Episode Transcript
[00:00:07] Speaker A: Welcome to id the future. I'm your guest host, Ira Berkowitz, speaking to you from the ancient yet modern city of Jerusalem, where I live and work. I teach, write, and do personal counseling. Here in my neighborhood of Har Nof on the western side of the city, lives one of my culture heroes, Doctor Lee Spettner. Through his books, not by chance and the Evolution Revolution, he's given me and many others a real education about Darwinism and its limitations.
Doctor Spetner is a physicist with a PhD from MIT who taught graduate level courses at Johns Hopkins University, worked for decades in military electronics, R and D, and then worked for twelve years in cancer research.
Besides his two books, hes written many articles and he holds a few patents besides. Doctor Spetner, its an honor to have you with me in the studio today.
[00:00:53] Speaker B: Its a pleasure to be here, Ira.
[00:00:55] Speaker A: Well, Doctor Spettner, youre skeptical of modern evolutionary theory, but you do believe that natural selection does account for some evolution, is that correct?
[00:01:04] Speaker B: Well, partially. I think natural selection is overblown. I think it has some kind of an effect, but I don't think it's as pervasive as the current theory of evolution takes it. For natural selection is supposed to work on random mutations that occur spontaneously. And it turns out that the mutations that are important in the evolution that we actually see are non random mutations. They're non random changes in the genome, and natural selection plays a very small role in that.
[00:01:38] Speaker A: So let's start with some of the problems in your first book. Not by chance, you write that a mutant with a selective advantage still doesn't have a much better chance of surviving than other individuals of the same species. Why is that?
[00:01:50] Speaker B: Well, because the selective advantage that the evolutionists assume in their theory is always a very small advantage.
That means that a mutant may have an advantage that it can reproduce 1% better on the average than its cousins, and that means that it has a very small probability that it will actually reproduce enough to take over the population.
These are all random processes.
They work according to probabilities. And the probability of a mutant with a 1% selection advantage may have a 2% probability of actually taking over the.
[00:02:38] Speaker A: Population, because that individual isn't that much better off than his cousins.
[00:02:43] Speaker B: That's right, it's not that much better off. And it's subject to many, many events that have nothing to do with disadvantage. It could get killed by a falling boulder or something like that. So it has a probability of survival, a probability of taking over the population, but it has a far greater chance of becoming extinct.
[00:03:09] Speaker A: Doctor Saunder, what if the population is small? So wouldn't a small population make the survival and eventual dominance of a positive mutation more likely? Okay, it's not a much more adapted organism, but it's got a smaller field in which to play.
[00:03:25] Speaker B: Well, I think the thing about small population is that the small number of individuals means that it's much less likely for a random mutation that they require to occur. So that already means that the probability of something evolving in a small population is less than in a large population.
[00:03:45] Speaker A: Why is that? Why is it less likely to occur if the population is small?
[00:03:50] Speaker B: Because the numbers of individuals are smaller. We're working on the occurrence of a random mutation that should occur in any one individual. Now, if I only have one individual in a population, then the probability of a random mutation being adaptive is whatever number it turns out to be. This is part of their theory that actually there are no such things.
And as you make the population larger and larger, there's a larger pool of individuals, larger pool of genomes in which mutations can happen. So the probability of getting a beneficial mutation in a large population is greater than the probability of getting one in a small population.
[00:04:39] Speaker A: Makes sense. Okay, but we've been assuming a low mutation rate, right?
[00:04:43] Speaker B: We've been assuming a mutation rate that we actually observe.
[00:04:46] Speaker A: Okay, let's say it was higher. In any case, Tom Schneider created an EV program, which you criticized, where the mutation rate was quite a bit higher. Would that create the information buildup required for natural selection? You said no. Why?
[00:05:00] Speaker B: Well, in a computer simulation, you can create information with a high enough mutation rate. But that mutation rate would have to be so high that if it would occur across a genome in an actual organism, the population would die out, because most of these mutations would be deleterious.
[00:05:22] Speaker A: So the higher the mutation rate means, okay, we've got more adaptive mutations, but correspondingly, we have many more deleterious mutations.
[00:05:33] Speaker B: That's correct. And in a computer simulation, you don't have to worry about the deleterious mutations. You don't even consider the population dying out. He's just looking for the increase of information. And you can get an increase of information with a high enough mutation rate.
[00:05:51] Speaker A: We can keep our pixels going no matter what.
[00:05:53] Speaker B: Yeah, sure.
[00:05:55] Speaker A: Okay. There was a case. Doctor Ed Max challenged you, though, where there is a case of a high random mutation rate, it does add information to the genome. It's the case of mutations occurring in b lymphocytes in the vertebrate immune system. So you'll have to fill us in on what that means, and then tell us why you don't agree with Doctor Max after all.
[00:06:18] Speaker B: Well, actually, he posted this essay on the Internet saying that here's an example in the immune system, where random mutations do create information. And he emailed me and asked me if I would be willing to comment on this, and my comment was that they indeed do add information in the immune system. But the point is that these mutations are not in the part of the genome that reproduces. They don't go on to the next generation. They're only somatic mutations, and they occur in a very small portion of the genome. They occur only at the times when they're needed. What they're doing there is matching something about an incoming pathogenic bacterium that might harm the system. They try to match onto it so that they can create an antibody that will oppose the incoming pathogen. And these mutations are very well controlled by the cell. As I say, they're only in a very small portion, a specific portion of the genome, and they occur only when they're needed and they're stimulated by the incoming pathogen. So everything is really well controlled in the cell. And if this kind of mutation were just random and spread out over the whole genome and not controlled the way it is in practice, the organism would die out.
[00:07:58] Speaker A: And you said that it's only somatic. What do you mean by that?
[00:08:01] Speaker B: Somatic means it happens in the body cells and not in the germ cells. The germ cells are the ones that contribute to the next generation.
[00:08:09] Speaker A: So the next generation is no better off because of this process.
[00:08:13] Speaker B: The next generation is completely independent of what happened here, because these don't occur in the germ cells. That's right.
[00:08:21] Speaker A: Okay, Doctor Spetner, you've pointed out that almost all point mutations are recessive. So that's another limitation that makes the survival of positive mutations even less likely than we might have thought. Right?
[00:08:32] Speaker B: Yeah, that's true, because a recessive mutation is not expressed in the phenotype, in the actual organism. So that if a beneficial mutation is recessive, which they usually are, then they're not expressed in the phenotype, and natural selection doesn't have anything to work on. So they would have to be expressed in both chromosomes that are received from the two parents, which means that a single mutation would never be acted upon by natural selection, because it would never be expressed. The only way that this would happen with a recessive mutation is that if two mutants, one male and one female, happened to meet and reproduce, then there is a likelihood that each one of these would contribute the adaptive mutation to the next generation. Even that isn't certain, but that's a very improbable thing to happen, and that's why the fact that the mutations are recessive is another strike against the evolution here.
[00:09:44] Speaker A: So adaptive mutations are becoming rarer and rarer.
[00:09:49] Speaker B: Yeah, if they're based on random mutations.
[00:09:52] Speaker A: If it's random.
One last issue, which you make a big deal of, and I think the math is going to be too hard for all of us without a scorecard. So we'll speak about it in general. You followed some important evolutionary scientists and said in your first book that let's grant 500 steps to get from one species to the next. Now, we have millions of years at our disposal. We have got only 500 steps. It seems to be not very many in relationships, years that we've got. Why are we never going to get there anyway?
[00:10:29] Speaker B: Well, 500 steps was an estimate of the number of evolutionary steps. That is, random mutation followed by natural selection to go from one species to another. Now, let's take the horse evolution, which was the example that I used.
Now, the horse evolution was supposed to have taken place in something like 50 to 60 million years. That's lots of millions of years, but it is something. But the number of species that we have to go through, then it's quite large, because to generate the entire evolutionary series of the horse, it generated one genus after another, and there were about half a dozen genera that it went through to get from the first horse to the present day horse. Now, each one of these, then, in, say, 60 million years, took 10 million years, and from one genera to the next, took about a chain of ten species, had to evolve one after the other to go from one genus to another, so that you're left with 1 million years for each genus. So this 500 steps had to occur in 1 billion years and not in millions of million years.
[00:11:55] Speaker A: So we're never going to get there. Well, the deck seems to be stacked against random mutations leading to speciation. And as you write, the chances of a new organ coming to existence would therefore be even smaller. It's hard enough to get from one species of horse to another. It would be much harder to create the liver, for example.
[00:12:12] Speaker B: Yeah, well, even from one species to another, I mean, we don't even know what the details are of changing the organs in a species. But true, to get a liver is not an easy task. A lot of different enzymes have to be manufactured and evolved, whatever. And this is, it's very hard to explain how these things could evolve in some detail by random mutations and natural selection.
[00:12:39] Speaker A: Thank you, Doctor Spettner, for talking to us today. And if our listeners really want to get the full account of what Doctor Spettner has to say, they should buy us two books, not by chance and the Evolution Revolution, both available on Amazon. This is Ira Berkowitz from Jerusalem. Thank you for listening to intelligent design. The future.
This program was recorded by Discovery Institute's center for Science and Culture. Id the Future is copyright Discovery Institute. For more information, visit intelligentdesign.org and idthefuture.com.
