Posted on 04/10/2005 3:53:04 AM PDT by PatrickHenry
A pro-evolution group has organized what appears to be a successful boycott of Kansas hearings on intelligent design.
Alexa Posny, a deputy commissioner with the state department of education, told the Kansas City Star that only one person has agreed to testify on the pro-evolution side for the hearings scheduled for May.
"We have contacted scientists from all over the world," Posny said. "There isn't anywhere else we can go."
Harry McDonald, head of Kansas Citizens for Science, charged that the hearings, called by a conservative majority on the state board of education, have a pre-ordained outcome.He said that testifying would only make intelligent design appear legitimate.
"Intelligent design is not going to get its forum, at least not one in which they can say that scientists participated," he said.
Backers of intelligent design, the claim that a supreme being guided evolution, say it is a theory with scientific backing. Opponents believe it is an attempt to smuggle religion into public education.
OTOH, when the public (government) funds research then the work product is in the public domain - any and every business can use it. The exception of course is funding of research pertaining to national defense.
IMHO, we need both kinds of research. It just seems to me that scientists might not be as business-minded as they could be to make things more efficient.
For instance, if the "unaffiliated" (academia) cancer researchers in Illinois formed an association and pooled their nickles and dimes to hire the specific skills needed to handle the grants, they might have more time to "do" the science.
Any hoot, those are my musings...
My sincere condolences, Doc, on this wretched state of affairs. Plus it is an appalling thing to turn a scientist into a hat-in-your-hand fund-raiser, and bookkeeper to boot.
In a prelude to going over his exchange with Max, Spetner says
NDT (Neo-Darwinian theory) is a theory that is supposed to account for the natural development of all life from a simple beginning. I dont know why we need such a theory, because the development of life from a simple beginning is not an observable. The theory is gratuitous; it comes to account for something that was never observed.Actually, evolutionary thinking goes like this.
One observes present life.
One then assumes that it arose in a natural way.
One then concocts a theory (e.g., the NDT) to account for the observation, given the assumption.I suppose that if the theory were really a good one, and could really explain well how life could have developed in a natural way, it would lend some credence to the assumption that life did indeed develop in a natural way. But it is not a good theory, and it does not account for what it is supposed to. Evolutionists, realizing this, have lately been reduced to arguing that if no one has a better theory that can account for the natural origin of life, then one must accept NDT. As you will see from some of Maxs comments below, he also adopts this approach. I dont know why NDT merits the pedestal on which evolutionists have put it.
Now lets get back to the probability of occurrence of one of those evolutionary steps of Maxs. Since they are chance events, we cannot say with any certainty that they will happen. The best we can do is to say with what probability such an event will occur. So, evolutionists have offered us a theory (NDT) that postulates a long string of random events to account for the existence of life, assuming it developed in a natural way. If the probability of those events were to turn out to be close to 1, then one could say that the theory accounts for the observation. On the other hand, if, according to the theory, the probability of those events were very low, one would have to say that the theory does not account for the observation. If a theory predicts observed events to be highly improbable, then one cannot justifiably say that the theory accounts for those events.
You would think that, since the issue of the probabilities of the evolutionary events is so crucial to the validity of the theory, the advocates of evolution would have calculated the necessary probabilities to make their case. But they havent. Since they have not made these calculations, Max is not entitled to assume that evolutionary steps can occur.
There is some difficulty in calculating these probabilities because the values of the relevant parameters are not all known. In my book, I addressed the problem of the probability of getting enough successful evolutionary steps to account for the evolution of the horse. In spite of the difficulties I just mentioned, I was able to calculate an important result. I found that either the probability of the horse evolving was impossibly low, or else convergent evolution cannot occur. This result refutes NDT, and with it Evolution A. Not only is Maxs point here not substantiated, it stands refuted."
Later, he says
In the final paragraph of my original critique, I said the following:The mutations needed for macroevolution have never been observed. No random mutations that could represent the mutations required by NDT that have been examined on the molecular level have added any information. The question I address is: Are the mutations that have been observed the kind the theory needs for support? The answer turns out to be NO! Many have lost information. To support NDT one would have to show many examples of random mutations that add information. Unless the aggregate results of the genetic experiments performed until now is a grossly biased sample, we can safely dismiss Neo-Darwinian theory as an explanation of how life developed from a single simple source.
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 the mechanism of NDT can result in Evolution A. Most evolutionists assume that long sequences of microevolutionary events can produce Evolution A, 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 have a hard time telling what it is.)
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. The concept of the adaptive landscape is useful here. This concept was first introduced by Sewall Wright[1], but now nucleotide sequences of the mean population genome have taken the place of Wrights gene combinations. There are a great many adaptive hills of various heights spread over the genomic landscape. NDT then says that it should be possible to continue to climb an adaptive hill to a large global maximum (or near-maximum), one base change at a time, without getting hung up on a small local maximum. No one has ever shown this to be possible.
Evolutionists often claim that if the evolutionary process were hung up on a small local adaptive maximum, a large genetic change like a recombination, or other genetic rearrangement, could bring it to another hill that has a higher peak, and place it higher up on that hill than it was before. 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 precisionnot 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 no one can think of any other way that beneficial mutations might occur in the absence of a law requiring them to occur. 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 for a population to escape from a local small adaptive maximum.
There is then a discussion about several mutations and whether they are information adding mutations or not. To me Spetner has a much better argument. Max argues at one point that the loss of antibiotic binding, causing bacteria to become streptomycin resistant, represents a GAIN of information. Spetner explained earlier in the piece what he means by information - in a nutshell, information = specificity.
Max: there are several other ways of considering how mutations affect information. In my view, even if all S12 mutations that caused streptomycin resistance abolished antibiotic binding, a reasonable argument could still be made that such mutations represent a gain of information rather than a loss. In the universe of all the possible S12 amino acid sequences that can function in the ribosome, essentially all S12 proteins found in wild-type bacteria (i.e., those grown in the absence of streptomycin) bind to this antibiotic. The S12 sequences that allow bacterial growth in the presence of streptomycin represent a small subset of the universe of observed functional S12 sequences. Therefore by growing bacteria in streptomycin we select for a specific and small subset of possible S12 sequences; thus it might be argued that we have forced a small increase the information content of the genome by narrowing the choice of S12 sequences.
Spetner: I cannot agree with what you wrote here. The wild-type S12 proteins that bind to the streptomycin molecule also form a subset of the universe of all possible S12 proteins. The set of S12 proteins that allow bacterial growth in streptomycin (i.e. that do not bind to the antibiotic) form a disparate subset of the universe of S12 proteins. My intuition tells me that the set that binds (the susceptible set) is smaller, and therefore has a smaller entropy, than the set that does not bind (the resistant set). Mutations that appear in the presence of the antibiotic convert one subset to the other. A mutation that transfers the enzyme from a low-entropy set to a higher-entropy set loses information; it does not gain it.
Max: Alternatively, it could just as well be argued that in all cases of single amino acid replacements there has been no change in information content at all, in that any given amino acid sequence is equally improbable compared with any other amino acid sequence of the same length.
Spetner: This is not a useful concept. It is like the pleading of the poker player who had a bust hand. When it came to the call, his opponent showed four aces. He pleaded that his bust hand was just as improbable, and therefore worth as much, as the four-aces, and suggested they split the pot. Hes right about the probabilities of the two hands, but in the context of poker, four aces win and the bust hand loses. Although in the context of the organisms survival in streptomycin, the degraded specificity of the S12 protein is beneficial, in the context of evolution, it is a dead end and it loses.
Finally the example Max cited of information adding mutations:
Maxs field of expertise is the immune system. This is the field in which he does research and in which he has published. In his original posting, his pièce de résistance was the presentation of somatic mutations in B lymphocytes (B cells) of the vertebrate immune system as examples of random mutations that add information. He implied that Evolution A 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. They are random, however, 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 Evolution A could be achieved through such mutations, and I shall show why.
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, which allegedly 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 highmore than a million times normal germ-line mutation rates. For this reason they are called hypermutations. If an organism had a germline 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 region encoding selected portions of the variable part of the antibody.
The mutation rate of the hypermutating part of the B cells genome is usually about 10-3 per base pair per replication[5], and it can be as high as 10-2 per base pair per replication[6]. These rates cannot produce Darwinian evolution. If a genome were to mutate at this rate, there would be, on the average, several mutations in every gene, with a high probability that many of them would be fatal for the organism. 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 (complementarity-determining regions) 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. 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 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: The theoretical argument hinges on the fact that the benefit that accrues to the immune system is a nonlinear function of the mutation rate. 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[7]. 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 one of the many lowest and not on one of the few highest in the landscape. It will then get stuck on a low local maximum of adaptivity and will not be able to move from it. That is particularly likely because the steps it takes are very smallonly 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[8]. 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, several adaptive mutations must occur independently and randomly at each step.
Hypermutation in the B cells does this. It quickly 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 informationeven over long times. I shall explain why. The effects of mutation rate are nonlinear. Consider a population of antigen-activated B cells of, say, a billion individuals, which is smaller than the typical number. In two weeks, there will be about 30 generations. Lets say the population size is 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 independent 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. If the mutation rate is 1 per 100, these numbers would be correspondingly larger.
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 were doing this experiment with a population of a billion bacteria. Then, in one generation, there will be an average of one change in any particular base in some one individual. 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. Ive 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. As far as I can tell from my reading of the literature, the mechanism of somatic hypermutation in B-cells is not currently known.
Spetner: On the contrary, my objection is well supported in the professional literature. The somatic hypermutations you cite do indeed require special enzymes, and is not the kind of mutations held to be responsible for the variation required in NDT. These mutations, unlike ordinary errors in DNA replication in the germline, are under precise control in the cell. They are turned on exactly when they are needed, and they are 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. They do not occur at any other place in the genome. 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 mechanismhypermutation does not happen by chance. Thus, even 14 years ago, a popular textbook in cell biology said[9], There must exist mechanisms that direct mutational activity to variable-region sequences. How this might occur is not known; possibly some sequence in the area of the variable region directs a special enzyme system to carry out point replacements of nucleotides independent of template specification. (my emphasis)
Informed current opinion on the subject of somatic hypermutations is overwhelmingly (and perhaps even unanimously) in favor of the suggestion that they are produced by a special mechanism requiring special enzymes that are unlike the spontaneous germline mutations assumed to be responsible for evolution. Experts in this field are very clear on this point. Let me just bring you a few quotes from a recent paper by Robert Blanden and his colleagues[10], in which they describe important characteristics of somatic mutations, and note how they differ from germline mutations [all emphases are mine (LMS)]:
The accumulated findings strongly suggest a complex mechanism [for hypermutation], which is unlikely to employ simple error-prone DNA repair processes involving DNA template directed DNA synthesis.
there should logically be a mechanism to ensure that when successful mutation has taken place, there is no further mutation which may destroy successful V(D)J sequences.
Let me also bring you a few quotes from another recent paper by David Winter & Patricia Gearhart (whom you may even know) on the subject of somatic hypermutations[11]:
The pattern of somatic mutations in rearranged variable (V) genes differs from the pattern of meiotic mutations, indicating that a different mechanism generates hypermutations than generates spontaneous mutation.
somatic hypermutations may be derived by different mutational processes than meiotic mutations.
The evidence suggests a model of hypermutation in which the DNA sequence of the immunoglobulin region directs the rearranged variable gene to a point on the nuclear matrix where both transcription and hypermutation occur.
B cells that are stimulated by antigen activate an error-prone hypermutation mechanism to introduce point substitutions throughout the V region.
it has been shown that areas containing transcription promoters and enhancers are required for [hyper]mutation
It thus seems quite clear 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. This is your field of expertise, Ed. Please let me know if you agree or disagree.
Max: 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.
Spetner: It should be clear from what I have written above that the hypermutation in B cells cannot serve as a prototype for the random mutations required by NDT to account for evolution. There is no known mechanism for mutation in germ cells that is comparable to the hypermutation in B cells. The example of hypermutation cannot be used to support your contention that random mutations in germ cells can build up information in the genome to explain Evolution A.
Max: 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? 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: Your comparison is fallacious. 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 (as explained above). It is not Science.
I have not asked for a mathematical-like proof for evolution. But for heavens sake, how about exercising some scientific discipline? Scenarios and just-so stories cannot substitute for proof. There is no proof of Evolution A that is of a standard that would be acceptable in any other scientific area. My conclusion: If this is the only example of confirmed information adding mutations, it would serve more as a refutation of evolution than a confirmation. As Spetner says: "To support NDT one would have to show many examples of random mutations that add information. Unless the aggregate results of the genetic experiments performed until now is a grossly biased sample, we can safely dismiss Neo-Darwinian theory as an explanation of how life developed from a single simple source."
Until you have a rebuttal that actually addresses the issue of naturalistic presuppositions, you may NOT claim that science by definition excludes the supernatural. This claim is, in fact, prejudiced, historically ignorant, philosophically unaware, and uses the word "science" like the curtain of the great OZ.
A point that some of us have been arguing for many years on these crevo thread is thus: "scientific" is not synonomous with atheistic premises, nor is it "unscientific" to have theistic premises. Both are mere starting points, though which starting point you adopt will have a tremendous influence on how you observe (percieve) things. Neither starting point has ANYTHING to do with methodology, though current scientific methodology seems to have arrisen from a bizzare and interesting mix of Greek philosophy and Christian theology. Yes, dear reader, the true roots of modern "science" are firmly implanted in Christian theological implications, with an assist by Aristotle. It wasn't until Darwin and Huxley that these theological implications were denied and deemed unecssary, only to be ultimately replaced by nothing. So now we have this strange, illogical premise in modern "science" that nothing created everything out of nothing for no purpose. Hence metaphysical naturalism.
Since either starting point has no bearing on methodology, then where is the difference? Well, it seems the difference lies on how one interprets the data. If one is starting from a naturalistic premise, the data is going to be interpreted somewhat differently from that of a person with a theistic premise, as chronic_loser along with various others have been taking great pains to make evident.
An example of how this works is morphology. An evolutionist will look at the amazing similiarities between all mamals, and conlcude that they all came from a common ancestor. A creationist will look at the amazing variations between all mamals, and conclude that is is evidence of a powerful and creative supreme being, who enjoys variations on a central theme.
Another example is paleontology. An evolutionst sees it as a record of transitional forms from the common beginnings in the great primordial soup. A creationist sees it as "snap-shots" of creations of a supreme being throughout time.
Again, the real issue is not methodology or data, but the interpretation of the data based on your worldview.
The movement since the mid 1800's to eliminate the supernatural from the definition of science is actually a systematic and intentional campaign by atheists to put God in the closet. This has nothing to do with science, but everything to do with humanistic, materialistic ideology.
For instance, if the "unaffiliated" (academia) cancer researchers in Illinois formed an association and pooled their nickles and dimes to hire the specific skills needed to handle the grants, they might have more time to "do" the science.
Say Alamo-Girl, have you read Michael Crichton's latest book State of Fear? He seems to be advocating a similar approach in the afterward/appendix of his book.
It's been a while since I've been near a computer, and this was the first post I had.
I must say this is an EXCELLENT post and bears repeating to all who will listen.
Good post Ronzo, thanks for your input!
Thank you for the kind words Mac! It's good to know there's at least one person reading my silly musings!
Thank you so much for the great post and the book recommendation!
Excellent post/essay, Ronzo! Thank you so very much!
So the next question would be: which worldview assumes that natural phenomena are regular and constant over time; which worldview assumes that causes can be discovered through research; which worldview assumes that an omniscient designer intentionally made parasites that eat the eyes of infants; which worldview assumes that disease is a natural phenomenon amenable to medicine; which worldview outlawed anesthesia for women in childbirth because God said they should suffer; and finally, which worldview has actually done honest research for five hundred years, and which worldview burned Bruno for speculating the stars were suns with planets?
You are correct. It's all a matter of worldview.
Are you suggesting that a scientific statement can be predicated upon the assumption of the existence of supernatural entities?
Yes.
Creationists have yet to demonstrate the existence of their proposed mechanism for the origin of the species.
Evolutionists are suffering from the same problem, as far as creationists are concerned.
Thank you so much for the great post and the book recommendation!
I HIGHLY recommend State of Fear. I encourage you to purchase it and read it as soon as possible! (Crichton really deserves your money, and you may want to look into some of his information and ideas further...)
It is an excellent demonstration of how limited interpretations, hand-picked evidence and ideology can drive science into poor conclusions.
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