deepen the cup and you start to add a lens, it gets better and better and better. But he said, what causes a spot to be light sensitive hardly concerns us more than how life itself originated.

Now, he was writing in the 19th century; he had no idea what cells contained, or what molecules were. And it turns out that the simple light-sensitive spot is horrendously complex. In the first steps of vision, a photon of light comes in and hits your retina, and it interacts with a little molecule called retinal, which is a derivative of vitamin A. And ordinarily, it’s shaped like this, bent like my elbow here. 

But when the photon hits it, it snaps out and changes shape. And that causes a change in the shape of the protein called rhodopsin, to which it’s bound. And the change in the shape of rhodopsin allows it to interact with another protein called transducin. And the rhodopsin-transducin complex now activates another protein called a kinase, which eventually causes calcium to come into the cell, and that sends an electrical signal down to the brain. And that’s kind of a little cartoon overview of the complexity of vision. 

But when you look at it at that level, you see, what do you mean, a simple light-sensitive spot? Where did that come from? And then the little cup cell shape; in the absence of proteins, the kind of fatty outside of a cell would be like a soap bubble. What causes a cell to have a little cup in it? It turns out Darwin hadn’t the foggiest idea, and it would be extremely complex to produce that. So there are a lot of organisms in the world, a lot of variety. If you just line things up, say, this looks kind of like this, and this looks like this, you'd build a story. But when you look closely with the least bit of skepticism, you see huge problems for Darwin’s theory.

Let me give you kind of an analogy from our everyday world. You know, you could say, back in the day, computers were pretty slow. They didn’t have much memory; they were, you know, 16 KB or whatever. Then we got 20 KB, and look, here was a 30 KB and a megabyte and a gigabyte. They must have evolved from each other. You know, it probably wouldn’t take much to change one into the other. But if you are an engineer, you know that a lot of thinking, a lot of design changes went into all of those new technologies that can’t be explained by accidents. The same thing is very, very likely for such things as the eye. 

Here is one more point to make on this topic. What Grok told you is at the gross anatomy level. That was the explanation Darwin presented in the 19th century. That’s been more than 150 years. Biology has progressed enormously since then. And yet, that’s still the explanation. There are no improvements; people don’t know how the molecular changes could have occurred.They might see some similarities and say, maybe this came from that, but nobody has even tried to show that it could happen by random changes plus selection.

Mr. Jekielek:

So, this is really, really interesting because basically, you know, I think what it showed me, and there’s plausibility in the intermediate species. The thing that you’re always looking for is sort of the intermediate species. You know, you’ve got the light spot on this end, you’ve got the full eye on this end, and you’ve got all these sorts of intermediate organisms, whether in the fossil record or existing or whatever, and then you have a plasmagazine. 

But the bottom line is, you’re saying that it’s these changes at the molecular level that ultimately drive these realities. So to get a light-sensitive spot at all, you actually need a great many mutations, not just one or two or three. And now we’re talking, you know, these sort of unimaginable orders of magnitude numbers.

Mr. Behe:

Yes, that’s exactly correct. Interestingly, you asked Grok. I later asked a different AI program. I said, give me the best evidence for eye evolution, and it gave pretty much the same story that you recounted. And then I said, okay, but all of those are just due to similarity. They just point to the idea of common descent. Maybe this came from that, but it doesn’t say how Darwin’s mechanism of random mutation and selection could have produced it. You know, what’s the evidence for that?

That second question to AI comes back and says, you got me. There’s not that much evidence to directly connect these, but we do know that mutations happen. And we do know, and so then they'll go back to sickle cell or antibiotic resistance. So the point is that all of these connections are being made in the minds of Darwinian biologists. They have a theory and they say, this would fit into it and this fits into it.

Back in Darwin’s time, that was a perfectly fine attitude to have because he didn’t have any way to test it. But now, 150 years later, we do have ways to test Darwin’s mechanism. And people have done it in the laboratory and other places. And they give absolutely no indication that it has the capacity to build coherent, complex systems.

Mr. Jekielek:

Quite the opposite.

Mr. Behe:

Well, it depends on how you define settled science. The large majority of scientists, if asked on a questionnaire if they believe Darwinian evolution is the full explanation for life, a lot of them, probably two-thirds, will say yes. But very few of them look into the questions that we are talking about today. Textbooks that I read accepted it for the same reason I did before I began to question it. 

On the other hand, there’s a large undercurrent of unrest in evolutionary biology. I would guess that a third, maybe more, maybe even half of evolutionary biologists think that Darwin’s theory is incomplete and that a different theory is called for. I am a proponent of intelligent design. I think that things look designed because they were designed, and that you need intelligent direction to make a lot of these complex systems, just like you do in our everyday world. 

But other folks question the Darwinian mechanism but don’t go that far. They propose other things. There’s something called the extended evolutionary synthesis, which talks about different mechanisms, like maybe cells can build themselves, or maybe when you get to a certain level of complexity, new systems kind of automatically fall out of that. None of these alternative explanations has attracted a majority or a large following, but they do show that there’s a lot of murmuring going on in the community.

Unfortunately, when you get an explicit public challenge to Darwin, such as, say, a group of parents saying, we want our children to be taught that there are questions about Darwin’s theory being raised in the professional literature, then the scientific community has this unfortunate tendency to circle the wagons and say, no, we are the only ones who are allowed to say what is correct or not correct in science. 

This gives the impression from public dust-ups that the scientific community is of one mind. But that’s not true. And even if it were, that’s just a question of what scientists believe, which is a kind of a sociological question. It’s not the same question as what the evidence supports, which is what we’re trying to discuss here.

Mr. Jekielek:

You know, in my undergrad, I was in an honors biology program and sort of getting very interested in evolution. By third year, I had the sense that Darwinian evolution didn’t explain the diversity of life in its entirety, right? And I was always, in fact, I had conversations with my professors, including someone named Dolph Schluter, who was kind of amazing. He’s done some amazing experimental work on sticklebacks back in the day. I had him for a class and just said, isn’t it interesting that many people believe deeply that this is the whole story when it’s clearly not? 

That said, someone who was with me in my thinking, in this very small class of 20 people who were all planning to become professors or something like that, he was someone who started off as a creationist, a devout evangelical Christian. But later, when I talked to him, and after my life took a very different turn, he told me, actually, looking at the DNA sequencing across all sorts of different species and comparing them, this actually convinced me that Darwinian evolution was the main driving mechanism, even though I didn’t believe that back in the day. 

By the way, he became a biology professor himself, working on Drosophila and also fruit flies. But I thought that was very interesting. Of course, he stayed a devout Christian and so forth. At this data of sequencing and the relatedness based on this commonality in DNA sequencing between presumably forms or species that look similar or are purported to have come from a common ancestor or believed to, according to the theory, that was convincing to him. What do you think about that evidence, which also developed quite a bit due to the increase in DNA sequencing and so forth?

Mr. Behe:

Distinctions. When you talk about evolution, you can easily get sidetracked and have fruitless discussions unless you make some basic distinctions. And one is the relatedness of species, the idea of common descent that, you know, back in the day there were organisms that over time changed and gave rise to organisms as we see today.

And the second thing is Darwin’s mechanism for explaining how that could happen, which was random changes and natural selection. Darwin’s theory is not just a theory of descent, it’s a theory of transformation. How did things change? How did we get new things? It does fine, but the relatedness of species was known before Darwin. People thought that they could classify organisms into different categories. These days, since Darwin, we think of common descent because that was one aspect of his theory.

But the main question, the most important scientific and arguably philosophical, even theological question, is the difference between randomness and purpose. Could these changes that impress us as clearly designed? You look at some of the systems in a cell, I always focus on the bacterial flagellum, because that’s an easy one to see or the eye. These things that look clearly designed, could they have arisen by chance, even slowly over numerous steps?

Mr. Jekielek:

Like a flagellum, actually, when you look at it closely, it literally functions like a motor. It’s fascinating.

Mr. Behe:

It really is. An outboard motor. Yes, this bacterial flagellum helps bacteria swim through. And it’s got a motor, it’s got a stator, it’s got bushing material. It’s got dozens of components that are needed. So the question is, could something like that arise by random mutation and natural selection? You could trace the genes for something. You could, well, back to the idea of common descent, the evidence that your friend from college is pointing to is all evidence for common descent. 

But the question is, you know, okay, so, suppose that an organism gave rise, an ancestor of mammals gave rise to bats and whales and dogs. That’s interesting if you can find the same genes, similar ones, in those different branches. But how in the world could that happen? How do a bat and a whale get numerous successive slight modifications, as Darwin proposed? It’s interesting to the great majority of people. 

You say, let’s focus on a simple system and test what random changes and selection do here. And a number of scientists have done that with bacteria and yeast, little single-celled creatures in their labs. And what they see is much different from what you would need to produce complex new systems. 

So we can see the similarities, but the question is, what caused the differences? Similarities relate to common descent. Differences relate to Darwin’s mechanism. And it’s only the differences—how do new things appear? How do they get built up? That’s the only thing that really involves philosophy, design versus chance, whatever is associated with that.

Mr. Jekielek:

I think one thing that people might say in response is, well, you know, we’re dealing in this very small period of time when we look at the history of life and the history of even human beings, or certainly the Earth and so forth. So, right now, when we’re doing these experiments, there’s just not a lot of time. But if you have enough time, I guess it’s sort of like this argument that if you put however many, I think they say, monkeys typing on typewriters, there’s one scenario out of a billion, billion, billion, billion that they would write a Shakespearean play or something. I forget how the argument goes, right? But so it would kind of be a similar argument saying, yes, okay, you know, that molecular flagellum, you need all these pieces to happen, but, you know, maybe with enough time there was this, all of a sudden, all of these things came together all at once by chance.

Mr. Behe:

Yes, that’s interesting.

Mr. Jekielek:

Or is that a faith position in itself? I’m kind of curious what you think about that.

Mr. Behe:

Well, the monkey thing is around, but most people disregard it because it’s so fantastically improbable that it’s essentially impossible. Turns out, if you do the math with the Darwinian random mutation and selection for molecular machinery, it comes close to the monkeys. It’s so fantastically improbable. That’s why a lot of evolutionary biologists never talk about the probability of things happening because it’s so grim.But here’s another way of looking at it, and it kind of pertains to recent work in the laboratory in the past couple decades.

Suppose our monkeys were typing away, but in fact, half of their keys or two-thirds of their keys had whiteout on them. Instead of ink, they had whiteout, so that as they typed, they'd erase some of the stuff they typed already. In fact, they did that more easily than typing new letters. Now you just get maybe a fragment, a letter here, two letters here; the rest are whited out. And then, even with a very large amount of time, it converges to never being able to do that.

Mr. Jekielek:

Okay, so I want to jump in here. That’s fascinating, right? Because basically, now you’re talking about your third book, right, Darwin Devolves, right? And basically, your argument is that most of the mutations that happen knock something out, are not additive, and are not creating something. They’re just degrading something, right?

Mr. Behe:

Yes, that’s right. Well, this information is relatively recent as these things go, just a couple decades old. And of course, the problem with evolution, people would say we can’t follow evolution because you'd take so many generations. You need large numbers of organisms to do statistics and random mutations. But scientists have said, well, we can grow bacteria. We can grow small single-celled creatures in huge numbers in the laboratory. And maybe then, with all these huge numbers, and bacteria reproduce quickly, so they go through a number of generations in a short time. Maybe then we can get to see what evolution can do. There have been a number of experiments, but one in particular is really, really impressive.

It was started by a man named Richard Lenski at Michigan State University in the early 1990s. And he decided to grow a bacterium called Escherichia coli [E. coli], in a dozen replica flasks just to repeat the experiment. And in one flask, in a small amount of liquid, he could grow a hundred million bacteria. And the bacteria would reproduce six times a day. And then the next morning he would come in and take a little bit of each of the flasks and put it in a fresh flask and grow them for another six generations.

Next day, another 70,000 generations now, and a cumulative population of trillions of bacteria. And with those numbers, you can definitely see the trend evolution is making. And in the early days, he saw that some cells would change their shape, they‘d become a little bit bigger, and they’d grow faster, and they'd do better, and take over the colony. So, mutation and selection, you know, you could see it right there before your eyes.But he couldn’t tell why, because the changes, again, mutations are changes in DNA.

And in 1990, it was really, really difficult to try to sequence DNA, determine the exact progression of nucleotides, and see where they changed in the mutant and follow that. But as, so he just published papers about how cool evolution was because he would see these changes. But then about 10, 15 years later, science developed the technology to easily to sequence DNA in even entire organisms. So these E. coli have a genome of 4 million base pairs, and yet, with computers and automated machinery, you can look through those.

And the long and the short is that the most beneficial mutation that Lenski’s work showed was where a couple of genes a row, something called the ribose operon, was blown apart by a deletion mutation. That is, fragments of that in some replication or other processes were knocked out of the cell. And it no longer made those genes. And that helped the bacterium grow faster. It could grow about 5 per cent faster than the precursor bacterium.It doesn’t sound like a lot, but 5 per cent means that in 20 generations it will have taken over the flask. 

And then he looked at other ones, and the next six were ones in which other genes were deleted or broken or changes that would not allow them to work anymore. And 10 years after that, they published the definitive paper where they listed the top 50-ish or so mutations that helped it grow best, fastest in his lab. And the long and the short is that of the top 50 mutations, roughly 50 were ones that broke or degraded the genes in which the mutation occurred. There were no new molecular machines, there were no new genes, there was just a loss of genes. 

And this is our best evidence now of what evolution can do. We’re looking in real time at random changes in natural selection. All this other stuff, which Grok tells you about eyeballs, that’s just somebody imagining what they think could happen. This is what happens. 

If you think about it briefly, you say, well, of course, that makes sense because genes are really big. And to break it, you could hit it anywhere, just like you could take a hammer and hit your computer in a lot of different places and cause it to stop functioning. But if you want to change a gene, you’ve got to just, let’s make a change here, just like a change in the mechanism of a watch. You can’t do it randomly, you’ve got to change a specific thing. 

So the thing is, there are many different ways to change a gene to break it, so that happens a lot faster. And when you have thousands upon thousands of different components doing different things in a complex organism, something oftentimes has a beneficial effect. And so those things will be selected first because they come along first. And that’s easy to understand. And that’s what we see in the laboratory. 

And all of the constructive behavior of Darwin’s mechanism is all in the imaginations of people. It might have been a good idea when Darwin first proposed it, but now we see that, in fact, Darwinian processes work, they work by mutation and selection, but most frequently the mutation is degradative. So, ironically, Darwin’s mechanism is strongly devolutionary in the sense that it works by degrading stuff. It lives by squandering genetic information for short-term gain, and that’s not the kind of mechanism you'd expect to build up stuff over the long term.

Mr. Jekielek:

So you’re saying the majority are degradative, right? Basically, broken genes, but that means that some are indeed creative. What about those?

Mr. Behe:

Actually, no. There’s only one in the entire Lenski experiment of 50,000-plus generations that even he argues might be constructive, and that’s when E. coli usually can’t eat a chemical called citrate. Citrate is like citric acid, you know, it’s in oranges and so on. And it’s a chemical that they had in their nutrient broth for technical reasons. 

But normal E. coli can’t eat that because while it has all of the machinery inside the cell to eat it or metabolize the citrate, another machine called a transporter has to actively pull the citrate in from outside into the inside. If that citrate transporter isn’t there, then it can’t get in. And it turns out that normal E. coli, in the presence of oxygen, which was present there, doesn’t make the transporter because it does other metabolic activities. 

But a mutation came along in Lenski’s experiment where the gene for the citrate transporter was replicated. It was put near the control region of another gene, which is turned on in the presence of oxygen. So, the long and the short is that this pre-existing transporter was now turned on in the presence of oxygen, and so the citrate could be pulled in and the pre-existing machinery could metabolize it.

But in his experiment, that change allowed the mutant bacteria now to have a new food source that was not available to all the non-mutants, and so it quickly took over the colony. I myself would argue that that’s kind of a sideways mutation because you’re just kind of rearranging pre-existing elements, not making a new thing. But let’s leave it, I don’t think that’s the important thing because it’s overwhelmed by degradative mutations. The strain in which that happened had already suffered a dozen degradative mutations. 

As a matter of fact, it became what Lenski called a mutator species because its DNA repair mechanism was broken, and that allowed mutations to accumulate much, much faster than they normally do. And that new citrate-using line of E. coli, they’ve grown that by itself for another 10,000 generations or so. To adjust to its new metabolic profile. And it has done this by losing dozens of other genes. So, whether you think the odd mutation you could argue is constructive, it’s overwhelmed by degradative mutations.

Mr. Jekielek:

I mean, absolutely fascinating.

Mr. Behe:

Yes, it was unexpected, too.

Mr. Jekielek:

You mentioned that you’re a Catholic and you mentioned that you favor intelligent design as an explanation. I think a typical argument that I hear from people who are religious and who favor intelligent design is that you have a preconceived notion of a creator, and now you’re trying to explain that using the best available science, and not the other way around. How do you respond?

Mr. Behe:

Yes, that may be the case for some people. It’s not my story, though. Yes, I’m a Catholic. I’ve always been religious and continue to be. But I was taught Darwin’s theory of evolution in parochial school and in high school biology classes. And we were always told that, well, you know, God is the author of life, but if he wanted to make it by natural processes or some other way, who are we to tell him otherwise? That sounded great to me.  

So I always kind of had a theistic, evolutionary view that God made the laws of nature and things developed from there. And all of my instructors in my classes in college and graduate school told me that Darwin’s theory was true. I was perfectly happy with that. But I didn’t become skeptical until I read a skeptical book on evolution. 

It was called, Evolution: a Theory in Crisis, by a geneticist named Michael Denton, back in the mid-80s. He raised a number of problems for Darwin’s theory that I had never heard discussed before. And here I was at the time, I was, you know, a professor setting up my lab, and I got into biochemistry because I wanted to figure out how life worked. And yet, none of my professors in school had ever raised any of this.

Immediately, in biochemistry, you study these very complex systems. And you know, I had always wondered, well, frequently wondered, you know, how did that evolve? And then I say, I guess somebody knows. Turn the page or do something else. But after reading this skeptical book, I said, who has explained this? So I went to the library, looked in the journals, and found that nobody had. There were no papers. The best you'd see is an explanation of a complex system, and at the end, isn’t it wonderful what Darwinian evolution can do for us? 

So at that point, I got mad because I thought I was being led to believe something not because the evidence for it was conclusive, but because that’s just the way you’re supposed to think these days. And that was the turning point in my thinking on Darwinian evolution. So I didn’t, I didn’t turn against it because of religious considerations, but for scientific considerations. And I guess also because of personal ones, I felt misled. And so I’ve kind of stayed with it these past 30 years now.

Mr. Jekielek:

Evolution has been worked on as a theory for a very long time. And a lot of scientists in the biological field and beyond accept it, right? And now, of course, that doesn’t mean it’s the whole truth. Theory doesn’t mean it’s the whole truth. No one, I think we’re, as scientists, we know that, but it’s considered to be, you know, the best we’ve got, right? And is that the same as saying Darwinian evolution, the way it works in our world today? It kind of is, right?

Mr. Behe:

It depends on who you talk to and at what level you’re talking.Biologists believe in evolution as common descent. That is, most organisms have derived by birth and descent and modification somehow from earlier organisms. So, everybody will agree on that. Strict Darwinism of the, say, Richard Dawkins variety has lost popularity even in the professional biological community over the past number of decades. So, more and more people are speculating. 

They see that Darwin’s theory can’t account for a number of different things, and people are casting about for something new. So, if you are asking if the scientific community agrees on evolution, yes, they agree on evolution as common descent. Even then, around the edges, there are some questions. But the mechanism, how in the world could such a thing happen, which was always the big question, remains wide open.

Mr. Jekielek:

I’ve been thinking a lot about this over the years. You know, why some people, many people, feel to me to be very, that I’ve spoken with, very determined and with a fervor of sorts to say, no, it’s absolutely, actually, Darwinian evolution explains us, explains human beings, right, for example, right? That we’re just kind of part of a biological system. We’re not special. We’re not created in God’s image, as multiple faiths, religious faiths, would say. 

It just struck me, it took on, for some people, a kind of a religious quality. Like, people really wanted to believe that we’re just another one of these pieces of the biological system and not something special, which is what we were taught back in the day, a few generations back. What do you think about that?

Mr. Behe:

People are not just scientists, or even scientists are not just scientists. People have beliefs and foundational views. And whenever the topic turns to some very basic aspect of the world, whether it’s how our minds work, where did we come from, where did the universe come from, then, you know, if science says something, then people whose worldview it doesn’t fit into will start to object. 

And you see that way back in the history of science, too. If you just go back to, say, when the Big Bang Theory was first proposed, the Big Bang Theory, of course, says that the universe began in a small space and exploded. And a lot of people quickly saw that that had theistic implications. Maybe this was, you know, let there be light or creation of it.

Mr. Jekielek:

There’s an origin. There’s a very specific origin as opposed to everything just being static forever, which was another theory, right?

Mr. Behe:

Yes, which was the popular view before the 1930s when the Big Bang, or at least the expansion of the universe, was noticed. A lot of people thought that had theistic implications, and a lot of people hated that, including many scientists. You can find some juicy quotes from scientists of the day denouncing the Big Bang theorist. My favorite is actually from later than that. 

In the late 1970s, the editor of the journal Nature, which is the most prominent science journal in the world, wrote a column with the interesting title, Down with the Big Bang. In it, he said that the Big Bang is a creationist theory and is philosophically unacceptable. So here’s a guy; he’s not going to accept the Big Bang theory because it just disturbs him. He wants a… 

Mr. Jekielek:

Naturalistic, not a creationist. 

Mr. Behe:

Exactly, completely naturalistic.

Mr. Jekielek:

Even though it’s not necessarily that way, right?

Mr. Behe:

Yes, if you’re asking what the evidence shows, that’s a different question. He says, I don’t care what the evidence shows. Maybe it shows this, but I know, because I have my presumptions, that it’s going to show something compatible with a naturalistic explanation. You see it these days in explanations of the mind. 

Some people say the mind has to be just the same thing as the brain and nothing more. If you ask them how that happens, they can’t tell you. You can point to all sorts of spiffy things that minds can do that they can’t explain. But nonetheless, because they don’t want there to be something beyond matter and energy—a materialistic point of view—they will resist that.

With biology, with evolution, with the development of all sorts of things, people don’t know how that could happen. Even Richard Dawkins couldn’t tell you how a molecular machine could be produced. But they know that it happened by chance plus selection because they have a more fundamental understanding of how things are supposed to work, and they want to fit that into it.

Mr. Jekielek:

To be testable scientifically, it has to be falsifiable, right? So, explain to me how, well, first of all, maybe explain to me the simplest possible definition of what intelligent design theory is and how it is indeed falsifiable.

Mr. Behe:

Intelligent design essentially says that some features of the world are better explained by positing an intelligent mind than random mutation plus selection. Or, a better way to look at it, one I use, is that whenever we see a number of parts that have been put together in a relationship for a purpose, like, say, a mousetrap, we always conclude that they were arranged through the intervention of a mind because only minds have purpose everywhere, and we’ve seen it not only at the large level, all the way down to the molecular level; we see that. 

So, intelligent design says we see parts arranged at the molecular level for a purpose, and therefore that requires purposeful design. The flip side of that is that, well, that’s the explanation. So, alternative explanations that don’t invoke intelligence must be incorrect. The Darwinian claim that you could get these things by random mutation and natural selection is wrong. And that’s how you could falsify intelligent design, just by showing that Darwinian processes can do what its proponents claim for it. 

So, if Richard Lenski went into his lab and grew his bacteria for 50,000 generations, and some new molecular machine that wasn’t there before was put together, it had a number of different components. If it was doing something fancy, you know, what it is doesn’t really matter, then my sort of intelligent design claims would be blown out of the water. And it’s interesting to then say, what would falsify the claim that Darwinian processes, say, made a bacterial flagellum? 

You could do the same thing. Suppose Richard Lenski went in and first took out all the genes—you can do that these days—take out all the genes for a flagellum from E. coli and let it grow under conditions where it would be beneficial for it to move. And after 50,000 generations, it didn’t do much. Maybe it deleted another gene or two.

Mr. Jekielek:

We did that, or we could do that?

Mr. Behe:

We could do that. We could do that, okay. The point is, I’m saying that would be a way to test it. But I predict that Richard Lenski would not then say Darwinism was false because it did not make a complex system. He'd say you had to wait longer; you had to use a different strain of E. coli. You had to use different conditions. It could have been anything else. So, the point is that intelligent design folks like myself are oftentimes asked, you know, is your theory unfalsifiable? or how would you do that?

But my point is that it’s easy to falsify intelligent design. Just show me a random process that does something fancy. On the other hand, it’s very, very difficult to falsify Darwinian claims because they could always say, it probably would have, should have gone this way or that way or the other way. They could always find an excuse.

Mr. Jekielek:

Well, they'll just say there’s not enough time.

Mr. Behe:

Exactly, yes. Even someone like Stephen Jay Gould once said, if you ran evolution again, you wouldn’t get the same thing. So they could always say, well, we ran it again. Well, we didn’t get anything this time, but probably we got it, you know, it happened before. But it’s very difficult to think of something that would falsify.

Mr. Jekielek:

Oh, wait, so bottom line is you’re saying that evolution, Darwinian evolution as a theory, is not falsifiable.

Mr. Behe:

That is correct, yes.

Mr. Jekielek:

How do people respond when you tell them this?

Mr. Behe:

They often say, aha, it’s easy to falsify evolution. All you would have to do is find a fossil out of place in the fossil record. And a favorite is, say, suppose a fossil of a bunny rabbit was unearthed in Precambrian rocks, and Cambrian is when the multicellular creatures started to appear that would show that evolution was false. And the response is, well, if that shows evolution is false, it’s a pretty fragile theory. It depends on the next fossil. You mean all this other evidence would be entirely falsified? The second thing is that, you know, fossils have been discovered earlier than they were predicted to all the time. And people just say, oh, boy, look at that.

Mr. Jekielek:

That’s what I was thinking. There’s all sorts of things that are found that don’t fit. And people just say, oh, that’s an anomaly. 

Mr. Behe:

Exactly. So, yes, it would be very difficult to falsify evolutionary stuff.

Mr. Jekielek:

Well, this has been an absolutely fascinating conversation. Perhaps a final thought now as we finish up?

Mr. Behe:

Again, we started out and said my most startling moment in this whole thing was at the beginning when I found out that the evidence that I thought supported a major claim of how the world worked was not there. So, just a kind of a proverb here, you’ve always got to do your own homework on these big questions. Don’t take The New York Times story on it as the final word, even big name people on any particular issue. You gotta look around, read different points of view, make up your own mind.

Mr. Jekielek:

Well, Michael Behe, it’s such a pleasure to have had you on.

Mr. Behe:

Thanks very much. It was a grand time.

This interview was partially edited for clarity and brevity.