That's because Creationists demand that the transition happen in one generation, when evolutions says the transition happens very slowly over many many generations.There have been no Macro-evolution observations.
There have been no observations of mutations causing one kind of organism to change to a destinct new kind of organism.
Increasing new & beneficial Genetic information,scientists know of no viable method for nature to add appreciable amounts of new & beneficial Genetic information to a gene pool.
Another problem for evolutionist is all observed mutations, after millions of observations, mutations are caused by the sorting or loss of pre-existing Genetic data not new data,this is called gene depletion.
And even if Creationists were to observe say a worm-like caterpillar change into a winged flying insect right before their eyes, they would simply say it is the same insect. (sarcasm)
And a virus has been known to add new and beneficial genetic information allowing it to prey on an increasing number of hosts.
Now let me introduce you to a fellow evolutionist DR. Lee Spetner that shows what you say is not possible. I will also show you why it's not possible from another view.
Lee Spetner/Edward Max Dialogue
Dr. Lee Spetner
continuing an exchange with Dr. Edward E. Max
© 2001 L.M. Spetner. All Rights Reserved.
fter I posted my critique of Edward E. Maxs essay, Max posted our dialogue with additional comments to my responses. The order of topics in his posting does not correspond exactly to the order of my posting, but both postings are fairly accurate representations of our dialogue. The following is my latest response (23 May 2001) in a form that reproduces his posting into which I have inserted my comments. I have identified each of our statements as he has reproduced them by putting our names in boldface followed by a colon. My new comments are inserted into the text in small caps inside square brackets and identified by "LMS".
Introduction
Spetner: I am writing this essay in response to a request from Edward E. Max to comment on his posting The Evolution of Improved Fitness (updated July 12 1999). His essay is an attempt to defend evolutionary theory against attacks by creationists. Although Max scored some points against some alleged creationist arguments, he failed to defend Darwinian evolution against my attack on it in my book Not By Chance. He did not mention my book in his posting, but he referred to my book in his request for my comments. I shall also take this opportunity to clarify some issues in my book about which some readers have written me.
The principle message of evolution is that all life descended with modification from a putative single primitive source. I call this the grand sweep of evolution. The mechanism offered for the process of modification is basically the Darwinian one of a long series of steps of random variation, each followed by natural selection. The variation is generally understood today to be random mutations in the DNA.
That primitive source of life is assumed to be sufficiently simple that it could have arisen from nonliving material by chance. There is no theory today that can account for such an event, but I shall not address that issue here. That is for another place and another time. What is relevant to this discussion is that the requirement that life arose spontaneously sets, at the very least, a stringent upper limit on the complexity and information content of the putative first organism that could reproduce itself, and thus serve as a vehicle from which to launch Darwinian evolution. The issue I address here is the alleged development of all life by the Neo-Darwinian process of random mutation and natural selection, starting from a sufficiently simple beginning.
Despite the insistence of evolutionists that evolution is a fact, it is really no more than an improbable story. No one has ever shown that macroevolution can work. Most evolutionists assume that macroevolution is just a long sequence of microevolutionary events, but no one has ever shown it to be so. (Those few evolutionists who hold that macroevolution is really different from microevolution have changed their story several times since they first came out with it, and their mechanism is so fuzzy that I cannot tell what it is. John Maynard Smith seems to be of a similar opinion.)
For the grand process of evolution to work, long sequences of beneficial mutations must be possible, each building on the previous one and conferring a selective advantage on the organism. The process must be able to lead not only from one species to another, but to the entire advance of life from a simple beginning to the full complexity of life today. There must be a long series of possible mutations, each of which conferring a selective advantage on the organism so that natural selection can make it take over the population. Moreover, there must be not just one, but a great many such series.
The chain must be continuous in that at each stage a change of a single base pair somewhere in the genome can lead to a more adaptive organism in some environmental context. That is, it should be possible to continue to climb an adaptive hill, one base change after another, without getting hung up on a local adaptive maximum. No one has ever shown this to be possible.
Now one might say that if evolution were hung up on a local Maximum, a large genetic change like a recombination or a transposition could bring it to another higher peak. Large adaptive changes are, however, highly improbable. They are orders of magnitude less probable than getting an adaptive change with a single nucleotide substitution, which is itself improbable. No one has shown this to be possible either.
Moreover, as I have noted in my book, the large mutations such as recombinations and transpositions are mediated by special enzymes and are executed with precision - not the sort of doings one would expect of events that were supposed to be the products of chance. Evolutionists chose the mechanism of randomness, by the way, because we cant think of any other way beneficial mutations might occur in the absence of a law that might govern them. Genetic rearrangements may not be really random at all. They do not seem to qualify as the random mutations Neo-Darwinists can invoke whenever needed to escape from a local adaptive Maximum.
Evolutionists can argue, and rightly so, that we have no way of observing long series of mutations, since our observation time is limited to a relatively short interval. Our genetic observations over the past 100 years are more like a snapshot of evolution rather than a representative interval in which we can search for the required long series of changes. But our inability to observe such series cannot be used as a justification for the assumption that the series Darwinian theory requires indeed exist.
Max: I agree that there are no definitive examples where a macroevolutionary change (such as the development of cetaceans from terrestrial mammals) has been shown to result from a specific chain of mutations. And I agree with your further comment that we have no way of observing a long series of mutations. But you go on to say that our inability to observe such series cannot be used as a justification for the assumption that the series Darwinian theory requires indeed exist. An equally reasonable conclusion, in my view, would be that our inability to observe such series cannot be used as a justification for the assumption that such a series of mutations did NOT occur.
Spetner: Now Ed, thats ridiculous! Those two statements are not symmetrical. I dont have to assume the series did not occur to make a case for the inadequacy of NDT. You, who are basing your theory of evolution on the occurrence of such a series, are required to show that it exists, or at least that it is likely to exist. You are obliged to show an existence. I am not obliged to prove a non-existence.
[LMS: IN MAXS POSTING HE MOVED THIS REMARK OF MINE TO A LATER POINT IN THE DIALOGUE. I ORIGINALLY HAD IT HERE, AND HERE IS WHERE IT BELONGS.]
Max: In the absence of conclusive data defining such a series, if we want to distinguish between various hypotheses to explain the origin of species we must rely on other data, such as from various laboratory model systems that show adaptations in short enough timeframes that we can observe them. Then we must extrapolate as best we can the information learned from these model systems to the questions of species origins. This extrapolation from laboratory model systems to systems unobservable in the laboratory is the method of science common to medicine, astronomy, chemistry, meteorology, physics, etc.
I think there is some semantic confusion here about the word justification in Spetners sentence But our inability to observe such series cannot be used as a justification for the assumption that the series Darwinian theory requires indeed exist. He is correct that acceptance of the NDT implies the belief that a series of successive mutations (including duplications and translocations) occurred in the evolution of an ancient primitive genome into the complex genome of a modern species. Because we can access only genomes of modern (or very recent) species, we can never obtain the direct evidencei.e., a complete list of those mutationsthat some anti-evolutionists (e.g. Behe) seem to think would be necessary to support NDT.
[LMS: MAXS STATEMENT HERE IS A DISTORTION OF MY ARGUMENT INTO AN EXTREME POSITION. I NEITHER SAID NOR IMPLIED THAT EVOLUTIONISTS MUST OBTAIN...A COMPLETE LIST OF THOSE MUTATIONS REQUIRED FOR NDT. I DO MAINTAIN, HOWEVER, THAT THEY SHOULD AT LEAST ACCEPT THE RESPONSIBILITY OF SHOWING THAT NDT IS REASONABLY SUPPORTED BY EVIDENCE. THEY HAVE NOT DONE THAT. THE MECHANISM OF NDT CONSISTS OF TWO BASIC STEPS. AN ADAPTIVE MUTATION MUST BE ACHIEVED, AND THEN NATURAL SELECTION MUST OPERATE TO ENABLE IT TO TAKE OVER THE POPULATION. EVOLUTIONISTS ARE OBLIGATED TO SHOW THAT BOTH THESE STEPS ARE REASONABLY SUPPORTED BY EVIDENCE IF THEY ARE TO MAKE A CASE FOR NDT. MOST OF THEIR EFFORTS ALONG THESE LINES HAVE BEEN LIMITED TO ARGUING FOR NATURAL SELECTION. THEY USUALLY DO NOT DEAL WITH THE PROBABILITY OF ACHIEVING AN ADAPTIVE MUTATION. THEY MERELY ASSUME ONE WILL BE AVAILABLE WHENEVER IT IS NEEDED.]
In the absence of such direct evidence, it seems pointless to argue which side is obliged to provide what indirect evidence; certainly neither side can hope for anything close to proof. Although Spetner denies that he is obliged to prove a non-existence of such a chain of mutations, his whole effort in the correspondence seems to be directed to just that aim. Evolutionists have the job of defending the reasonableness of such a series of mutations. I believe that Spetner would agree with this.
[LMS: RIGHT. EVOLUTIONISTS DO HAVE THAT JOB AS AN OBLIGATION, AND THEY HAVE FAILED TO FULFILL IT. I AM NOT OBLIGED TO PROVE A NON-EXISTENCE. BUT IN MY BOOK, I HAVE MADE A GOOD CASE FOR THE UNREASONABLENESS OF THE EVOLUTIONISTS TACIT ASSUMPTIONS OF THE UNIVERSAL AVAILABILITY OF ADAPTIVE MUTATIONS, AND I HAVE GIVEN SOME OF THOSE ARGUMENTS IN THIS DIALOGUE.]
Spetner: But the argument against Darwinian theory is considerably stronger than that. The theory requires there be a vast number of possible point mutations which, coupled with natural selection, can produce the evolutionary advances that could produce the grand sweep of evolution. Because there must be a large number of qualifying mutations, at least a few of them should have been observed in some of the many genetics laboratories around the world. All the mutations in these long series must not only confer selective advantage on the organism but they must, on the average, also contribute to the information, or complexity, increase that surely distinguishes present-day life from the putative primitive organism.
These mutations must have whatever characteristics are necessary for them to serve as elements of the grand sweep of evolution. Thus, for a mutation to qualify as a representative member of the required multitude of long series that are supposed to produce evolution, it must bring new information not just to the genome of the organism, but the information must be new to the entire biocosm. The horizontal transfer of a gene from one species to another is not information new to the biocosm. To show evolution in action, one must at least demonstrate examples of a mutation that can serve as a prototype of those required by the theory. Such a mutation must be one that could be a contributing member of a series of mutations that could lead to the vast increase in information required by the theory. Thus, for example, a mutation that disables a repressor gene causing a constitutive synthesis of an enzyme might be advantageous to an organism under special circumstances, but the disabling of a gene does not represent the mutations required by the theory.
Max devotes a good portion of his essay to refuting what he calls the creationist argument against evolution. Although some opponents of evolutionary theory may have advanced the arguments he attacks, those arguments are in large measure straw men that Max busies himself with refuting. If some creationists have claimed that all mutations are harmful, they would be wrong, but Maxs observation that there are mutations that are beneficial, while true, is hardly a telling argument for evolution.
The B-Cell Hypermutation Model
Max: The next major point of discussion in the correspondence has been about how well the model of immunoglobulin gene somatic hypermutation in B cells serves as an analog to genomic mutation in evolution. The following section contains the salient points of our exchange about this question, beginning with Spetners initial response to my essay on Talk.Origins.
Spetner: Maxs pièce de résistance was the somatic mutations in B lymphocytes (B cells) of the vertebrate immune system as examples of random mutations that add information. He implied that Evolution could follow this method to achieve baboons from bacteria. I agree with him that these mutations add information to the B-cell genome. I also agree that they are random, but they are random only in the base changes they make; they are not random in where in the genome they can occur. More important, I do not agree that the grand sweep of evolution could be achieved through such mutations.
Although the somatic mutations to which Max referred are point mutations that do indeed add information to the genome of the B cells, they cannot be applied to Darwinian evolution. These are not the kind of mutations that can operate as the random mutations required by NDT that can, through chance errors, build information one base change at a time.
For one thing, the rate of the somatic mutations in the immune system is extremely high - more than a million times normal mutation rates. For this reason they are called hypermutations. If an organism had a mutation rate that was even a small fraction of this rate it could not survive. For a second thing, the hypermutations in the B cells are restricted to a specific tiny portion of the genome, where they can do no harm but only good. The entire genome of the B cell could not mutate at this rate; the hypermutation must be restricted only to the portion that encodes selected portions of the variable part of the antibody.
The mutation rate of the hypermutating part of the B cells genome is about one per thousand base pairs per replication (Darnell et al., 1986, Molecular Cell Biology, Scientific American Books, p. 1116.), and it can be as high as one in 500 base pairs per replication (Shen, 1998 Science 280: 1750). These rates are incompatible with Darwinian evolution. If an organisms genome were to mutate at this rate, there would be, on the average, about one mutation in every gene, with a high probability that many of them would be fatal for the organism. No, Darwinian evolution could not occur with such rates.
These high rates are essential for the working of the immune system. In each replication of a B cell, about 30 of the 300 or so gene regions encoding the CDRs will have a mutation. A lower mutation rate would make for a less efficient immune system. The high mutation rates, so necessary for the immune system, if applied to an entire organism for evolutionary purposes, would be fatal many times over.
Note that these hypermutations are limited to a restricted portion of the genome. Moreover, the hypermutations are mediated by special enzymes. Thus, although the hypermutations are random in the changes they make in the bases of the genome, they are not random in the positions in which they occur. They occur only in the small region in which they are needed, and occur there through enzymes that apparently play only that role. Furthermore, they occur only when they are switched on by the controlling mechanism of B-cell maturation. Thus it is clear that the hypermutations in B cells cannot serve as a prototype for the random mutations required for NDT.
Max: You agreed with me that the model system of random somatic mutations and selection that occurs in immunoglobulin genes in B lymphocytes can add information to the B-cell genome. I am glad that you accept the idea that random mutation and selection can lead to an increase in information, since this idea directly refutes the notion of Dembski and others who believe that there is some theoretical bar that would prevent achieving what they call complex specified information through random mutation and selection. (Incidentally, I dont think they would appreciate your characterization of them as straw men.") However, you then go on to declare that the B cell example is a poor model for what happens in Darwinian evolution, and you cite two reasons: (1) the mutation rate in this model is much higher than what is seen in non-immunoglobulin genes and in non-B-cells; and (2) these hypermutations are mediated by special enzymes. With regard to your first point, I agree that the mutation rate is higher in the B cell example than in evolution, but I fail to see why that fact weakens the usefulness of the example as a model for evolution. If adaptive mutations that increase information in the genome of a B lymphocyte population can occur over one week given a high mutation rate, what theoretical argument would lead you to reject the idea that adaptive mutations that increase information in the genome of a germ cell population could occur over many millions of years given a much lower mutation rate?
Spetner: [LMS: IN HIS POSTING, MAX MOVED MY ANSWER FROM HERE TO A LATER POINT IN THE DIALOGUE, BUT THIS IS WHERE I ORIGINALLY PUT IT, AND THIS IS WHERE IT BELONGS.]
The theoretical argument is the following. Evolution requires a long series of steps each consisting of an adaptive mutation followed by natural selection. In this series, each mutation must have a higher selective value than the previous. Thus, the evolving population moves across the adaptive landscape always rising toward higher adaptivity. It is generally accepted that the adaptive landscape is not just one big smooth hill with a single Maximum, but it is many hills of many different heights. Most likely, the population is on a hill that is not the highest in the landscape. It will then get stuck on a local Maximum of adaptivity and will not be able to move from it. This is particularly likely because the steps it takes are very small - only one nucleotide change at a time. The problem is compounded by the lack of freedom of a single nucleotide substitution to cause a change in the encoded amino acid. A single nucleotide substitution does not have the potential to change an amino acid to any one of the other 19. In general, its potential for change is limited to only 5 or 6 others. To evolve off the dead point of adaptivity, a larger step, such as the simultaneous change of more than one nucleotide, is required. Moreover, the probability is close to 1 that a single mutation in a population, even though it is adaptive, will disappear without taking over the population (see my book, Chapter 3). Therefore, many adaptive mutations must occur at each step.
The hypermutation in the B cells does this. It achieves all possible single, double, and triple mutations for the immune system, which allows them to obtain the information necessary to match a new antigen. Ordinary mutations, at the normal low rate, cannot add this information - even over long times. I shall explain why. Consider a population of antigen-activated B cells of, say, a billion individuals. In two weeks, there will be about 30 generations. Lets say the population size will remain stable, so in two weeks there will be a total of 30 billion replications. With a mutation rate of 1 per 1000 nucleotides per replication, there will be an average of 30 million changes in any particular nucleotide during a two-week period. The probability of getting two particular nucleotides to change is one per million replications. Thus in two weeks, there will be an average of 30 thousand changes in any two particular nucleotides. There will be an average of 30 changes in any three particular nucleotides.
How many generations, and how long, would it take to get a particular multiple nucleotide change in a germ cell to have an effect on Neo-Darwinian evolution? Here, the mutation rate is about one per billion nucleotides per replication. Lets suppose we're doing this experiment with a population of a billion bacteria. Then, in one generation, there will be an average of one change in a particular base. A particular double base change has a probability of one per quintillion, or 10-18. To get one of these would take a billion generations, or about 100,000 years. To get a triple change would take 1014, or a hundred trillion, years. That is why a long waiting time cannot compensate for a low mutation rate. I've given numbers here for a laboratory experiment with bacteria. Many more mutations would be expected world-wide. But the same kind of thing has to happen under NDT with multicelled animals as well. With vertebrates, for example, the breeding populations seldom exceed a few thousand. Multicelled animals would have many fewer mutations than those cited above for bacteria.
Max: Your second objection to the somatic mutation model in B-cells, that special enzymes are involved, is unsupportable.
[LMS: ON THE CONTRARY, I HAVE SHOWN IT IS WELL SUPPORTED (SEE BELOW).]
As far as I can tell from my reading of the literature, the mechanism of somatic hypermutation in B-cells is not currently known.
[LMS: TO WHAT EXTENT THE MECHANISM IS KNOWN IS IRRELEVANT TO THIS DISCUSSION. THE POINT IS THAT THE CONSENSUS AMONG EXPERTS IS THAT SUCH A MECHANISM EXISTS FOR B-CELL MUTATION, AND DOES NOT EXIST FOR GERMLINE MUTATION.]
The mechanism could perhaps involve special enzymes that create mutations, but an alternative possibility is that the high rate of accumulation of mutations simply reflects selective inhibition of normal proof-reading mechanisms. But again, I fail to see why the source of the random mutations should influence the general validity of the conclusion that random mutations and selection can increase genomic information, or why you feel that these mutations cannot serve as a model for evolutionary adaptations.
Indeed, both the rate and predominant mechanism of mutation may be different in different species of organisms, depending on whether they have more or less exposure to cosmic rays and other environmental mutagens, and depending on the nature and robustness of their genomic error-correction mechanisms. Therefore, if we accept your argument against extrapolation from B cell adaptation to species adaptation, should we reject the extrapolation of any information learned from studying one organism to understand adaptations in a second organism, unless it is shown that both the rate and mechanism of mutation are the same in both organisms?
[LMS: HERE AGAIN, MAX DISTORTS MY ARGUMENT INTO AN EXTREME POSITION AND THEN RESPONDS TO THAT EXTREME POSITION.]
In my view this would be like refusing to use the gravitational constant determined in laboratories on earth to analyze stellar physics. Such a reluctance to extrapolate would certainly prevent the use of modern organisms as a basis for understanding evolutionary events that occurred millions of years ago (which may be precisely your intent). I sometimes hear arguments like yours from creationists who are demanding rigorous proof of evolution. These creationists do not seem to understand the distinction between mathematics, where a rigorous proof is expected, versus most experimental and observational science, where all we are seeking is the best theory that explains observed data. Of course it is possible to extrapolate unreasonably, but I do not see that you have shown how evolutionary theory (or my essay) does this.
Spetner: Extrapolations made in astrophysics and cosmology may not be entirely valid, but at least they are reasonable based on everything we know. The extrapolation you propose from B-cell hypermutation to Neo-Darwinian evolution is unreasonable based on present knowledge, and it is therefore unjustified.
[LMS: THIS ANSWER OF MINE SOMEHOW GOT MOVED AWAY FROM THIS PLACE WHERE IT BELONGS.]
Yes, Ed, the hypermutation in the B cells cannot be a prototype of the kind of mutation required by NDT for Evolution A for the two reasons I gave. You question both those reasons, so I shall elaborate to explain to you why they are valid reasons for rejecting your example of B-cell hypermutation as support for NDT.
One of my arguments to invalidate hypermutation as a model for NDT is that this kind of mutation requires special enzymes", and is not the kind of mutations held to be responsible for the variation required in NDT. You rejected that argument as unsupportable, but that rejection is unjustified. These mutations, unlike ordinary errors in DNA replication in the germline, are turned on precisely when they are needed and turned off when they have done their job. They are accurately targeted to the very small regions of the genome where they can provide variability to the CDRs, which form the antibody binding site. Although the mechanism of this precisely targeted phenomenon is not yet known in complete detail, enough is known to say that there has to be a mechanism - it doesnt just happen by chance.
Max: {At this point Spetner quotes a number of speculative statements in the scientific literature, to the effect that B cell somatic hypermutation involves a special mechanism.
[LMS: MAX DID NOT REPRODUCE HERE THE REFERENCES I CITED. I WONT REPEAT THEM HERE, BUT THEY CAN BE SEEN IN MY PREVIOUS POSTING. MAX CALLS MY CITED REFERENCES SPECULATIVE", AND THAT MIGHT CREATE THE IMPRESSION THAT THEY ARE NOT REPRESENTATIVE OF RELIABLE SCIENTIFIC OPINION. THAT IMPRESSION IS FALSE. THE REFERENCES ARE FROM MAINSTREAM EXPERTS IN THE FIELD, ALL AGREEING THAT THERE IS A SPECIAL MECHANISM FOR HYPERMUTATIONS THAT IS NOT AVAILABLE TO GERMLINE MUTATIONS. THEY ARE SPECULATIVE ONLY IN THE SENSE THAT THESE PAPERS WERE SPECULATING ABOUT WHAT THE MECHANISM COULD BE. BUT THERE IS NO SPECULATION ABOUT THE EXISTENCE OF THE MECHANISM. ALL AGREED TO THAT, WHICH IS THE ONLY POINT I INTENDED, AND NEED, TO MAKE.]
The enzymes involved in somatic hypermutation in B cells remain unknown, so if Spetner is correct that special enzymes is supportable, he is correct only in the sense that the idea of special enzymes is supported by speculation in the literature. It is unsupported by any evidence, which is what I meant by unsupportable.
[LMS: MAX IS WRONG. THE EXISTENCE OF A MECHANISM IS SUPPORTED BY A LOT OF EVIDENCE, AS REFERRED TO IN THE PAPERS I CITED.]
To be fair I should note that an enzyme known as Activation Induced Deaminase (AID), reported after my initial comments to Spetner, has been shown necessary for somatic hypermutation to occur, but it is not clear whether this enzyme participates directly in the introduction of mutations. Indeed, since absence of AID also blocks isotype switch recombination, a phenomenon not obviously related to hypermutation, and also leads to enlarged germinal centers, it is possible that this enzyme is required for a step in B cell developmental maturation that triggers both hypermutation and switch recombination, and that the enzyme plays no direct role in mutating DNA. In any case, I never have questioned the idea that somatic hypermutation in B cells involves a special mechanism"; the question of whether unique enzymes are directly involved in creating the mutations seems to me rather tangential to the present discussion, but it is accurate to say that this question has not been settled as of yet.}
[LMS: SINCE MAX HERE ACKNOWLEDGES THAT HYPERMUTATIONS MAKE USE OF A SPECIAL MECHANISM NOT AVAILABLE TO GERMLINE MUTATION, HE IS LOGICALLY OBLIGATED TO CONCEDE TO ME THAT HIS EXAMPLE OF HYPERMUTATIONS CREATING INFORMATION IN THE B-CELL GENOME BY RANDOM MUTATIONS AND SELECTION CANNOT BE USED TO DEMONSTRATE THE POSSIBILITY THAT RANDOM MUTATIONS IN THE GERMLINE CAN CREATE INFORMATION FOR EVOLUTION. THIS CONCESSION ON HIS PART SHOULD LOGICALLY END OUR DEBATE. THE PRECISE NATURE OF THE MECHANISM OF HYPERMUTATION IS NOT SETTLED, BUT THE EXISTENCE OF SUCH A MECHANISM IS A CONSENSUS AMONG THE EXPERTS. FURTHERMORE, THE EXISTENCE OF A SPECIAL MECHANISM WITH ITS SPECIAL ENZYMES THAT PERMITS THE HYPERMUTATIONS TO DO THEIR JOB IN THE IMMUNE SYSTEM IS NOT TANGENTIAL TO OUR DISCUSSION. THE MECHANISM, WHATEVER ITS NATURE, IS WHAT PERMITS HYPERMUTATIONS CREATE INFORMATION FOR THE IMMUNE SYSTEM. SUCH A MECHANISM IS NOT AVAILABLE FOR GERM LINE MUTATIONS TO MAKE EVOLUTION POSSIBLE, AND THEREFORE MAXS EXAMPLE OF B-CELL HYPERMUTATION TO SHOW THAT INFORMATION CAN BE GENERATED IN EVOLUTION IS INVALID.]
Spetner: It thus seems quite clear to me that informed opinion in this field supports my contention and rejects your suggestion that an alternative possibility is that the high rate of accumulation of mutations simply reflects selective inhibition of normal proof-reading mechanisms". Please let me know if you agree or disagree.
Max: {As indicated above, I disagree.}
[LMS: MAX IS, OF COURSE, WRONG IN DISAGREEING, AS EXPLAINED ABOVE]
Spetner: You ask, why does the existence of a special mechanism for the hypermutation in B cells preclude the example from being a model of mutations for NDT? The simple answer is that if you really want to suggest that mutations for NDT are capable of hypermutations as are the B cells, you have to show two things. First you have to show that such a highly complex system with its requisite enzymes actually exists in germ cells, where they can play a role in evolution. As far as I know, there is no such mechanism in germ cells. If you know of anything like this please let me know.
Max: {I have pointed out that the enzymatic mechanisms creating somatic mutations in B cells is not known. I have never claimed that it is the same mechanism as causes mutations in germ cells where they play a role in phylogenetic evolution, so I am not obligated to show what Spetner says I am.}
[LMS: THIS IS ANOTHER EXAMPLE OF DISTORTING THE ARGUMENT. IF MAX WANTS TO USE B-CELL HYPERMUTATIONS AS A DEMONSTRATION OF THE CAPABILITY OF GERMLINE MUTATIONS TO GENERATE THE INFORMATION REQUIRED FOR EVOLUTION (WHICH WAS THE MAIN PURPOSE OF HIS ESSAY) THEN HE IS OBLIGATED TO SHOW THAT GERMLINE MUTATION HAS THE SAME CAPABILITY AS B-CELL MUTATION. THAT IS NOT TO SAY THAT IT HAS THE SAME MECHANISM, BUT IT MUST HAVE A COMPARABLE MECHANISM. SINCE NO SUCH MECHANISM IS KNOWN FOR GERMLINE MUTATIONS, THE MAIN THESIS OF MAXS ESSAY FALLS.]
Spetner: Furthermore, according to the evolutionary paradigm, you must account for the origin and development of such a mechanism in the germline, or at the very least, you must suggest how such a development could reasonably occur. You are obligated to do this because you hold that all characteristics of life have evolved through random variation and natural selection.
Max: {Here Spetner, like Behe, seems to demand that I provide an origin and development scenario that he knows he will be able to disparage as another just-so story.
[LMS: I HAVE ASKED HIM TO BRING AN ARGUMENT. I DIDNT ASK FOR A SCENARIO". HIS PROBLEM, BUT NOT MY PROBLEM, IS THAT A FICTIONAL SCENARIO IS THE ONLY KIND OF ARGUMENT HE HAS, AND ITS NOT SCIENTIFIC.]
Furthermore, the question of how somatic hypermutation evolved is totally irrelevant to the question of whether it is a good model for the efficacy of random mutation and selection in promoting increased fitness, which is the subject of my Talk.Origins essay.}
[LMS: THIS IS AN OTHER DISTORTION OF MY STATEMENT ABOVE. I DID NOT ASK FOR A DESCRIPTION OF HOW HYPERMUTATION EVOLVED. I ASKED FOR ONE ABOUT HOW A COMPARABLE MECHANISM IN THE GERMLINE COULD EVOLVE. ITS NOT IRRELEVANT BECAUSE IF ONE IS TRYING TO JUSTIFY NEO-DARWINIAN THEORY (NDT), THEN ONE WOULD BE ON SHAKY GROUND TO SUGGEST IT DEPENDS ON THE EXISTENCE OF A MECHANISM WHOSE OWN ORIGIN CANNOT BE ACCOUNTED FOR BY NDT]
Spetner: You are not entitled to postulate a mechanism that could not have evolved. Such a mechanism of germline mutation would have to produce accurately targeted mutations that could play a role in evolution. For such a system to develop by Neo-Darwinian evolution, a long series of evolutionary steps in ordinary evolution would have to play the role of a single step in the evolution of this mechanism, because selection here is based on successful evolution of the ordinary kind. Thus if a million generations are necessary for the evolution and perfection of a new phenotypic character, then a million times that, or a trillion generations, would be required for the evolution and perfection of this mechanism.
Max: {These are totally unsupported quantitative speculations.}
[LMS: MAX MUST THINK HE CAN DISPARAGE MY QUANTITATIVE ESTIMATES BY THIS STATEMENT. MY ARGUMENT ABOVE IS A TYPICAL KIND OF ARGUMENT USED IN ANY QUANTITATIVE SCIENCE TO ACHIEVE SOME ROUGH QUANTITATIVE ESTIMATES, USUALLY REFERRED TO AS BACK-OF-THE-ENVELOPE CALCULATIONS. IT PROVIDES AN ADEQUATE ESTIMATE FOR OUR DISCUSSION, EVEN THOUGH IT IS NOT PRECISE.]
Spetner: It seems to me that any selective pressure to raise the spontaneous mutation to benefit evolution would be overwhelmed by the selective pressure to keep the mutation rate low. Perhaps Ill look into the mathematics of such a phenomenon and prepare a paper on it.
Max: I still fail to see how the particular enzymes involved have any bearing on the applicability of the model to Darwinian species evolution. Indeed, a variety of laboratory mechanisms for generating mutations in antibody genes (chemical mutagens, randomized oligonucleotides, etc.) all lead to pools of mutated antibody genes from which higher affinity proteins can be obtained, so the principle that random mutation and selection can lead to improved function appears to be independent of the mechanism of generating the mutations.
There is no logical reason why mutation and selection in species adaptation should be strictly dependent on the mechanism of mutation either; indeed, a variety of different mechanisms are known to contribute to varying extents under different conditions, including copying errors, radiation, chemical mutagens, slipped mispairing, deamination, etc.
[LMS: THE IMPORTANT FEATURE OF THE MECHANISM OF HYPERMUTATIONS IS ITS ABILITY (1) TO TURN THE MUTATIONS ON WHEN THEY ARE NEEDED, AND OFF AGAIN WHEN THEIR JOB IS DONE, AND (2) TO CONFINE THE MUTATIONS TO A RESTRICTED PORTION OF THE GENOME WHERE THEY CAN DO NO HARM, AND CAN ONLY DO GOOD. HYPERMUTATIONS HAVE A MECHANISM WITH THESE CHARACTERISTICS AND GERMLINE MUTATIONS DO NOT. SEE MY NEXT COMMENT. THE MECHANISMS MAX CITED HERE FOR GERMLINE MUTATIONS DO NOT ADDRESS THESE QUESTIONS AND IS THUS IRRELEVANT TO THE DISCUSSION.]
Spetner: You are missing my point. I am not focusing on the source of mutation as the distinguishing factor between the somatic mutations and germline mutations, but I am noting that the hypermutations do have a special mechanism that controls them whereas the germline mutations have no such mechanism available. The important features of the somatic mutations that are unavailable to germline mutations include some (unknown) trigger that turns them on at the right time and directs them to the right place on the genome. Without these controls, hypermutations would destroy the B cells.
Max: Clearly, the lower rate of mutation that occurs in the germline does not destroy genomes for the next generation. Is this rate high enough to generate enough mutations to account for adaptive phylogenetic evolution? This is a critical issue, and while I dont have a quantitative answer, I dont find Spetners negative answer to this question supported by convincing logic. He makes reference to his book as offering some arguments, but has not discussed this evidence in our correspondence.
[LMS: AGAIN, MAX DODGES THE POINT. MY POINT IS NOT ONE OF ABSOLUTE MUTATION RATES. HE SAYS WE DONT KNOW IF THE NORMAL GERMLINE MUTATION RATE IS ENOUGH TO PRODUCE THE ADAPTIVE MUTATIONS. ALTHOUGH WE DONT KNOW ANY HARD STATISTICS ON ADAPTIVE MUTATIONS, THERE IS GOOD EVIDENCE THAT THERE ARE NOT ENOUGH OF THEM OCCURRING AT RANDOM TO MAKE NDT WORK, AS I HAVE NOTED IN MY BOOK. BUT THAT IS NOT THE POINT IN THIS STAGE OF THE DIALOGUE. THE POINT HERE IS THAT MAX IS TRYING TO USE THE EXAMPLE OF THE GENOMIC INFORMATION GENERATED BY HYPERMUTATIONS IN THE IMMUNE SYSTEM TO DEMONSTRATE THAT GERMLINE MUTATIONS CAN LIKEWISE GENERATE THE INFORMATION NEEDED BY NDT. I HAVE SIMPLY POINTED OUT THAT HYPERMUTATIONS HAVE SOME ADVANTAGES THAT GERMLINE MUTATIONS DO NOT. AND THESE ADVANTAGES ARE PRECISELY WHAT MAKES HYPERMUTATIONS ADD INFORMATION TO THE GENOME. THAT POINT IS SUFFICIENT TO DISQUALIFY HIS EXAMPLE AND NULLIFY ITS FORCE.]
On the question of the frequency of mutation, in your last posting you included numerical models for B cell hypermutation and for species mutation, and arrived at conclusions by reasoning that I find illogical. You calculate the time required for one, two or three particular nucleotide changes to occur as though these calculations would be relevant to the times required for changes to occur in either B cell or species adaptations. Your reasoning seems to be predicated on the following logic. (1) By single nucleotide mutations, most triplet codons of amino acids can be mutated to code for only 5 or 6 different altered amino acids out of the 20 amino acid constituents of proteins. (2) This limitation would restrict the changes available by single nucleotide changes, such that certain adaptive changes would require two or three particular nucleotide mutations in order avoid getting stuck on a low local Maximum of activity in the adaptive landscape.
[LMS: MAX IS LEAVING OUT THE NEXT IMPORTANT STEPS IN THE LOGIC. THEY ARE: (3) THE RESTRICTION ON THE CHANGES THAT COULD BE MADE IN ONE MUTATION RESTRICT THE FIELD OF MUTATIONS HAVING SELECTIVE VALUE. (4) A TRIPLE MUTATION CAN REACH ANY ONE OF THE FULL FIELD OF 19 AMINO-ACID CHANGES. FOR THIS FIELD TO BE AVAILABLE TO A CHAIN OF THREE SINGLE MUTATIONS, EACH OF THEM WOULD HAVE TO HAVE POSITIVE SELECTIVE VALUE, A REQUIREMENT NOT NECESSARY FOR A TRIPLE MUTATION.]
Your reasoning seems flawed to me in part because you are considering the time to achieve a particular change rather than the time necessary to achieve an improvement in function. The illogic of this is similar to that of equating the odds of being dealt any hand that beats a bust hand with the odds of being dealt a particular poker hand that beats a bust hand.
Spetner: I am considering in my analysis what would be analogous to being dealt any hand that beats (i.e., that has a higher selective value than) a given hand.
Max: This seems to be contradicted by the following sentences Spetner wrote (quoted a few paragraphs back): With a mutation rate of 1 per 1000 nucleotides per replication, there will be an average of 30 million changes in any particular nucleotide during a two-week period. The probability of getting two particular nucleotides to change is one per million replications. Thus in two weeks, there will be an average of 30 thousand changes in any two particular nucleotides. There will be an average of 30 changes in any three particular nucleotides.
[LMS: I DO NOT SEE ANY CONTRADICTION.]
Particular nucleotides will be generated by mutation at a far lower frequency than adaptive mutations, as discussed below.}
[LMS: THE READER CAN SEE THAT MAX MUST HAVE MISUNDERSTOOD THE POINT I MADE. SEE MY COMMENTS ABOVE.]
The B-cell system selects for improvements in function and not for particular sequences. Furthermore, there is no reason to assume that the highest theoretical peaks on the adaptive landscape are ever achieved - either by the B cell system or Darwinian species evolution. Finally, there is no reason to assume that functional improvements cannot arise from the small subset of amino acid replacements accessible from single nucleotide changes.
Spetner: On the contrary, there is no justification in assuming that one can always obtain a selective advantage with one nucleotide substitution.
Max: I am not assuming a priori that one can ALWAYS obtain a selective advantage with one nucleotide substitution. But where this has been investigated by experimentally mutating immunoglobulin genes to introduce single mutations corresponding to changes observed in natural somatic hypermutation, it has been found that improvements in antibody affinity can be attributed to specific single nucleotide changes; so it is reasonable to assume that this potential is not so rare as to require the assumption that most increases in antibody affinity require multiple simultaneous mutations.
Indeed, if one looks at actual sequences of somatically mutated antibody genes (e.g. Cumano and Rajewsky EMBO J 5:2459, 1986, Figure 2), one finds plenty of single nucleotide mutations that change amino acids, and their presence at a frequency higher than would be predicted by random mutations suggests that most have been selected for on the basis of improved antigen binding. (In this study of nine somatically mutated antibodies, there were 23 amino acid changes caused by single mutations within a codon, and only 4 caused by double mutations; in addition there were only 6 silent single mutations, i.e., not causing amino acid changes.)
Spetner: This is all consistent with what I have written. I do not say that an adaptive mutation cannot be achieved by a single mutation. I only say that the target set of single mutations is smaller than that for single plus double mutations, which in turn is smaller than that for single plus double plus triple, etc. I do not claim that functional improvements cannot be achieved by single mutations, only that the choice is much wider for multiple mutations. For example, three single mutations are not the equivalent of a triple mutation. The first mutation will not remain in the population unless it has a selective advantage. I am sure you will agree that it is possible for a triple nucleotide substitution to have a selective advantage without any single one of them having an advantage. In fact, I would say that is the most likely case.
Max: If single nucleotide changes can lead to selection for improved function, then if one wants to calculate the time necessary to achieve the even greater improvement that might be achieved by three mutations, this time would be found not by a calculation like yours, based on the product of the odds for a single mutation, but rather by multiplying the time for a single adaptive nucleotide mutation by three. Suppose it would take one week for the first adaptive change. By the selection mechanism in the germinal center, the population of B cells would soon be overtaken by B cells with this first change, so that the time required for the second adaptive change would again be one week; and similarly the third change would require a third week to yield a protein of even greater affinity than could be achieved by one or two amino acid replacements.
Spetner: You are assuming that the single mutation will be selected. I say that is unlikely. The time to achieve a triple change would be equal to the sum of the times necessary to get a single one only if all those single changes had selective value, and that is too unlikely to bank on.
Max: What is the basis for your judgment that such selectable single nucleotide mutations are too unlikely"?
[LMS: MAX IS THE ONE WHO IS TRYING TO SHOW THAT HIS EXAMPLE OF B-CELL HYPERMUTATIONS DEMONSTRATES THE ABILITY OF GERMLINE MUTATIONS TO ACHIEVE DARWINIAN EVOLUTION. HIS ARGUMENT IS BASED ON THE TACIT ASSUMPTION THAT GERMLINE MUTATIONS CAN DO ANYTHING THE SOMATIC HYPERMUTATIONS CAN DO. I HAVE NOTED THAT HYPERMUTATIONS HAVE ADVANTAGES THAT GERMLINE MUTATIONS DO NOT HAVE. WITHOUT THESE ADVANTAGES, B CELLS CANNOT GENERATE THE INFORMATION THE ANTIBODIES NEED. ONE OF THESE ADVANTAGES IS THE ABILITY TO GENERATE A LARGE NUMBER OF DOUBLE AND TRIPLE MUTATIONS. IS MAX HERE TRYING TO ARGUE THAT THREE SINGLE MUTATIONS AT THE LOW RATE OF THE GERMLINE MUTATIONS ARE AS LIKELY TO PRODUCE AN ADAPTIVE IMPROVEMENT AS A TRIPLE MUTATION AT THE HIGH RATE IN THE B CELL? HE CANNOT SHOW THAT. IF THAT IS HIS THRUST, HE IS WRONG. CLEARLY THE FORMER IS LESS LIKELY TO PRODUCE ADAPTIVITY IN ALL OF THREE SUCCESSIVE MUTATIONS THAN THE LATTER IS TO PRODUCE IN ONLY ONE MUTATION. DOES HIS ARGUMENT REST ON CHALLENGING ME TO SHOW JUST HOW UNLIKELY ARE THREE ADAPTIVE MUTATIONS IN A ROW? IF SO, IT IS A POOR ARGUMENT.]
A similar argument would apply to estimates for adaptive mutations in bacteria. Because of the flawed assumptions built into your approach it seems to me that your calculations grossly overstate the time required for evolving adaptive changes by random mutation and selection.
Spetner: My assumptions are not flawed. You just dont understand them. Read again what I wrote above and see if you dont agree with me.
Max: {I have reread what Spetner wrote. He agrees that single nucleotide changes can lead to selectable advantages (even if the available codons are restricted so the scope of amino acid changes is less than would be possible with multiple simultaneous mutations). Such selectable single mutations could spread throughout the population, to be followed by successive additional selectable point mutations. By this model, three selectable point mutations could occur in a time frame measured by three times the time for a single mutation, rather than taking the time necessary for three simultaneous mutations as Spetner has calculated. We both agree that simultaneous double and triple mutations have greater scope for amino acid replacement, but are very rare. I honestly do not understand the basis for our disagreement here, but perhaps Spetner will clarify why he considers evolution by successive single selectable point mutations too unlikely even though he agrees that single point mutations leading to selectable advantage can occur.}
[LMS: I AM DISAPPOINTED THAT MAX DOES NOT UNDERSTAND MY POINT. IT IS NOT THAT I NECESSARILY CLAIM HERE THAT SUCCESSIVE POINT MUTATIONS ARE TOO UNLIKELY", ALTHOUGH THEY ARE AND THERE IS EVIDENCE FOR IT. BUT THE POINT HERE IS THE AVAILABILITY TO B CELLS OF A HIGHER RATE OF MULTIPLE MUTATIONS PROVIDES THEM WITH GREATER SCOPE FOR ACHIEVING ADAPTIVE IMPROVEMENTS THAN ARE AVAILABLE TO GERMLINE MUTATIONS. THE POINT THAT MAX SEEMS TO MISS HERE IS THAT A TRIPLE MUTATION CAN BE ADAPTIVE EVEN THOUGH EACH NUCLEOTIDE CHANGE INDIVIDUALLY IS NOT. THESE MUTATIONS ARE AVAILABLE TO HYPERMUTATION, BUT NOT TO GERMLINE MUTATION. UNLESS EACH INDIVIDUAL CHANGE IS ADAPTIVE, A TRIPLE CHANGE CAN BE ACHIEVED BY THREE SINGLE MUTATIONS ONLY IF THE THREE OCCUR BY CHANCE WITHOUT SELECTION. THIS IS WHY SUCH AN EVENT HAS A PROBABILITY OF THE CUBE OF THAT OF A SINGLE MUTATION, AND THAT IS WHY THE TIME TO ACHIEVE SUCH AN UNLIKELY EVENT IS SO ENORMOUS. I HOPE I HAVE NOW MADE IT SUFFICIENTLY CLEAR FOR MAX TO SEE MY POINT.]
The Role of Gene Duplication
Max: In his first response to my essay, Spetner was critical of the role he thought I claimed for gene duplication in evolution. When he understood that he had originally misread the essay, he had no quarrel with this aspect. Here is the short discussion of this point.
Spetner: Max cited gene duplication as an example of a mutation that increases information. A favorite scenario for molecular evolution is that a gene gets duplicated and then gradually mutates to become something useful that did not exist before. Such a proposed scenario does not constitute evidence for evolution, it proves nothing, and indeed such a scenario itself requires proof. I do not, of course, mean to say that one has to prove that genes can be duplicated. That is well known. But gene duplication alone does not constitute an increase of information in the biocosm or even in the genome of the organism itself. Two copies of todays newspaper contain no more information than one copy. Gene duplication, in any case, cannot play the role of the mutations that could produce the grand sweep of evolution.
Gene duplication alone cannot add information to the genome. The purpose of the gene duplication in the above scenario is simply to provide raw material from which a new gene could evolve without having to give up any functions the organism already had. New information would then supposedly be built up by point mutations and natural selection. And this is precisely the process I discussed in my book and about which I said that all known examples of these mutations lose information rather than gain it. Note that I did not say that it is impossible in principle for random mutations to add information to the genome. But it just turns out that that is what has been found.
Max: You state: Max cited gene duplication as an example of a mutation that increases information. On the contrary, I believe that I was careful to avoid saying that gene duplication alone increases information. I do not believe such a statement is correct and agree fully with your statement that Two copies of todays newspaper contain no more information than one copy.". Please let me know exactly what words in my essay (or in my letter to you) suggested that I believed duplication by itself increases information, and I will try to change the phraseology so as to reduce the likelihood that other readers will misconstrue my meaning.
On the other hand - and this is the major point of all that follows - I do believe that gene duplication is a critical component of what I will call the evolutionary triad: namely gene duplication, random mutation and selection. To illustrate the role of gene duplication in this triad, lets extend your own newspaper analogy. Suppose we have a copy of the early edition of todays newspaper and a copy of the final edition. In the final edition several paragraphs of certain articles have been altered to include late breaking events. Each article has remained the same length in the two editions because certain less important information in each article was deleted to make room for the late breaking news. Now it is clear that having these two copies of todays newspaper does give us more information than either copy alone, since the early edition lacks the late breaking events and the late edition lacks the information that was deleted to make room for the late breaking news.
You seem to allude to this possibility in evolution when you suggest that in the evolutionary model, after gene duplication [n]ew information would then supposedly be built up by point mutations and natural selection."
Spetner: You deny suggesting that gene duplication alone adds information. I accept your denial and I apologize for incorrectly attributing that view to you. What led me to believe that you did suggest this is the statement in point 1 of your letter to me, saying. Gene duplications occur, and there is no reason to postulate supernatural processes to account for them. ...Does the ID argument about impossibility of naturalistic information increase include an assumption that naturalistic gene duplications cannot occur? This is what led me to think that you were suggesting gene duplications as a method of adding information.
[LMS: IN MY FIRST POSTING OF OUR DISCUSSION, I LEFT OUT THIS PART OF THE DISCUSSION, BECAUSE IT WAS MY MISUNDERSTANDING OF WHAT HE WROTE. MAX WAS UPSET ABOUT MY LEAVING THAT OUT. IF HE WANTS TO ENJOY A SMALL TRIUMPH IN NOTING THAT I MISUNDERSTOOD HIM, THEN I AM MORE THAN HAPPY TO LET HIM DO SO.]
Interpretations of the Word Evolution
Max: Spetner tried to clarify different interpretations of evolution that frequently cause people confusion if one meaning is intended but another is meant. (For the text of Spetners comments on this issue, I have taken his True.Origins posting, which begins with this discussion.) I countered that there were several more identifiable meanings of evolution, and that Spetner seemed to be avoiding the burden of having to defend his position by being intentionally vague about where he stood. My response to this point has not been answered.
[LMS: I FRANKLY DO NOT SEE WHAT MAX WANTS TO ARGUE ABOUT HERE. IT SEEMS TO ME THAT HE IS NIT PICKING. MY PURPOSE IN NOTING THE TWO EXTREME USES OF THE WORD EVOLUTION WAS SIMPLY TO CLARIFY A CONFUSION POPULAR WITH EVOLUTIONISTS, AS CAN BE SEEN FROM MY COMMENTS BELOW. THERE IS NO NEED FOR ME TO CONSIDER ALL OTHER USES OF THE WORD EVOLUTION". THE TWO EXTREMES ARE SUFFICIENT FOR MY PURPOSE. I REALLY DONT KNOW WHAT IS BOTHERING MAX HERE. I DONT KNOW WHY HE THINKS I MUST WRITE A TREATISE ON ALL POSSIBLE USES OF THE TERM EVOLUTION.]
Spetner: At the outset, I shall establish an important and necessary guideline in this discussion of evolution. The word evolution is generally used in at least two different senses, and the distinction between them is important. On the one hand, the word evolution is used to denote the descent of all life from a putative single primitive source. It is the grand sweep of evolution that is supposed to have led from a simple beginning, something perhaps simpler than a bacterium, to all organisms living today, including humans. This descent is supposed to have occurred through purely natural means. Neo-Darwinian theory (NDT), which is the prevailing theory of evolution, teaches that this development occurred through random heritable variations in the organisms followed by natural selection. I shall denote the word evolution used in this sense as Evolution A. When evolution is discussed for popular consumption, it is most often Evolution A.
The second sense in which the word evolution is used is to denote any kind of change of a population. The change can sometimes occur in response to environmental pressure (artificial or natural selection), and sometimes it can just be random (genetic drift). I shall denote the word used in this second sense as Evolution B. Evolution B has been observed. Evolution A is an inference, but is not observable. The distinction between these two meanings of evolution parallels the distinction between macroevolution and microevolution, but the two pairs of terms are not identical. Evolution A is certainly what is called macroevolution, but what is called macroevolution is not identical with Evolution A. In any case, I prefer to use the A and B to avoid having to carry whatever baggage might go with the macro/micro distinction.
The distinction between these two meanings of evolution is often ignored by the defenders of Neo-Darwinian evolution. But the distinction is critical. The claim is made for Evolution A, but the proof offered is often limited to Evolution B. The implication is that the observation of Evolution B is a substantiation of Evolution A. But this is not so. Since Evolution A is not an observable, it can only be substantiated by circumstantial evidence. This circumstantial evidence is principally the fossil record, amino-acid-sequence comparisons, and comparative anatomy. Circumstantial evidence must be accompanied by a theory of how it relates to what is to be proved. NDT is generally accepted to be that theory. The strength of the circumstantial evidence for Evolution A can therefore be no better than the strength of NDT.
Max: I cant tell exactly what you accept in your distinction between Evolution A and Evolution B. I actually think that there are finer distinctions between the various meanings of evolution than encompassed by your A vs B.
[LMS: YES, FINER DISTINCTIONS CAN BE MADE, BUT THEY ARE IRRELEVANT TO THE POINT I WAS TRYING TO MAKE.]
I would distinguish several more possible meanings:
Living forms are different now from what they were in the past. This seems to be well documented by fossil evidence. This slow change is sometimes referred to as evolution.
Random mutation and selection can lead to microevolution, i.e., small changes in gene frequencies that follow an environmental shift and leave a population on average more fit to cope with the new environment. I think you accept this, since I think it corresponds to what you mean by Evolution B. I certainly accept it.
Various different modern species share a common ancestry. Since the time of the common ancestor, the divergence into the various modern species has involved changes much greater than microevolution. This is the idea of common descent. I am really not sure whether you accept this notion. I think there is excellent evidence for common descent of some groups of species, as outlined in my essay. If you do not accept common descent, at least for the cases I cite in my essay, I would be interested in hearing what alternative interpretations you can offer for the observations I cite in that essay. [I do not have that essay handy to check what you say. If you want my critique of that essay, ask me, and if I find the time I shall write one. Meanwhile, lets stick to my critique of your fitness essay.]
All of the nucleotide discrepancies between modern species, or between a modern species and its ancestral species, arose as a result of random mutation (including gene duplications, insertions and deletions caused by naturalistic processes) and natural selection, without the intervention of an intelligent designer. I do not believe that there is any evidence for the preceding statement, and indicate as much in my essay. Nor do I believe that an intelligent designer can be ruled out as an explanation for hurricanes, disease, or stock market fluctuations. However, I have never seen a convincing argument that an intelligent designer must be hypothesized in order to explain any of these kinds of events, or to explain species change through time.
[LMS: MAX IS THE ONE WHO IS BRINGING IN AN INTELLIGENT DESIGNER.", NOT ME. I DID NOT BRING IN THE NOTION OF AN INTELLIGENT DESIGNER, IN MY CRITIQUE OF MAXS ESSAY, AND I DONT THINK IT BELONGS IN THIS DISCUSSION. MY POINT IS THAT MAXS ESSAY DOES NOT LEND ANY SUPPORT TO NEO-DARWINIAN THEORY. THE GRATUITOUS INTRODUCTION OF AN INTELLIGENT-DESIGNER THEORY DOES NOT HELP HIS DEFENSE OF HIS ESSAY.]
The origin of life came about through exclusively naturalistic processes operating on prebiotic chemicals, which evolved into replicating life forms. We have almost no scientific evidence about the origin of life and so there is no scientific evidence to support a purely naturalistic origin of life. I feel the same way about this meaning of evolution as I do about #4.
In my judgment, there is good scientific evidence for #1, #2 and #3. From your dismissal of evidence for what you call Evolution A, I cant tell what you believe about #3. On #4 and #5 I assume we are in agreement on the insufficiency of scientific evidence to support a purely naturalistic mechanism, but we obviously differ on whether arguments such as yours are sufficient to rule out a purely naturalistic mechanism. I think that it would be an improvement in the dialogue/ document to clarify both of our opinions on these finer distinctions. Incidentally, I am not clear exactly on the difference you see between Evolution A and macroevolution.
[LMS: WHAT I CALLED EVOLUTION A IS A SUBSET OF WHAT IS CALLED MACROEVOLUTION. NOT ALL MACROEVOLUTION QUALIFIES AS EVOLUTION A. BUT LETS LEAVE THAT. I INTRODUCED THE TERM EVOLUTION A TO MAKE THINGS CLEARER. IF ITS ONLY MAKING THEM MORE COMPLICATED, THEN LETS DROP IT AND SUBSTITUTE FOR IT THE GRAND SWEEP OF EVOLUTION FROM SOME PUTATIVE PRIMITIVE ORGANISM TO ALL THE LIFE OF TODAY. SUBSTITUTE FOR EVOLUTION B THE SMALL CHANGE IN POPULATIONS THAT ARE ACTUALLY OBSERVED.]
I dont know what version of creation you accept, but it seems to me that even if the supernatural played a role in past events, those past events leave traces. By refusing to specify an alternative scenario that you consider more believable than evolution, you hide behind vagueness in order to avoid having to defend potential contradictions between your scenario and the traces from the past that point in a different direction.
[LMS: HERE MAX IS TRYING TO DRAW THE DISCUSSION OFF COURSE. THE POINT IS THAT HIS ESSAY OFFERS NO SUPPORT FOR NDT. I DID NOT INTRODUCE CREATION OR THEOLOGY INTO MY CRITIQUE OF HIS ESSAY BECAUSE THEY HAVE NO PLACE IN A SCIENTIFIC DISCUSSION. THEOLOGY IS NOT WITHIN HIS EXPERTISE, NOR DO I CLAIM IT TO BE WITHIN MINE. THIS STARTED OUT AS A SCIENTIFIC DISCUSSION AND I THINK IT SHOULD REMAIN SO.]
In my book, I did not quantify the information gain or loss in a mutation. I didnt do it mainly because I was reluctant to introduce equations and scare off the average reader. And anyway, I thought it rather obvious that a mutation that destroys the functionality of a gene (such as a repressor gene) is a loss of information. I also thought it rather obvious that a mutation that reduces the specificity of an enzyme is also a loss of information. But I shall take this opportunity to quantify the information difference before and after mutation in an important special case, which I described in my book.
DR. Lee Spetner is a creationist.
it is a living breathing human in the womb if that were not true why did God give that child an umbilical cord if you don't mind answering please ?
, a Hebrew abbreviation of shisha sedarim, the "six orders" of the Mishnah.
