Creation and Evolution (Part 19)

August 26, 2013     Time: 00:36:17

In our lessons, we have been thinking about the contemporary evolutionary paradigm. We saw that one aspect of that paradigm is the affirmation of the thesis of common descent. Last time I said that, in my assessment, it seemed to me that the evidence concerning the thesis of common descent was mixed. While the genetic evidence seemed to support the idea of common descent, nevertheless, the fossil evidence seemed to still run against it.


Question: I might have missed it, but . . . this whole genetic discussion seemed to me like the best argument for a common designer . . . Everything you look at in the world, you can generally tell (if it has any importance to it at all) the designer. Once you know a designer’s work, you can generally see characteristics of that designer’s work in a long strain of devices or designs. For example, an architect might have a habit of putting this little space or this particular feature in every house or building he designs. That seems to me like what all the evidence that you’ve given supports – a single designer.

Answer: I see. OK. As I said last time, one possible way of responding to this genetic similarity among all living things is that this shows, as you say, a trait in the designer to design things a certain way. I do think, though, in all honesty that that response is less persuasive when it comes to what I shared about these pseudogenes which are broken genes that have mutated in such a way as to become inoperative and no longer have their original function. And these get reproduced in organisms that are thought to have descended from earlier ones. And, as I said, it would be hard to see why, for example, an automotive designer would reproduce, say, a broken jack from one model of a car that won’t in fact jack the car up so that you can change the tire. Why would you reproduce that broken jack in another model? When it comes to something like that, then it does seem to be (at least to my mind) indicative that this could be the result of some sort of a genetic relationship between the two – that the one is descended from the earlier one and so these broken features get repeated. So while I think that is a possible response to the genetic similarity that we noted, it seems to me less persuasive with respect to these pseudogenes.

Question: It seems like we’ve come a long way in genetics but it seems still that we’ve got a long way to go. And to say that we know what a gene does and doesn’t do necessarily seems premature. Just the whole realm of coding and communication and all of that, it just seems like there could be multiple levels of that within the DNA structure. So to say absolutely that this is a broken gene may be presumptuous.

Answer: I hear you. That is a good point. Certainly, the discovery that junk DNA really has a function might be a lesson that would say we should be cautious about this. Then there are these master genes that simply switch others on and off that were discovered that previously were thought to be nonfunctional.[1] So that could be grounds for caution. I think you are right.

Question: . . . I think we have to agree that the limitation of our knowledge says that similarity does not prove descent. We can’t say, “Ah-ha! There it is! They are similar, therefore, it proves descent.” I think the argument on the other side is at least as powerful or more so that the only similarity is the similar designer. It is the same designer.

Answer: OK. That is basically similar to the earlier point.

Question: Isn’t there more to genetics, though, than just the similarity of the genes such as the addition of genetic information that would be necessary in order for one species to develop into another. Also, as far as genetics is concerned, shouldn’t the naturalist be able to prove that mutations are a force for positive change within the organism whereas it seems to the layman that most mutations are harmful.

Answer: All right, now, let me say a couple of things in response. This isn’t a debate between naturalists and theists. I don’t think we want to frame it that way. We are looking at this from a theistic perspective and we are asking “How did God bring about biological complexity?” Did he use prior organisms as ancestors for ones that later developed or are organisms created afresh, de novo[2]. So this isn’t a debate here between naturalism and theism, I think. But the other thing that I wanted to say is that I think the points that you are making about the deleterious effect of most mutations is really relevant to the third point that I want to talk about next – the explanatory mechanisms behind evolutionary change. You are suggesting that these mechanisms are not explanatorily adequate because of what you mentioned – the overriding, debilitating effect of mutations. I think that your point is really addressing what we are going to talk about rather than the thesis of common ancestry which would just be that things that we observe today are descended from prior living organisms.

Question: Following up on the pseudogenes, when Fuz Rana was here[3] I asked him about the pseudogenes. His comment was, yes, it certainly looks like common descent but you do have to keep in mind this is an inference and it is based on some assumptions. One assumption is that these genes really don’t have a function and maybe they do (echoing what someone said earlier). The other thing he pointed out, which was kind of interesting to me, was if you look at some of these pseudogenes, they have the same mutation that breaks them. That makes it look like it comes from a common ancestor and that broken chain gets inherited. Fuz was suggesting that maybe in some of these pseudogenes they have certain hotspots that make them more susceptible to mutations and it may just be a coincidence that two different species have the same mutation and that maybe that wouldn’t be so unlikely.

Answer: Wow. OK. Well, that would be a bold claim to write it off to just coincidence.

Scientific Extrapolation

What is the evidence then for Darwinism which, you will remember, we defined as the claim, or the thesis, that natural selection operating on random mutations accounts for grand evolutionary change? Before we look at the evidence specifically, I think it is worth emphasizing how extraordinary an extrapolation Darwinism involves. Many of us probably think that if random mutation and natural selection could explain, say, the evolution of the horse from a small multi-toed animal up to the beautiful animal with the single hoof that we see today that that would really be powerful evidence for the efficacy of these Darwinian mechanisms.[4] But in fact evolution within a single kind like this is nothing compared to the vast range of life. Well, you might think that if we could show that random mutation and natural selection could explain, say, how a bat and a whale could evolve from a common ancestor, that would certainly show the power of these evolutionary mechanisms. Well, I want to invite you to think again. Here I want to show our first PowerPoint slide [see Figure 1]:

Figure 1 - Metazoan Phylogeny

On this slide you see the various phyla, or major groups, of the animal kingdom. Now, notice that top group and that a bat and a whale are both mammals. That is just one of the subcategories under the Chordates. So along with reptiles and birds you have these mammals which belong to this single phylum of the Chordates. So even the evolution of a bat and a whale from a common ancestor is an utter triviality compared to the vast range of the animal kingdom. This would do nothing to explain, for example, how a bat and a sea urchin (which you see belongs to another phylum) could evolve from a common ancestor, not to speak of a bat and a sponge (which is yet a more distant phylum). So the extrapolation of these explanatory mechanisms from our limited experience to the sort of grand evolutionary story is an extrapolation of gargantuan proportions. If this extrapolation takes your breathe away, then take a look at the next slide [see Figure 2]:

Figure 2 - Universal Tree of Life[5]

The whole previous slide that we just looked at showing the different phyla of the animal kingdom – all of that, is contained on the little twig of that right hand branch under Eukarya where it says “Animals.” Animals! I love the modesty of that label – the whole of the animal kingdom – all of those phyla that we previously saw, all of that diversity – is contained on that little twig called “Animals.” Notice slightly to the right of that twig is another twig labeled “Plants.” Plants! The whole of the plant kingdom is contained on that little twig. And these are just two twigs on the branch of the Eukaryotes which are animals that have cells with a nucleus in them. There are still two other domains of the Bacteria and the Archaea to be accounted for. The extrapolation of the efficacy of these Darwinian mechanisms from experiments on peppered moths and finch beaks and fruit flies to the production and evolution of every living thing is a breathtaking extrapolation of gargantuan, brobdingnagian, proportions.

And we know that in science such extrapolations often fail. To give an illustration from a field I am familiar with: after Albert Einstein developed his Special Theory of Relativity in which he tried to eliminate absolute, uniform motion in favor of simply relative motion, he attempted to enunciate a general principle of relativity that would also relativize absolute rotation and acceleration so that all motion – not simply uniform motion, but even rotational and accelerated motion – would also be relativized to reference frames. But, in fact, this extrapolation failed. He was unable to successfully enunciate a general principle of relativity that would eliminate absolute rotation and acceleration.[6] Instead what he discovered was a radical new theory of gravity which was his greatest achievement. The General Theory of Relativity is not really a relativistic theory in the sense of eliminating absolute acceleration and rotation. It is a gravitational theory that enunciates a new theory of gravity to replace Newton’s theory. So, in fact, although Einstein had limited success in the Special Theory in eliminating absolute uniform motion, it turned out that that principle could not be extrapolated so as to relativize all motion. Similarly, we are compelled to ask, I think, in the case of these mechanisms of random mutation and natural selection, “What is the evidence for this extraordinary extrapolation from the limited development that we see though mutation and natural selection to the grand evolutionary scenario?”

Mechanisms of Biological Evolution

Typical of the evidence that is offered on behalf of these Darwinian mechanisms are things like the experience of breeders in breeding new kinds of roses, for example, or horses. The experiments with the peppered moths in England in which the light and dark moths varied in their proportion of the moth population based upon the amount of industrial pollution that darkened the trees in England. And then the development on the part of bacteria to drugs – the mutations that cause bacteria to become drug resistant so that we have to develop new drugs to fight these because they have mutated in such a way as to become resistant to the drugs that we have.

Let me say a word about each of these. Francisco Ayala whom I have quoted before – a prominent evolutionary biologist – appeals to the experience of breeders in producing new varieties of dogs and roses, for example, as evidence for the efficacy of these mechanisms of random mutation and natural selection. But I think you can see clearly that such experience does nothing to justify the extrapolation of these mechanisms to the production of the grand evolutionary story of life. In fact, quite the contrary – the experience of breeders tends to show the limits of these mechanisms in that the breeders bump up against limits beyond which they cannot produce desired variety. For example, despite decades of effort, breeders have never been able to get chickens to lay more than one egg per day. So breeding actually shows the limits of what natural selection and random mutation can accomplish.

Ayala also appeals to the famous peppered moth experiments. But all that happened in that case was that the proportion of light colored moths in the population decreased and the proportion of dark colored moths increased. But the light colored moths never evolved into dark colored moths. So taken as evidence of the power of natural selection and random mutation to produce grand evolutionary change – honestly, to call such evidence paltry would be to pay it an undue compliment.

Ayala also appeals to the finch beaks of different sizes that Darwin observed in his visit to the Galapagos Islands. But again, like the peppered moths, nothing here ever actually evolved. It is just that the proportion of finches with the large beaks increased during the drought or the dry season – they were better able to survive – and the proportion with the small beaks decreased because they were less able to survive in the dry climate. But once the rains came again then the normal beak proportions in the finch population returned as the population increased.

Ayala also mentions the speciation that occurs in fruit flies in Hawaii.[7] This is a very interesting case. The Hawaiian Islands are extremely isolated and so they tend to be sealed off from outside influences. That is why there are no indigenous mammals, for example, in Hawaii. And yet, some five hundred species of fruit flies exist in the Hawaiian Islands. One fourth of all of the fruit fly species that exist in the entire world – there are about 2,000 in the entire world – exist in this tiny area on the Hawaiian Islands. This evidence points to their common ancestry and evolution – as they have mutated and evolved into a diversity of species. I think we can agree that this evidence in all plausibility points to their common ancestry and evolution and agree that this is well within the limits of what these Darwinian mechanisms can achieve. But, again, it hardly goes to justify the enormous extrapolation of the power of these mechanisms to yield the grand evolutionary scenario. All we have here is just speciation of fruit flies in the islands.

Finally, Ayala appeals to the ability of organisms to develop drug resistance and resistance to poisons through random mutation and selection. He points out how an unacceptably improbable double mutation – where a mutation would need to occur simultaneously at two places in the genetic structure – can happen one step at a time. So while it is unacceptably improbable to say that you can have a double mutation simultaneously, nevertheless, it can be achieved stepwise to produce cumulative change, such as producing drug resistant bacteria. Then he extrapolates this process to explain macroevolutionary change. But of course the question that we are asking here is, “Can the mechanisms be successfully extrapolated in that way?” In his most recent book, The Edge of Evolution[8], Michael Behe argues that the very evidence of organisms’ development of drug resistance is a powerful indication of the limits of what random mutation and natural selection can achieve with regard to evolutionary change. For example, Behe explains that malaria and the human immune system have been waging war against each other for over ten thousand years. Since the advent of modern science, human beings have been developing anti-malarial drugs to try to destroy the malarial organism. Unfortunately for us, the malarial population is huge. The average person infected with malaria has over one trillion malaria cells in his body. Therefore, malaria mutates extremely rapidly. As a result, it has been able to develop resistance to every drug that we’ve thrown at it. Simple, single point mutations are enough to make malaria drug resistant. For example, Behe says a mutation in one amino acid at point 108 in the human genome suffices to render malaria drug resistant to pyrimethamine.[9] On the other side, there is enormous selective pressure on the human immune system to develop some sort of defense against malaria, but it hasn’t done so. The human immune system has not been able to evolve a defense against malaria. Instead, what has happened, says Behe, is that a mutation has occurred in the human respiratory system, not in the immune system. There has been a mutation in our respiratory system which makes some people immune to malaria – namely, sickle cell hemoglobin.[10] Unfortunately, the downside is that this also produces sickle cell anemia which is eventually deadly.

This is where the story gets really interesting. Despite its incredible mutation rate that has enabled malaria to overcome every drug that we’ve hurled at it, malaria has never, in all of those thousands of years and trillions of mutations, been able to overcome sickle hemoglobin. Molecular biology explains why. Resistance to a drug can result from a simple, single point mutation. But overcoming sickle hemoglobin would require either multiple, simultaneous mutations or else a sequence of mutations occurring blindly which are just too improbable to occur. As a result, sickle hemoglobin has never been overcome by malaria. The mutations required are simply too improbable.

HIV supplies another case study. The HIV virus mutates ten thousand times faster than malaria, if you can imagine. In the last fifty years alone, the AIDS virus has mutated as much as all the cells that have ever existed upon earth. Can you imagine? It has tried out every possible combination of up to six point simultaneous mutations and it has become resistant to every drug that we’ve developed. But Behe says, “Yet through all of that, there have been no significant basic biochemical changes in the virus at all. . . . on a functional biochemical level the virus has been a complete stick-in-the-mud.”[11] Behe concludes, “The studies of malaria and HIV provide by far the best direct evidence of what evolution can do.”[12] He says,

. . . here we have genetic studies over thousands upon thousands of generations, of trillions upon trillions of organisms, and little of biochemical significance to show for it. . . . Our experience with HIV gives good reason to think that Darwinism doesn’t do much – even with billions of years and all the cells in the world at its disposal.[13]

Finally, recent studies on the bacterium E. coli have yielded similar results. Richard Lenski and his colleagues recently released their data on studies of E. coli in which they did research on 40,000 generations of E. coli grown in the laboratory. They discovered that while there were a couple score of beneficial mutations (and this speaks to an earlier question) that occurred in these E. coli bacteria; nevertheless, these mutations were degradative, or degenerative, in nature. That is to say they involved the loss of genetic information or the loss of protein function. They were beneficial, but they resulted in the loss of genetic information. So there is no indication that these bacteria were on their way toward building new complex systems. Lenski’s work lines up very well with the results of malarial and HIV findings. In huge numbers of tries, one sees minor changes, mostly degradative, but no new complex systems evolve.

Now, malaria, HIV, and E. coli represent three fundamentally different forms of life. The malarial organism is a eukaryote; that is to say, it is an organism having a nucleus.[14] HIV is a virus. E. coli is a bacterium – it is a prokaryote, they don’t have a nucleus. So we have here three fundamentally different forms of life, a eukaryote, a virus and a prokaryote. And in each case the evidence for the efficacy of the Darwinian mechanisms is the same – it just doesn’t do very much. I quote from Michael Behe’s online blog:

Instead of imagining what the power of random mutation and selection might do, we can look at examples of what it has done. And when we do look at the best, clearest examples, the results are, to say the least, quite modest. Time and again we see that random mutations are incoherent and much more likely to degrade a genome than to add to it — and these are the positively-selected, “beneficial” random mutations.[15]

He says, “There is no evidence that Darwinian processes can take the multiple, coherent steps needed to build new molecular machinery . . . that fills the cell.”[16] Thus the argument from the ability of organisms to develop drug resistance seems to completely backfire. Far from providing evidence of the power of the Darwinian mechanisms to produce grand evolutionary change, the experience of scientists with drug resistance in bacteria and viruses and malaria reveals the severe limits of those mechanisms.

So, again I ask: where is the evidence for the extraordinary extrapolation that Darwinism involves? Behe says that the evidence for common descent seems compelling. He affirms the thesis of common descent that we looked at. “. . . the evidence for common descent seems compelling. . . . [but] except at life’s periphery, the evidence for a pivotal role for random mutations is terrible.”[17] If Behe is wrong about this then I simply want to know – what is the evidence? I am genuinely open to it but what is it? What is the evidence that would justify this grand evolutionary extrapolation?

I have to say when I, as an objective observer, look at the evidence it seems to me that we haven’t been shown yet any good reason to think that these Darwinian mechanisms are sufficient to explain the extraordinary diversity of life that we see on this planet during the amount of time that is available.

In their book, The Anthropic Cosmological Principle, the physicists John Barrow and Frank Tipler list ten steps in the course of human evolution such as the development of photosynthesis, the development of an endoskeleton and so forth.[18] Ten steps in the course of human evolution, each of which is so improbable that before it would occur the sun would cease to be a main sequence star and would incinerate the earth. Included in these steps are things like the development of a DNA-based genetic code, the evolution of aerobic respiration, the evolution of glucose fermentation to pyruvic acid, the development of an endoskeleton, and so on and so forth. Ten steps in the course of human evolution, each of which is so improbable that before it would occur, the sun would have gone through the entire course of its stellar evolution and incinerated the earth. As a result, they report that “there has developed a general consensus among evolutionists that the evolution of intelligent life, comparable in information processing ability to that of homo sapiens is so improbable that it is unlikely to have occurred on any other planet in the entire visible universe.”[19] So according to Barrow and Tipler, the consensus of the evolutionary biologists themselves is that the evolution of intelligent life is so improbable it is unlikely to have taken place anywhere else in the entire visible universe. But then that raises the obvious question – why think that it has evolved on this planet by these Darwinian mechanisms?[20] Indeed, doesn’t the evidence suggest just the opposite? In fact, Tipler himself now believes that the process of evolution must have been guided by some kind of intelligence.

So how do we put this together? Well, I am rather skeptical of these mechanisms of the Darwinian theory of biological evolution. I think the whole story hasn’t been told here yet. So even if the thesis of common ancestry is true, these mechanisms that have thus far been suggested seem to be inadequate to explain the biological complexity that we have today. There is something more going on here than just random mutation and natural selection.[21]

[1] 5:03

[2]De novo” is Latin for “anew” or “from the beginning.” In the field of genetics, “de novo” can refer to a genetic mutation that neither parent possessed nor transmitted to the child organism.

[3] Dr. Fazale “Fuz” Rana is a member of the organization “Reasons To Believe” ( was recently at Dr. Craig’s church to present his ideas on creationism and evolution. This questioner is referring to this visit by Dr. Rana.

[4] 10:20

[5] This “universal tree of life” diagram is from Francisco J. Ayala, Darwin and Intelligent Design, (Minneapolis, MN: Fortress Press, 2006), p. 42. The root of the tree labeled “LUCA” stands for the “Last Universal Common Ancestor.”

[6] 15:03

[7] 20:02

[8] Michael J. Behe, The Edge of Evolution: The Search for the Limits of Darwinism, (New York, NY: Free Press, 2007).

[9] Ibid., p. 75.

[10] 25:05

[11] Ibid., p. 139.

[12] Ibid., p. 140.

[13] Ibid., pp. 140, 154-55.

[14] 30:03

[15] Michael Behe, “Response to Kenneth R. Miller”, July 11, 2007 blog post at (accessed April 16, 2013).

[16] Behe, The Edge of Evolution, p. 162.

[17] Ibid., pp. 3-4.

[18] John Barrow, Frank Tipler, The Anthropic Cosmological Principle, (Oxford: Clarendon Press, 1986), pp. 561-65.

[19] Ibid., p. 133.

[20] 35:07

[21] Total Running Time: 36:16 (Copyright © 2013 William Lane Craig)