Paul Nelson, Evolution, or design ?

Paul Nelson, Evolution, or design ? 

I transcribed it for who is too lazy to see the video, but its worth to watch, a great speech:

https://reasonandscience.catsboard.com/t2310-paul-nelson-evolution-or-design


https://www.youtube.com/watch?v=0snNuOiZF_k



http://mediacenter.saddleback.com/mc/m/7ece8




Let me tell you where we are going. I am giving you in the next half hour or so, some detailed evidence pointing unmistakenly to intelligent design in biology. Unmistakenly in the sense that the evidence is so strong that it's really the only reasonable interpretation of what we see that it is designed. Now you can have a skeptical moment, and say: But Paul, i know the majority of the scientific community, of the biological community, rejects intelligent design, so if the evidence is so strong, why do they not accept it ? Well, that is the second part of my subtitle, and see, there is a play on words there. We go on, what does the evidence of nature, but also of the nature of evidence. The evidence is a transaction, between the world, and you, and in fact of the people. In Illinois, where I live, we have an unhappy practice to put our governors in jail. Our current, or our last governor, Robin Goiwitch, which is, as you know, doing some very hard federal time right now, there were two trials for Robin Goiwitch, the first one ended in a mistrial, they had to do it again. But how is a mistrial even possible? Well, its possible, because of a member of this jury, said: I am unpersuasive by the evidence, and there was nothing that anyone at that room could do to get her to change her mind.And they had to tell the judge, we had a mistrial, and we have to do it again. So think about what evidence is while you go through this talk, and we are gone at the end ask this question and see why it is that this evidence is unpersuasive to the majority of the scientific community, and I tell you, I give you some sort of forecast, it has nothing to do with the evidence itself, but what we gonna let this evidence tell us. 

Alright, its funny what you remember from college, i used to go at the office hours to one of my mentors, he was a brilliant atheist philosopher of science, I won't mention his name because he is still alive, and very active, and these were private conversations. He was a brilliant man, and i was being scared to go to see him because i knew he would try to take my arguments apart. But not only did i have to face this guy, who actually ended up and  recommended me to gradual school, and face his intellect, I had to look at this photograph. Now many of you know who this is, its one of the most influential intellects of the twentieth century, Bertrand Russell, intellectualist, logician, philosopher, social critic, educator, atheist, whose ideas strongly influenced 20st-century philosophy and science. Nearly at the end of his life, he was asked by very brave reporter ( I would not have the guts to do this ) but they asked him : What would you say if after death he realised that his consciousness was continuing, and there was God looking at him, in other words, they said to him, Dr. Russell, what would you say, if you met God, after your death ? And he said: I should reproach him for not give us enough evidence. In other words, i remained an atheist throughout my life, he played around in his late teens with theism and rejected it, and was a lifelong atheist, because the evidence in some sense was insufficient to show God's existence. 
  So think about it this way, here is Atheismville, very nice town, kind like Sweden, here is Belief and, and you have an atheist friend, or maybe he is agnostic, he lives in Atheismville, in the suburb, and you are gonna try to persuade him that God is real. Christianity, that's a bigger challenge, just want to acknowledge him that there is a God, that made the universe. So you sit down, there is a road by the way that connect the two towns, you sit down in your car, turn up the ignition, and he looks at your evidence gage, and says, we just never get there. You barely got a quarter tank. That's a long road. You have to get that red all the way up to that gage if you expect me to get over to Beliefland. This view treats evidence quantitatively, something that you can pile up, and at a certain point, its compulsion, the atheist says, ok you piled up enough, now i get to believe. Now i told you, i am skeptical towards that view of evidence, because that does not evaluate the role of that individual to evaluate the evidence. In that failed Robin Goiwitch trial, eleven jurors were convinced he was guilty, one was not, and it would not matter how high they piled it, she just would not change her mind, because of that transaction. Now we need to notice, that Russells view that there was not enough evidence, was rather recent in human thinking. This is Isaac Newton, one of the founders of western science, and in his book, the optics, in fact, right through all of his writings, Newton was absolutely sure that the evidence pointed to a creator. A being, incorporeal, living, intelligent, omnipresent, a being, that made the world and everything that we see, and science itself, he didnt give it that name, but he called it natural philosophy, science itself had value, in part because it pointed us to a creator. See, you might say, alright, but what happened to the evidence ?

 What happened between Newton, and Russell? Here is a little timeline: You can put Russell in there, in the nineteen sixties, and put there " i would approach God for not giving enough evidence", and you can put Newton in there in the time of the scientific revolution. Something happened in that intervening period, how science viewed the evidence. Well, what really happened was the Darwinian revolution. In particular, the mechanism of natural selection to explain what appeared to be intelligently designed in living things. For Newton, there was clear evidence for intelligent design in biology, and it wasn't there for Russell, and that is because Darwins proposal for natural selection changed how people viewed living things. In particular, it seemed to offer a strictly natural process for the origin of the biological designs. So, Richard Dawkins puts it this way: The theory of natural selection provides a mechanistic, causal account of how living things came to look as if they had been designed for a purpose. Came to look as if.  In other words you look at the eye, the eye of an eagle, or you look at the brain of an octopus, which is rather sophisticated, there are some vertebrates that are smart, look at any biological design, it seems there were an intellect that put it together, and Dawkins says: it only appears that way, because natural selection explains, and we now know better. And this view is very widely held by biologists. Ernst Mayr, for instance, that had a long career at Harvard, he died at 100 years of age, said : Natural selection is so important for evolutionary biologists because it seems to explain or it does explain the design of living things, that is a natural process, instead of by divine action. So to understand what happened to the evidence, we need to look at natural selection, and ask does it actually explain what evolutionary biologists say that it does?  That will be our case study, this morning. Before we get there thow, i gonna give you a very interesting historical detail. Bertrand Russell had a very high regard for the power of the intelligent design argument. You know there are several classical arguments for God's existence. The ontological argument, the moral and so forth, he thought all of them had some kind of logical flaw, but when it came to designing, he said: this argument actually works. It depends what the evidence shows, so in this passage, he says : This argument contends that , on a survey of the known world, we find things that cannot plausibly be explained as the product of blind natural forces, but are much more reasonably to be regarded as evidence of a beneficent purpose.

 That is something with an intellect, with a mind like ours: This argument has no formal logical defect, its premises are empirical, and its conclusions professes to be reached in accordance with the usual canons of empirical inference. The way that we do in science. So he says: The question wheter it is to be accepted or not turns, therefore not on general metaphysical questions, but on comparatively detailed considerations. Now what does he mean by that? What he means is that you've got to have to look at the evidence in detail. So that's what we are going to do, dig deep, and what cause can explain the biological evidence, and what i wanna do is a little case study here, in a puzzle, that Dawkins and Mayr say, natural selection explains. And that's the origin of animal body plans. Now, think about what you want a theory of evolution to do. If you are a biologist, or just a curious human being. You wouldn't be content with that theory if it just would explain why one moth has slightly more pigments in its wing than another. You wanna know where did the moth itself come from. Where did oak trees, and blue whales, and bacteria, and human beings themselves, where did we come from, the organisms, so that's the question we are looking at. So here is a little worm, it's very small, its about thousand cells, and you can find these worms in the soil, if you have a pretty powerful hand microscope you can see them, they consume bacteria. Here is a fruit fly, they are actually quite small, but beautiful, they have brilliant red eyes, or there is the purple sea urchin, which is you go here, at Lagoona beach, you see lots of these things, flourishing along the Pacific coast, now you know this, they do not have the same overall architecture. A worm is a worm, a fly is a fly, and a urchin is a urchin. Their architectures are different. They are not the same kind of living thing, and it's not easy to interconvert them. So this is gonna be a real challenge for evolution. Where did these different architectures come from? So first if we gonna evaluate natural selection, we need to understand how natural selection operates. Now let me stretch this thing, natural selection is a real process, we have a lot of examples of it in fact, my wife is a pediatrician, in Chicago, and during her training, she was told to tell patients, don't expect if you have a minor infection, to go home with an antibiotic today, because we have a tendency to abuse antibiotics, take them until the symptoms go away, but put the rest of the medicine in the cabinet, in the bathroom, if enough of us do that, over and over, that antibiotic is then less effective, the next time, we need to kill some bacteria, because of the power of natural selection. So natural selection is real, the question is, does it do, what evolutionary biologists claim that it can.  So here is a little formulation of how natural selection works.

 3 conditions have to be satisfied. The first one is variation. So we need differences. Here are some tigers, and that poor guy at left side got to say, man i have no stripes, i am barely a tiger, i don't know what i am, but i got no stripes, that's variation within that species. you can see the differences there. Here are some stickleback fishes, all within the same species, and you can see there are lots of differences within those various fishes, and those differences between tigers, and fish, and in this case, ladybugs, may make a difference between the offspring that they make. And of course, if we look in our species, homo sapiens, we have a tremendous variety of differences, just within this auditorium, you look around, and you see a lot of variation. So that's the first condition, you need to have a lots of differences, and they need to make a difference in the number of offspring they leave, more or less, so here is the little cartoon showing a tree, and a single-celled organism, the yellow tree is favoured, under the selective condition that we have set up, so that that condition is maintained, the orange tree disappears, and over time, there is a shift of the population, so the yellow tree dominates, and you need to be able to past it on. You got to be able to transmit that variation to your offspring. If you can't there is gonna be a problem, but if those 3 conditions are satisfied, natural selection will occur, as night follows day. So we go back here and see, we started out with orange, and yellow, that black bar represents the selective condition, we end up just with yellow, because the orange creatures couldn't survive. Think about this like 3 legs of a stool. You got to have them all to have natural selection to operate. But the bottom line is which we will be looking at is if you can't leave offspring, you are at a dead end, as far as evolution is concerned. So think about it at this way: imagine someone with the intellect of Albert Einstein and the physique of Michael Phelps. Put those two together. Absolute brilliance and intelligence, and olimpical specimen in regard of physical characteristics, one problem: that guy is sterile. His testicles are not producing any sperm. It doesn't matter what else is right with him. He is a dead end, and invisible to evolution, because he can't leave any offspring, And here is Paul Nelson, which obviously does not have the physique of Michael Phelbs, but in march 16 , 1992, me and my wife, we successfully passed DNA to the next generation. so in that sense, i am more fit, than that hypothetical, superintellectual swimmer. If you have kids, but you are not happy about your physical condition, just remember, you got kids, you are fit, as far what evolution is concerned. But here is a problem for natural selection. Claims that are made on its behalf are rarely backed up with evidential support.

 Rarely. Richard Dawkins will make a claim like this. But if you go actually to the scientific literature, as i do professionally, and look for the evidence, where natural selection is actually shown to be causally effective on building eyes, or ears, or brains, or wings, or nervous systems, its just not there, and in fact, this has been know for a long time, even at the zenith, even at its most popular period, in the 1960's, natural selection left many evolutionary biologists very unhappy. So Mr. Waddington, who was a embryologist, who worked closely with the core of the evolutionary community, to try out sort out evolution, at the famous meeting in Philadelphia, in 1966, he said, evolution, the textbook theory that explains what we wanted to, what he called the whole real guts of evolution, left at the outside the mathematical theory, and by that he means, the mathematical expression of natural selection.  In particular, this problem ( of body plan variations) is unsolved. Its wide open. And there is, of course, a greater part of body plans, you come to recognize these even as a small child, you can distinguish a spider from a sea star. They are just not the same organisms, they have fundamentally different architectures, of course, we belong to that group at the lower right, the chordates, if evolution cannot explain these differences, the theory is in deep trouble. Now, text book theory, the theory that you would get at a public high school, or university, at UCLA, holds, that all the animals stem from a common ancestor. That funny shaped thing at the bottom , they are called urbilaterian, thats just a fancy name for an organism with bilateral symmetry. We are bilaterally symmetrical, an arm on the side, an arm on the side, an eye and eye, you can put a dividing line on the middle of us, and have roughly mirror images on either side, even if our internal organs aren't quite symmetrical. That theory has never been demonstrated. Urbilateria is hypothetical, there are two different ways to drawing it there, one has a few more details than the other, thats a hypothetical construct to tie together what are in fact two very different kind of organisms. This problem is an unsolved problem in the origin of animals is well known within the discipline of evolutionary biology. Wallace Arthur is the english development geneticist. I met him when i was a graduate student in Chicago, and in the late 80ies he was becoming very unhappy with textbook theory, and in a publication at that time, he said : We don't really know how body plans originate.

 And the examples we have in our text books, aren't adequate. So what he calls the Biston Betularia, thats the name for the famous peppered moth from England, which may be many of you remember from textbooks of biology. Thats a classical example of natural selection in action, where pollution changes the color of the environment such that the light colored moths are preferentially preyed by birds because they can better see them while the dark moths have better camouflage and what happens in that process is that the whole population shifts . Example of natural selection but Wallace says that really does not explain where the moth came from. Eric Davidson, from Caltech in Pasadena, in a paper a few years ago, said, what we see with things like moth, for this is the question where these came from, these are fundamentally different problems, as differences between apples and oranges. And we cannot understand the origin of the moth itself, just from the small-scale evolution that we see, we can go back in the history of evolutionary theory, in the last century, and find the point where the mistake was made. Now it was not really a mistake. Every time you do science, you have to make assumptions about the world. And the founders of textbook evolutionary theory said, lest assume, that micro, or small scale evolution, and macro, or large scale evolution, are the same. Just add time to micro, and you get macro. Dobzhansky, who is one of the founders of textbook theory, in the mid-thirties, said : We can't observe macro evolution , it took place over a long time, so what we have to do, is take micro evolution and extrapolate that over a long time, and he said, we do this reluctantly, we put a reluctant sign of quality between micro and macroevolution, and we push our investigations as far as we can, on basis of that assumption, what he called a working hypothesis. Now the thing is that a working hypothesis can work out to be false. And i think thats whats happened. So here is Dobzhansys view. We start with population A, we will let time run, and what will happen, is if the variation is operating with natural selection continues to arise, we make a change that occurs , indicated there by the letter C, we didn't anticipate by the basis of the starting population, but, given enough time, and enough variation, natural selection will relentlessly move that population to new points. So, micro equals macro, just given enough time, well, that's not true, and its well known within evolutionary biology, infact John McDonald, the geneticist at Georgia tec, called it a great Darwinian paradox. He said, we've known this for twenty years, that micro does not scale to macro, well, this was published when i was a undergraduate, and many in the room were not even born. This problem has persisted for a long time indeed. Now this should alert your philosophical radar, how can an unsolved problem in evolution thats central for self-persist for so long ? I tell you, we will come back to this at the very end, it has to do with what we will permit the evidence to tell us, alright, we will come back to that. But the problem arises in the intersection of 3 ideas, or 3 parts of biological knowledge, one is how animal development works, one is the theory, that may be false, that all animals are related by common ancestry, and then the third is natural selection. And the paradox arises from a junction from what we know of each of those areas. Think about it this way: what do we know from development: We know how all animals are built. They start from one fertilized single egg. Thats how you began your existence, me, and so forth, most, but not all animals start that way. 

The earliest stage of that process determines what follows. Certainly, no human parent sitting in an obstetrics waiting room wants to hear the doctors mouth: Mr. Nelson your daughter has a macromutation. Your newborn baby has a macro-mutation. Because we know that those kinds of changes is destructive. Because they happen usually early in development in cascade throughout the whole process. So, for going to change the form of an animal, you have to start early because that's the place where the form is being put in place, but now the paradox arises: Those kind of mutations are the least tolerated by the embryo, the earlier you go in development, the more destructive the mutations are, because they affect more cells downstream, bad effects cascade downstream, and typically destroy the organism. And this was discovered in flies, as a Nobel prize-winning piece of research, by this team, Christiane Nuesslein, and Eric Wieschaus, in the late 1970ies, and early 80ies, in Europe. As I said, what they did, they looked at the problem right where these 3 circles come together, and what they did was a kind of reverse engeneering. Using fruit flies, they interrupted their genes. Marching down the chromosomes the fruit flies, disrupting genes, one after another, they asked the organism, what happens if we hit that gene. Will you develop ? So we start on the left, with the egg, we have this long development process which leads to the fly, and by disrupting genes, and their protein products by their different development, they ask the fruitfly, did you need that protein, for normal development. Or if we disrupt that protein, that gene, and its protein product, what will be the downstream consequences. What they found is quite remarkable. Now i told you there will be details, this is one of the details: This is their figure from their paper in nature, that ended up them winning the Nobel prize. On the left side, it shows the normal larval form of the flies. So in the four columns there, and the left-hand side of each of them, it shows if you want the maget form, its quite small, it's very hard to see with your naked eye, but you can see it quite easily with a low powered microscope, that's what a fruit fly magget normally looks like, and the sections that are colored in pink are the sections that will be affected by the mutations they induced. Now the columns on the right are the embryos that have been mutated. And you can see that their form is very different than their normal form. Its truncated, and its sometimes much smaller, all the embryos at the right-hand columns are dead. They are not going anywhere. Because the consequences for normal fruit fly development are so severe that it destroys the organism. And this is in fact how they figured out how the development worked. Perturb it, and reverse engineer it, disrupt the process and then look what is affecting what. And they quickly realized that if you want a fruit fly at all, you cannot perturb its early development. The problem is for macro-evolution to occur is that is exactly the place where the mutations have to take place. So you have this paradox. Hence you have this Darwinian paradox: In order to macro-evolve a species, if you will, you need to have early acting viable mutations. Thow those are the ones that are by far the most destructive. Which means that natural selection cannot operate. Natural selection thow it is a natural process, it is powerless to effect macro-evolution because the kind of variation that it needs is too destructive to animals. Ann Gauger who is the developmental biologist and cell biologist that i work with at Discovery Institute: Ann and i have compared this to what we call a magic bridge.

 Ok, this would be right at home of an Indiana Jones movie. The bridge is magin in the following sense: Start on the left, and you start now walking on the bridge. As long as you keep moving, towards the right, towards the other side of the bridge, you will be there beneath your feet. The minute you stop and look over your side, the bridge disappears, and you fall towards the chasm. See how it would fit in a movie, because of a real bridge aren't like that, but development is very much like that. Because only on the right, does reproductive capability arise. Yes, reproductive capability, being able to make copies of your genes, passing them on, is necessary for natural selection, so how did natural selection build that bridge of natural development, if one of its conditions is way on the other side. This problem has never been solved by evolutionary theory. And it's not because natural selection is not real. It's real. It's just not the right kind of process to build things that didn't  even exist before. In particular to build animals that didnt exist before. And the consequences for the Darwinian hypothesis, are profound. I showed you this slide before, This is what you get in a textbook, it says that all different animal groups came from this unknown ancestor that we call urbilaterian. Ur, by the way, is a prefix meaning original. You see in biblical studies, referring to the ur-texts, that gave rise to the books of the bible that  we see. So that original bilateral form, if it was an animal, it had probably a few thousand cells, the same problem would arise. If it was an animal, it would have gone through a development process, to change it into a anthropod, or a chordate, in other words, one of these different architectures would require the disrupting of its early development, and we have exactly the same problem again. There is no reason to think that thing were different at the pre-Cambrian, than they are today. Well, i told you, this is a problem that i encountered first as a student, much skinnier and with a lot more hair, a long time ago, i am telling you, its well known, its a well-known problem, so John McDonald in the early 80ies, and this is another detail, in technical language, let me translate it for you. He is saying that " Those loci that are obviously variable within natural populations do not seem to lie at the basis of many major adaptive changes, while those loci that seemingly do constitute the foundation of many, if not most, major adaptive changes, apparently are not variable within natural populations". And if you look around this room, there is a lot of variation.

 Hair color, height, eye color, you name it, homo sapiens has a lot of variations, Those genes do not affect the overall body plans. What does not vary ? The genes that build your brain stem. The genes that give your heart, that are connected to the lungs, genes that give you a spinal colon, and so forth, variations on those most fundamental systems don't happen. because they have to happen early , and when they happen early, the bad effects cascade downstream, and the organism is destroyed. You certainly know this from your own experience, and you can see it , for instance not only in homo sapiens, but also if you breed dogs,  there are certain kinds of variations that certain species simply will not tolerate. Eric Davidson is quite outspoken about this : In a paper last year , he said, textbook theory gives rise to lethal errors. You don't need to read of all that, i am telling you what he is saying. He is saying: what we see as viable variation in populations today, does not affect macro-evolution. To build body-plans where they did not exist before, it needs a totally different kind of theory. He said: What you learn in a textbook, the last sentence of that statement was : all the basic statements on these textbooks are basically counterfactual. Andreas Wagner, who is a evolutionary biologist in Zurich, said: We don't know, how natural selection operates. This article, again, from last year, he said: Natural selection alone is not sufficient. It may explain the survival of the fittest, but it cannot explain the arrival of it. Alright. Bottom line. Research on evolution done within the darwinian framework in the past 30 years has actually discovered that that framework is actually false. And right now, if you go to a evolutionary meeting as i do, with regularity, you will find people talk about this, it doesn't make it sway into CBS specials, or into textbooks, or into the public face of science, but believe me, its quite real. So where do we go ? Its time to go back to the philosophy of science, and the second part of my subtitle, the nature of evidence. If you see something like this , and  you take it seriously, it tells you something about nature herself. It tells you to look for a kind of cause. If you will build that magic bridge of development, where once the egg begins to divide, its gonna be all the way over , in our case to the trillions of cells, you see in a newborn baby,  that kind of process is telling you look forward to a particular kind of cause. One, they can do the following. they can aim to a distant functional target. Natural selection is very powerful, but it has no foresight. Its powerful, but very very dumb. It cannot look into the future to build something, that will be needed in the distance. What kind of cause can re-use modules ? You know the proteins in your body are reused over and over and over, in different settings. Its remarkable that the number of proteins that you have is not that much larger than the number of proteins that i showed you, earlier, its remarkably close. they have around 19000, we have around 22000 proteins. You were here last Sunday, and they were there in the soil. There is a huge difference because we have a huge amount of junk DNA. that's not junk at all. That is a very very sophisticated code, for reusing those proteins to build what you have. That makes you homo sapiens. What kind of cause can build different systems, different right from the start ? Establish primary discontinuities, where the system tells its parts what to do, you know there are proteins in your body that are identical to those in a fruit fly, by a few amino acids different, but in your body, those proteins will build a camera eye, and in a fruit fly a compound eye, what you've got there is the system is the whole, pointing to the parts what to do, top down, well , this is what can do then. Universally, uniquely, this is the only kind of cause that we can se.

 Now its the evidence. What are we gonna tell us? Now we are running into a philosophical barrier. It's not a scientific barrier. Because the scientific evidence is unequivocal. It's a philosophical barrier, and  its the worst kind of barrier to have. Because if you can't change it, if you can't find a way to change that barrier, it doesn't really matter what the evidence is, the philosophy will stand in your way. And the philosophical barrier comes to us from the 19th century. It was introduced by the Darwinian revolution itself, as a really more profound consequence of Darwin's ideas than the theory of evolution. Because that fell in a much deeper level. changing the nature of science itself. This essay in the early eighties, David Hull, was a brilliant historical philosopher of science at Northwestern said :  what Darwin did was not just to change how we thought about living things, but actually the change of science itself, and what happened was, a wall was thrown upon the evidence of biology, constraints of any possible solution that you can offer to a puzzle, you can think of this like a citywall, get inside the wall, inside you are aloud to work, outside you are like a barbarian. And what the wall says is that following: The statement of science must invoke only natural things and processes. Where natural is contrasted with intelligent. You are an intelligent cause. Every time that you answer a text message, or an email, or someone bumps your car, and leaves a phone number or apologizing, you know, you make an inference where the box on the bottom, intelligence, is absolutely essential for what you do as a rational human being. And it would be that way, if you were a atheist, or a agnostic, or a skeptic, or a Buddhist, or a Christian, it just wouldn't matter, all human beings use intelligence all the time, in their daily life, to explain what they see in the daily world. We know, its real, and the question is, are we allowed to use that concept of intelligence in biology, that made sense to Newton, to Kepler, and Boyle, and Galileo, and the founders of western science, was taken out of the toolkit of science in the 19th century, really, i think to the detriment of science, if we go back, there is our toolkit, restricted, but i think insufficient, if we go back to our initial diagram here, lets say you ve got the thing filled right up to the top, with all the evidence that someone ever wanted, you take that role seriously, of methodological naturalism, do you not allowed to infer intelligent cause, even if the evidence indicates that? this is pointless, there is no reason even to bother with it, the evidence will be powerless, and you have to say, you cant get from there to here, no matter what you show me. So when you think about this question, of the evidence of science, and belief in God, and what it might indicate, realize, its really not an evidential question, yes, evidence is important, but far more important in my experience, i think you will find this as well, is the influence of rules like this. The very worst philosophy of science they have because it puts a screen between you and nature itself. you know God could have put a barcode, in every living thing, if you take this rule, it prevents you to see the evidence, its there. This kind of evidence, that i think that biological development evidence reveals. Bottom line: Natural selection says almost nothing about macroevolution, for reasons having to do with natural selection itself.



The marriage of science to naturalism during the mid-to-late 18th century ministered most famously by the Scottish enlightenment philosopher; David Hume[1], symbolized the brokering of a union which was nothing short of a shotgun wedding of academia to ideology.
The union endures until today. Science, thus became the bride of a completely self-sufficient naturalistic worldview, a crooked union sealed by a single vow, as pervasive as it is perverse: “What science cannot tell us, mankind cannot know.”[2]

- Bo Jinn | Illogical Atheism: A Comprehensive Response to the Contemporary Freethinker from a Lapsed Agnostic
Ref.
[1] Hume is frequently directly and indirectly referenced by both Hitchens and Dawkins.
[2] Bertrand Russell

McDonald – The Great Darwinian Paradox

A reader has specifically asked that I look into the Great Darwinian Paradox as promoted by the authors associated with the Discovery Institute.  I say it this way very specifically, because the only references I can find to the paper that they claim presents said paradox is from Meyer, Behe, and Dembski.
Of course, behes darwins black box seems to have started it all

University of Georgia geneticist John McDonald notes a conundrum:
[ed note: the following is quoted from McDonald] “The results of the last 20 years of research on the genetic basis of adaptation has led us to a great Darwinian paradox.  Those [genes[ that are obviously variable within  natural populations do not seem to lie at the basis of many major adaptive changes, while those [genes] that seemingly do constitute the foundation of many, if not most, major adaptive changes apparently are not variable within natural populations.”

In Darwinism refuted, Jonathan Wells  says

Second, in order for natural selection to produce evolution, a population must include suitable variation.  No one doubts that natural populations include variations, but are those variations the kind that can lead to large-scale evolution?  Modern research on the genetic basis of adaptation suggests that they are not.  Geneticist John McDonald considers this “a great Darwinian paradox,” since those genes “that are obviously variable within populations do not seem to lie at the basis of many major adaptive changes,” while those that “seemingly do constitute the foundation of many, if not more, major adaptive changes apparently are not variable within natural populations.

The problem has led to what the geneticist John F. McDonald has called “a great Darwinian paradox”.  He notes that genes that vary within natural populations affect only minor aspects of form and function, while genes that govern major changes – the very stuff of macro evolution – apparently do not vary, or vary only to the detriment of the organism.  As he puts it, “those [genetic] loci that are obviously variable within natural populations do not seem to lie at the basis of many major adaptive changes, while those loci that seemingly do constitute the foundation of many if not most major adaptive changes are not variable…”  (all emphasis in original)

This problem has led to what J.F. McDonald has called “a great Darwinian paradox”.  He notes that genes that observed to vary within natural populations do not lead to major adaptive changes, while genes that could cause major changes – the very stuff of macroevolution – apparently do not vary.

Not the loss of the quoted material and that words like “many major” and “seemingly” and “apparently” have been replaced with “do not lead to” and “do not vary”
And, finally, we have Meyer’s Darwin’s Doubt  (in both chapters 13 and 16)

[Chapter 13] This problem has led to what Georgia Tech geneticist John F. McDonald has called a “great Darwinian paradox”.  He notes that the that are obviously variable within natural populations seem to only minor aspects of form and function – while those genes that govern major changes, the very stuff of macroevolution, apparently do not vary or vary only to the detriment of the organism.

Looking at this, we see something interesting.  Behe went from just a straight up quotation.  It’s been modified using almost the exact same language* and continue to add interpretations to the work.  We also see that Meyer is copying his own work from previous years. Why is this an awesome book again?
Thanks to another reader, I have gotten a copy of McDonald’s actual paper.  Reading it, I wonder how many of the Discovery Institute authors have actually read it.  How many have just taken what one of their fellows said previously and done what most 10th grade students do for research papers (i.e. change a few words in an attempt to avoid plagiarism).


By adding their own interpretation of the prior authors work (using secondary sources instead of primary sources), quite a bit of error has crept in.  I’m sure it’s just a bit of error, we all know that no creationist would say something that wasn’t true, especially if he is quoting an actual scientist’s paper.
No, I can’t do it, that level of sarcasm is too much for me.  These people are liars.  Either they are directly lying in order to make someone appear to say something that they actually didn’t or they are the worst researchers ever and shouldn’t be allowed to write non-fiction.  Which is it creationists?
What I continually find stunning is that creationists find a comment by a scientist (like McDonald or Gould or Darwin for that matter) and try to make it seem like the scientist is saying that there is a fundamental problem with evolution and therefore, design is a valid alternative.  McDonald is a geneticist with Georgia Tech, whose lab is currently doing cancer research.  In the late 90s, he was doing a lot of genome and evolution research.  He’s been doing this research for over three decades.
So why does a scientist think that there is a great Darwinian paradox and does it really mean that the ID guys have a leg up?
The paper in question is by John F. McDonald and titled “The Molecular Basis of Adaptation: A Critical Review of Relevant Ideas and Observations”  published in the Annual Review of Ecology and Systematics, Vol 14 (publish 1983).


Wait… what!?!?  It was suggested to me (a few weeks ago, by a scientist that I greatly respect) that references to things 10 years ago was too long ago.  Even Behe’s first use of this article was over ten years out of date.  We’re now rocking on nearly 30 years since the publication of this article.  At this point, the only way I would use an article like this is for historical purposes or for a piece of data established at the time and not contradicted since then.
So, Meyer, in Darwin’s Doubt, wants to hang his premise on three words written thirty years ago.  OK, well, let’s look to see what the article actually says.
The author states that his paper will focus on molecular events that “must have served as the source of adaptive evolution and will continue to do so.”  That’s a rather interesting statement coming from an author who, according to the DI crowd, thinks that there is a “great Darwinian paradox”.
McDonald continues by asking three questions.


What kinds of changes or variations in the hereditary material will result in the generation of adaptive phenotypes?

What is the origin of these variations?

What mechanisms amplify these variations in populations and species.

Far from saying that these kinds of things cannot happen, McDonald seems to be intending to explore the concepts and, hopefully, answer the questions that he asks.  (Spoiler alert: He does.)  We haven’t even read a full page of material here and already, it’s not looking good for the creationists.
McDonald talks a bit about the history of molecular biology, including the substantial levels of genetic variation in populations discovered in the 60s and 70s.
Then he discusses the first area of concern (I’ll try, but please ask me to explain if you get lost).  The concern, at the time, was that “why are the organisms in a population so variable”.  For example, humans have some 700+ variations of the HLA-B allele.  Why do all those variations exist?  If one of the alleles is “best”, then shouldn’t the others be “less fit” and slowly be eliminated from the gene pool?


I’ve even heard creationists use this as an attempt to support Young Earth Creationism.  If, they say, evolution is correct, then species will, over time, lose unfit alleles and they will all be very, very similar.  Since this isn’t the case, there must not be enough time for evolution to have acted and therefore the Earth is less than 10,000 years old.  I could drive an aircraft carrier through the holes in that argument.  But, if we ignore the conclusion, it really is a good question.
The conclusion at the time was that most of the variations were adaptively insignificant or neutral.  There was some uncertainty about whether there was enough non-neutral variation within populations for evolution to occur.
The argument is this:  If all these variations are effectively neutral (meaning there is no evolutionary significance), then how does evolution function when there’s nothing to work on?
In the late 70s and early 80s, geneticists began to realize that there was something else going on.  High school (and freshman college) biology rarely gets beyond the “DNA is the code for proteins” level of knowledge.  And this is probably where a lot of the problems lie.
The scientists of the time where beginning to see genes that didn’t code for proteins.  Instead, they were regulatory genes.  They controlled how and when other genes were activated.


Think of it this way.  There really isn’t a gene for height.  Tall people don’t have one allele and short people have a different allele.  Or even two or three alleles that combine to make tall, short, or something in between.  There is a human growth hormone produced during development.  And perhaps dozens of other genes that control how much and for how long that human growth hormone is produced.  Variations in the growth hormone DNA will probably result in a protein that doesn’t do what it’s supposed to (resulting in massive dwarfism or death).  However, variations in those regulatory genes won’t prevent the protein from working, just change how much is produced.  Less protein results in a shorter person.
The data, even in the early 80s, suggested that mutations respond to environmental forcing and that’s where McDonald is going with this.
McDonald then spends five pages discussing the evidence that supports the “Darwinian paradigm”.  He closes with the statement “In summary, there appear to be significant levels of regulatory gene variation within natural populations.”  He uses this figure to describe the hierarchical structure of gene regulatory networks.



Basically, mutations in the regulatory genes closer to the protein coding level (in this example R1 and R2) would have less of an effect on the phenotype than a gene like R3, at the bottom of the diagram, that controls many regulatory genes.  If R3 is mutated and doesn’t work, then everything else below it fails.  Genes like R3 are highly conserved within a population.  Where something like R1 might exhibit quite a bit of variation making (say if phenotype 1 is ‘height’).
Why don’t Meyer and the rest ever talk about those sections of the paper?  Nope, they only interested in one part… the part where Darwinism is called into question.
McDonald then spends six pages talking about how to determine the adaptive significance of this naturally occurring genetic variation.  There are no fewer than seven examples (keeping in mind that this is from 1983).  Then he talks about the “abundance of regulatory gene variation in natural populations, with potential adaptive significance”.
Note that this information is very, very different from the “do not vary” claims of Dembski and Meyer.
If you’re still here, stay with me.  We’re getting close.  I’m going to pull a few passages from the paper and we’ll get to the famous paradox.
On page 91, McDonald writes

Based upon the results presently available [ed: 1983], therefore, it is reasonable to conclude tentatively that much of the genetic variation that exists in natural populations has potential adaptive significance, at the least.

Now, why doesn’t Meyer and the rest mention this?  Because it directly contradicts their claims.  And they don’t want that.
McDonald explain why the quote I copied above is true, then says this.

As mentioned above, much of the adaptive genetic potential contained within populations may be conditional.  If this hypothesis is correct, it would present a formidable methodological problem for those attempting to evaluate the adaptive significance of naturally occurring genetic variation.  At the same time, however, the phenomenon of conditional adaptive significance seems to subvert many of the early theoretical objections based upon the concept of genetic load that were raised against the Darwinian paradigm.

Basically, this is saying that the fitness of an allele is conditional.  Think about sickle cell anemia here.  The sickle cell condition actually has some adaptational advantage, provided it exists in an environment with the malaria causing parasite.

Although the paleontologists’ objections are directly relevant only to Darwinian conceptions of evolutionary rates, they have indirectly cast doubt on Darwinian conceptions of the mode of evolution as well.  Even closely related species are frequently distinguished by major structural, functional, and/or behavioral characteristics that make them adapted to their particular niches.  however, since the magnitude of interspecific adaptive variation for the most part substantially exceeds the degree of phenotypic variation observed to be segregating intraspecifcially, it seems reasonable to conclude, as Darwin did, that selection gradually brings about major adaptive changes.

This is something that I didn’t realize had been known in 1983.  It’s certainly a well established fact now.  Basically, there is more variation within a population (think about the population of domestic dogs or people for that matter) than there is between other species (wolf, coyote, and dog for example).
Again, this is easy to show and it’s how evolution works.  Under certain conditions large dogs might have an advantage.  Under other conditions small dogs might have an advantage.  Which is more evolutionarily fit?  The question makes no sense because we don’t have any conditions to base a decision on.  Say something happens and domestic dogs have to survive without humans.  Big dogs are OK because they can tackle big prey.  Small dogss are OK because they can live on small prey and hide easily.  Medium dogs may get the worst of both worlds.  They are too small to get big prey, but to large to survive on small prey.  They are too small to fight effectively, but too large to hide effectively.  After a few generations, we have, for all practical purposes, a speciation event. We have big dogs, which never breed with small dogs.

 From the perspective of the neo-Darwinian geneticist, these challenges have been more irritating than devastating.  Effective counter arguments have been presented showing that strict gradualism is not an inherent characteristic of modern synthetic theory.Moreover, it has been pointed out that what a paleontologist considers a rapid rate of adaptive change may, in fact, be viewed as a quite comfortable pace by neo-Darwinian geneticists.  This the neo-Darwinian view of evolution, whereby adaptive genotypes are drawn from the store of genetic variation that segregates within species, is not necessarily incompatible with the evidence of rapid adaptive change. [my emphasis]

This paragraph pretty much dismantles the entire line of argumentation used by Meyer in Darwin’s Doubt.  I wonder if he even knows about?  The evidence suggests that Meyer has never read this article.  If he has, then he is lying about it.
This information, which really is devastating to Meyer’s claims, have been well known for almost 30 years prior to the publication of his book.  This would be the equivalent of someone writing a book about how there is no way fission could ever be used as a weapon… in 1974.
McDonald then gives two examples of what he’s talking about before stating

The problem for the Darwinian view, however, is that there has not been any variation observed within natural populations in those regulatory loci set deep within the control network (Figure 2), as was mentioned above.  In other words, the results of the last 20 years of research on the genetic basis of adaptation has led us to a great Darwinian paradox. Those loci that are obviously variable within natural populations do not seem to lie at the basis of many major adaptive changes, while those loci that seemingly do constitute the foundation of many, if not most, major adaptive changes apparently are not variable within natural populations.

A devastating problem for Darwinian evolution… unless one has actually been reading up to this point.  McDonald continues in the very next paragraph.

If the genetic material for major adaptive shifts is not present within species’ gene pools, it must be provided de novo by some sort of mutational events(s).

He then describes two experiments and provides references to two more than support this view.

These observations, and similar ones in other organisms, have currently led to the view that rapid genomic restructurings play an important role in the de novo establishment of reproductive isolation in higher eukaryotes.
As significant as molecular drive mechanisms may be for the rapid formation of prezygotic reproductive isolation, they are only one class of the macromutational processes that are now known to be occurring within the eukaryotic genome.  Recent findings indicate that pieces of DNA may not only become rapidly amplified, but they also may be deleted, rearranged, and translocated to new sites in the chromosome.  Evidence of these macromutations imparts an overall picture of the eukaryotic genome that is quite distinct from the rigid structure envisioned only a few years ago.  The genome is not static; it is dynamic.  Moreover, it may be playing a much more active role in the adaptive process than was previously believed.

Sorry for the long chunk of text, but this is really central to defeating even modern creationist claims… and it’s from 1983.  Meyer was an idiot for including this in his referenced materials.  Anyone who reads this article for understanding will see that Meyer’s arguments are utterly and completely wrong.  Additional support for these came very recently too.
Let me put in a few more quotes from the article, then I’ll do a quick sum up.

In this section, I have been arguing for a renewal of interest in the relative importance of mutation in evolution, since it is the only apparent source of the major regulatory chances seemingly associated with major adaptive shifts.
In fact, recent evidence suggests that the rates of many mutational events are not always low and constant, but rather that they may increase dramatically during periods of environmental challenge and the consequent organismal stress.  The implications for adaptation of such a scenario are significant; at precisely those challenging moments in evolutionary history when major adaptive shifts are required, genetic mechanisms exist that increase the probability that the appropriate variants will be provided.

He then provides a number of examples of this.
What he is saying, and Meyer is explicitly saying doesn’t happen, is that when there are major environmental stresses, mutation rates in the regulatory genes increase.  This provides for greater variation in future generations ensuring (hopefully) that at least some of the population survives.
Note what has happened in this article.  McDonald describes the history of the concept under discussion.  He describes the issues and the supporting evidence.  Then he describes the solution to the problem.  Meyer and the other creationists have focused on the problem, without mentioning that the solution (and supporting evidence) are contained just a few pages further in the article.
This is the kind of deceptive practice that most upsets me.  No, that’s not true, concern trolling pisses me off more.
I will close with one more statement from the paper.

The result of the analysis is that, although the basic Darwinian tenet of natural selection remains intact, the paradigm nevertheless needs significant revision.  The results of research in evolutionary genetics over the last 20 years indicate that the adaptively significant variation that exists within natural populations may not be the primary source of many, and perhaps most, of the major adaptive shifts that have occurred over time.  This paradox, coupled with recent molecular evidence that many, if not most, mutation events significantly increase in frequency in response to environmental stress, has prompted construction of the following “new wave” evolutionary paradigm.
According to this approach, species adapted to their particular ecological niche are effectively protected against most changes in their adaptive needs by the store of selectable variation that is present within their gene pools.  Environmental challenges that are stressful to organisms will elicit elevated rates of mutation, consequently increasing the level of genetic variation within the challenged population or species. The periodic introduction of mutational variation into populations has both positive and negative effects.  While the genetic load may be increased, this negative aspect can be more than offset by the generation of new, selectively advantageous alleles.

And this is just describing McDonald’s solution to the problem of the “great Darwinian paradox”.  It’s certainly not a death knell for evolution and anyone who actually reads the article will understand that.
Meyer and the other creationists are desperately hoping that no one will read the article and show them that they are no only wrong, but their arguments have been countered for decades before they even made the arguments.
How much of McDonald’s work here is accurate?  As I mentioned, the research in this is still going on, but it seems to me (from a 30,000 foot overview) that McDonald made some good points and some of the more recent research seems to support him, at least partially.
Of course, now we must ask Meyer and the others, why McDonald’s one statement, in the middle of this paper is acceptable for them to use to support their views, but the remainder of the paper is not.

http://www.skepticink.com/smilodonsretreat/2013/11/12/mcdonald-the-great-darwinian-paradox/

EARLY-ACTING BODY-PLAN MUTATIONS AND EMBRYONIC LETHALS


Darwins doubt page 196:

To create significant changes in the forms of animals requires attention to timing. Mutations in genes expressed late in the development of an animal will affect relatively few cells and architectural features. That’s because by late in development the basic outlines of the body plan have already been established. Late-acting mutations therefore cannot cause any significant or heritable changes in the form or body plan of the whole animal. Mutations that are expressed early in development, however, may affect many cells and could conceivably produce significant changes in the form or body plan, especially if these changes occur in key regulatory genes. Thus, mutations that are expressed early in the development of animals have probably the only realistic chance of producing large-scale macroevolutionary change.8 As evolutionary geneticists Bernard John and George Miklos explain,
“macroevolutionary change” requires changes in “very early embryogenesis.” Former Yale University evolutionary biologist Keith Thomson concurs: only mutations expressed early in the development of organisms can produce large-scale macroevolutionary change. Yet from the first experiments by geneticist T. H. Morgan systematically mutating fruit flies early in the twentieth century until today, as many model species have been subjected to mutagenesis, developmental biology has shown that mutations affecting body-plan formation expressed early in
development inevitably damage the organism.11 (See Fig. 13.2, for examples.) 



As one of the founders of neo-Darwinism geneticist R. A. Fisher noted, such mutations are “either definitely pathological (most often lethal) in their effects,” or they result in an organism that cannot survive “in the wild
state.” Normal development in any animal can be represented as an expanding network of decisions, where the earliest (upstream) decisions have greater impact than those occurring later. Regulatory genes and their DNA-binding protein products help to control this unfolding network of decisions— such that if regulatory proteins are altered or destroyed by mutation, the effects cascade downstream into the whole developmental process. The earlier the failure, the more widespread the destruction. Geneticist Bruce Wallace explains why early-acting mutations are thus overwhelmingly likely to disrupt animal development. “The extreme difficulty encountered,” he observes, “when attempting to transform one organism into another . . . still functional one lies in the difficulty in resetting a number of the many controlling switches in a manner that still allows for the individual’s orderly (somatic) development.”
 Nüsslein-Volhard and Wieschaus discovered this problem in experiments performed on fruit flies after their first Nobel Prize–winning efforts. In these later experiments they studied protein molecules that influence the organization of different types of cells early in the process of embryological development. These molecules, called “morphogens,” including one called Bicoid, are critical to establishing the fruit fly’s head-to-tail axis. They found that when these early-acting, body-planaffecting molecules are perturbed, development shuts down. When mutations occur in the gene that codes for Bicoid, the resulting embryos die—as they do in all other known cases in which mutations occur early in the regulatory genes that affect body-plan formation. There are good functional reasons for this, familiar to us from the logic of other complex systems. If an automaker modifies a car’s paint color or seat covers, nothing else needs to be altered for the car to operate, because the normal function of the car does not depend upon these features. But if an engineer changes the length of the piston rods in the car’s engine, and does not modify the crankshaft accordingly, the engine won’t run. Similarly, animal development is a tightly integrated process in which various proteins and cell structures depend upon each other for their function, and later events depend crucially on earlier events. As a result, one change early in the development of an animal will require a host of other coordinated changes in separate but functionally interrelated developmental processes and entities downstream. This tight functional integration helps explain why mutations early in development inevitably result in embryonic death and why even mutations expressed
somewhat later in development commonly leave organisms crippled. Looking more closely at a specific experimental result of this kind further illuminates the problem. A mutation in the regulatory Ultrabithorax gene (expressed midway in the development of a fly) produces an extra pair of wings on a normally two-winged creature. Although an extra set of wings may sound like a useful piece of equipment, it’s not at all. This “innovation” results in a crippled insect that cannot fly because it lacks, among other things, a musculature to support the use of its new wings. Because the developmental mutation was not accompanied by the many other coordinated
developmental changes that were needed to make the wings useful, the mutation is decidedly harmful.

My Discovery Institute colleague Paul Nelson, a philosopher of biology who specializes in evolutionary theory and developmental biology, summarizes the challenge to neo- Darwinism posed by animal development as three premises:
1. Animal body plans are built in each generation by a stepwise process, from the fertilized egg to the many cells of the adult. The earliest stages in this process determine what follows.
2. Thus, to evolve any body plan, mutations expressed early in development must occur, must be viable, and must be stably transmitted to offspring.
3. Such early-acting mutations of global effect on animal development, however, are those least likely to be tolerated by the embryo and, in fact, never have been tolerated in any animals that developmental biologists have studied.

“If the only kind of mutations that can conceivably produce enough morphological change to alter whole body plans never causes beneficial and heritable changes, then it is difficult to see how mutation and selection could ever produce new body plans in the first place.”

Thus, he concludes:
Research on animal development and macroevolution over the last thirty years—research done from within the neo-Darwinian framework—has shown that the neo-Darwinian explanation for the origin of new body plans is overwhelmingly likely to be false—and for reasons that Darwin himself would have understood.

Indeed, Darwin himself insisted that “nothing can be effected” by natural selection, “unless favorable variations occur.” Or as Swedish evolutionary biologist Søren Løvtrup succinctly explains: “Without variation, no selection; without selection, no evolution. This assertion is based on logic of the simplest kind. . . . Selection pressure as an evolutionary agent becomes void of sense unless the availability of the proper mutations is assumed.” Yet the “proper” kind of mutations—the mutations that produce favorable changes to early-acting, body-plan–shaping, regulatory genes—do not occur. Microevolutionary change is insufficient; macromutations—large-scale changes—are harmful. This paradox has beset Darwinism from its inception, but discoveries about the genetic regulation of development in animals have made this paradox more acute and cast serious doubt on the efficacy of the modern neo-Darwinian mechanism as an explanation for the new body plans that arise in the Cambrian period.



MAJOR BUT NOT VIABLE, VIABLE BUT NOT MAJOR

Despite the enthusiasm surrounding the field, evo-devo fails, and for an obvious reason: its main proposal, that early-acting developmental mutations can cause stably heritable, large-scale changes in animal body plans, contradicts the results of one hundred years of mutagenesis experiments.  the experiments of scientists such as Nüsslein-Volhard and Wieschaus have shown definitively that early-acting body-plan mutations invariably generate embryonic lethals—dead animals incapable of further evolution. The results of these experiments have generated the dilemma for evolutionary biologists that geneticist John McDonald aptly described as the “great Darwinian paradox.” Recall that McDonald noted that early-acting regulatory mutations do not produce viable alterations in form that will persist in populations, as evolution absolutely requires. Instead, these mutations are eliminated immediately by natural selection because of their invariably destructive consequences. On the other hand, later-acting mutations can generate viable changes in the features of animals, but these changes do not affect global animal architectures. This generates a dilemma: major changes are not viable; viable changes are not major. In neither case do the kinds of mutation that actually occur produce viable major changes of the kind necessary to build new body plans. In 2007, I coauthored a textbook with several colleagues titled Explore Evolution. In it, we explained this “either/or” (“major-not-viable, viable-not-major”) dilemma and suggested that it posed a challenge to theories that rely on the mutation and selection mechanism to explain the origin of major morphological changes. The National Center for Science Education (NCSE)—an influential activist group that opposes allowing students to learn about scientific criticisms of evolutionary theory—challenged our critique. They charged that our textbook “fails to acknowledge the extensive research on mutations in DNA sequences that do not encode proteins, but which have important morphological effects.” In other words, they claimed that some viable mutations do produce major large-scale changes.

Superficial changes in insect wing coloration thought to be caused by mutations in cis-regulatory elements. Such examples show that mutations that affect development and that also result in viable offspring tend to be minor. Courtesy National Academy of Sciences, U.S.A. The NCSE cited papers from the “evo-devo” literature claiming that a type of mutation in the regulatory regions of the genome, “cis-regulatory” regions, have been shown to produce large-scale changes in winged insects. According to the NCSE, mutations in these cis-regulatory elements (or CREs) are “considered by many evolutionary biologists to have the greatest potential for generating
evolutionary change.” What’s more, they insisted that “mutations in CREs play an important role in morphological evolution.” The NCSE cited a paper in the Proceedings of the National Academy of Sciences by three developmental biologists, Benjamin Prud’homme, Nicolas Gompel, and Sean B. Carroll. The paper did not show what the NCSE claimed, however. It did assert that changes in regulatory DNA produce “both relatively modest morphological differences among closely related species and more profound anatomical divergences among groups at higher taxonomical levels.” But the study only showed how changes in the cis-regulatory elements in fruit fly DNA might have affected the coloration of wing spots in several different types of flying insects. It did not report any significant change in the form or body plan of these insects. Instead, the study highlighted a clear case of a viable mutation generating merely a minor or superficial change (see Fig. 16.2).



Not surprisingly, many evolutionary biologists recognize that such regulatory mutations do not explain the evolution of new body plans. For example, Hopi Hoekstra, of Harvard University, and Jerry Coyne, two traditional neo-Darwinists, have published an article reviewing various evo-devo proposals in the journal Evolution. They note, “Genomic studies lend little support to the cisregulatory theory” of evolutionary change. They also argue, tellingly, that most cis-regulatory mutations result in the loss of genetic and anatomical traits, including a famous case in which evolutionary biologists attributed the loss of pelvic spines in stickleback fish to mutations in cis-regulatory elements. Yet, as they argue, “supporting the evo-devo claim that cis-regulatory changes are responsible for morphological innovations requires showing that promoters are important in the evolution of new traits, not just the losses of old ones.” Hoekstra and Coyne conclude, “There is no evidence at present that cisregulatory changes play a major role—much less a pre-eminent one—in adaptive evolution.” Given their commitment to neo-Darwinism, it’s fair to assume that Hoekstra and Coyne probably did not intend, in making this argument, to refute the NCSE’s criticism of our textbook Explore Evolution. Nevertheless, science, like politics, sometimes makes for strange bedfellows.

eles rapidamente perceberam que, se você quer uma mosca da fruta, você não pode perturbar o seu desenvolvimento inicial. O problema é para macro-evolução  ocorrer  que é exatamente o lugar onde as mutações têm de acontecer. Então você tem esse paradoxo. Daí você tem esse paradoxo darwiniano: A fim de ter macro-evolução de uma espécie, se quiser, você precisa ter  atuação de mutações viáveis logo no inicio do desenvolvimento. Mas esses são os que são de longe as mais destrutivas. O que significa que a seleção natural não pode operar. A seleção natural  é um processo natural, é impotente para efeito macro-evolução, porque o tipo de variação que ela precisa é muito destrutiva para os animais.