Uncommon Descent Serving The Intelligent Design Community

Cost of maintenance and construction of design, neutral theory supports ID and/or creation

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Most of biological ID literature is focused on Irreducible Complexity and Specified Complexity (Specified Improbability) and information theory, no free lunch, critique of OOL, the Cambrian explosion, etc,

But there is another line of argument that is devastating to the claims of mindless evolution that has been underappreciated partly because it is highly technical, and in many cases most biologists will not even learn it in detail, namely that most molecular evolution is non-Darwinian.

Here is the simplest way to understand why evolution is mostly non-Darwinian. The ability to select for or against a trait involves the cost of sacrificing individual lives. When we spend money we have a limited budget to buy things. From our budget we can select to have maintenance done on our houses, cars, computers, our bodies (healthcare) or we can buy other thing to accumulate possessions.

What Darwin and most Darwinists do not realize is that selection for individual traits likewise comes at cost. To select to maintain one part of the genome means that there is no budget to maintain another part of the genome. To select to construct new features of the genome means one must abandon the maintenance budget of another part. This will be true even if the selection process is done by an intelligent agency like a human. The reason most computerized “proofs” of evolutionism like Dawkins Weasel and Avida are invalid is they do not model the problem of cost of maintaining and constructing mutli gigabit complex designs.

To understand things more clearly, here is a hypothetical illustration. If an asexually reproducing species could only have one offspring, selection must necessarily be neutral because there is no reproductive excess, there is zero “money” to carry out selection. If there are harmful mutations along the way, oh well, no “money” of excess reproduction to fix it. This would be an extreme case of Muller’s ratchet where the bad irreversibly just keeps accumulating.

Now if an asexually reproducing species could have two offspring, it now has a little more “money” in the form of reproductive excess to select to maintain one trait that goes bad. Let’s say one of the two offspring develops a bad mutation and the other doesn’t. We can expend him, or dare I say “spend” him to fix the genome. But our selection budget would be blown if each of the kids develop 1 bad mutation each, and it would really be blown if they develop 100 bad mutations each! And at this point we are not even considering the budget needed to build new functional traits.

When we actually do careful accounting of the costs of natural selection envisioned by Darwin and Dawkins versus the available money of reproductive excess, we realize that if evolution happens, it must be mostly free of selection as a matter of principle, and thus mostly neutral. There is simply not enough “money” in the form of reproductive excess to maintain and construct complex designs composed of billions of nucleotide and epigenetic “traits”. There is some selection obviously, because there is some “money” to do a little bit, but not enough.

The accounting of the cost of selection can be done in a number of ways. One way to demonstrate this is through the equations of population genetics, and the other way is a computer simulation that does the accounting. One of the best, if not the best computer accounting simulations is Mendel’s Accountant written by the dream team of creationist population genetics. The irony then is population geneticists, PZ Myers, Larry Moran, the YECs have had a rare moment of agreement where they have all signed the claim, “most molecular evolution is non-Darwinian.”

But if most evolution is non-Darwinian, maintenance much less construction of design cannot be explained by Darwinism, then the case for ID is strengthened.

Now if most evolution had been non-Darwinian, one would rightly argue it would have been a random walk, and thus not much better than a tornado going trough a junkyard. Creationist have seized on this and said, “well we’re not a junkyard, therefore some non-random process must have created designs in nature, hence we are designed”. In contrast, Larry Moran and friends have said “evolution is a random walk and we are obviously junkyards and you’re an IDiot if you think biological organisms are mostly functional.”

[cross posted at CEU IDCS Cost of maintenance and construction of design, neutral theory supports ID and/or creation]

Comments
Thanks, jerry, that is a valiant stab at it. If adaptation includes things that are "maintained and evolved by means of natural selection", is then the proposal that exaptation did not involve natural selection or is not maintained by natural selection? The only way I can see that being true is if (i) they are admitting exaptation was pure dumb luck, a shot in the dark, or (ii) they are confused because they don't understand natural selection well enough to describe it properly (the more likely scenario, in my view). One foundational problem with the description they offer is that if we look at an adaptive feature, such as echolocation (according to the Berkeley website), they are saying that it "evolved" by natural selection and that its function has always been echolocation. So if the parts of the echolocation mechanism didn't serve some other function (as assumed), then they cannot have been built up slowly by natural selection. They must have come about by chance. All at once. Or by neutral theory, with no function at all, until one glorious day, Poof!, function burst onto the scene. In either case we are right back to Behe's irreducible complexity argument. Part of the alleged power of co-option is that it gives the evolutionary story a back door through which it can claim an irreducibly complex structure came about, without relying on the Poof! theory. But if we are to eschew the Poof! theory, such co-opted parts must have evolved and been preserved by natural selection and the newly irreducibly complex structure must also be preserved by natural selection. At any rate, I would be very interested to know how anyone thinks exaptation works, if not, after all, through the magic of natural selection. And how do we properly distinguish a feature with "current" function (which is, of course, all we can actually observe) from one with a co-opted part that had prior function? The main time someone tried to do this -- with the bacterial flagellum -- they got egg on their face when it was shown that, if anything, the flagellum would have preceded the Type III secretory system. In any case, most co-option claims are simply another just-so story, supported by little more than a few comparative analyses and a healthy dose of imagination. It seems the only reasonable alternative is to treat exaptation as a sub-category of adaptation. Alternatively, I'd very much like to know, if not natural selection, what power or process causes a biological feature to take on another role and remain in that new role in an organism?Eric Anderson
April 24, 2014
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Can someone explain to me the important distinction between “exaptation” and “adaptation”?
I don't know if I can but it may be worth while knowing what certain naturalists think. Here are Wikipedia's definitions:
An adaptation, also called an adaptive trait, in biology is a trait with a current functional role in the life history of an organism that is maintained and evolved by means of natural selection.
I believe this means a pre-existing coding sequence has multiple alleles and will be subject to some mutations and the specific sequences that will survive will depend upon natural selection. The sequences or characteristics that survive will depend upon the particular environment the population is in.
Exaptation (a replacement for the teleologically-loaded term "pre-adaptation") and the related term co-option describe a shift in the function of a trait during evolution. For example, a trait can evolve because it served one particular function, but subsequently it may come to serve another.
I believe this term applies to something that already exists and now has a different function. I believe one of the most famous recent examples is that part of flagellum is made up of parts that have other functions in different species. So a particular part was exapted to have a new use. If I am reading some of the Gould stuff correctly, it can also refer to a sequence that has no function but with a certain mutation can be functional. So mutation of non functional DNA can turn into functional DNA. This may be an example of exaptation too. Anyone else want to give it a shot.jerry
April 24, 2014
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So much for “free peer review”. Larry Moran is complaining about this blog post but doesn’t offer a counter-argument. Nor has anyone yet done so in the comments
Larry may not be happy with the way I characterized his position, but he doesn't seem to have much to criticize about my cost-of-selection argument. That's what I was more interested in anyway.scordova
April 23, 2014
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Bornagain said "Acartia_bogart @2, perhaps you would like to tell us how Natural Selection, a process selecting 3-Dimensional phenotypes, produces 4-Dimensional systems?:" I must admit that I read your comment several times and still do not understand what you are trying to say. Which means that you must be s genius or an idiot. I won't tell you which category I think you fall in.Acartia_bogart
April 23, 2014
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Can someone explain to me the important distinction between "exaptation" and "adaptation"? The explanation at the Berkeley website leaves a lot to be desired. http://evolution.berkeley.edu/evosite/evo101/IIIE5cExaptations.shtml They seem to focus on whether natural selection produced something for current function. (Certainly an unknowable, but let's set aside that gaping problem for a moment). In contrast, exaptation (we are informed) is a result of things like "co-option", and they use the term "co-option" as though it were a real process on its own separate from natural selection. What is co-option, if not another form of adaptation? How can co-option occur apart from natural selection? Does the feature just "poof" into its new role? Is not the feature maintained in that role after all by natural selection? If so, how does that role differ from natural selection's role in any other situation? Sadly, I note that they also talk of natural selection "producing" new features, which of course it doesn't. The whole "explanation" should drive any sane person to, if not downright reject the story, then at least toward some nagging doubts.Eric Anderson
April 23, 2014
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jerry: Unfortunately, I cannot get the article. The abstract, indeed, is not very informative, although I must say that the simple term "exaptation" is usually enough to make me mad. So, for the moment I will atick with Axe and Durston. :)gpuccio
April 23, 2014
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I provided this reference before on how a segment of the evolutionary biologist think: It is an article by jurgen Brosius http://www.bioone.org/doi/abs/10.1666/0094-8373%282005%29031%5B0001%3ADAEBAC%5D2.0.CO%3B2 If you can get the Brosius article, read it. He certainly has a non Darwinian approach that is naturalistic.. It is in a journal titled, Paleobiology (Paleobiology 31(sp5):1-16. 2005 ). He was recommended by Allen MacNeill and it is about change in the non-functional DNA due to mutation. His ideas are testable and are opposed to Axe and Durston.jerry
April 23, 2014
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Really? Where are the testable hypotheses for blind and undirected processes producing genomes?
I gave you the examples. People here tend to look at one side of the naturalist agenda and assume no other. They look at Darwinian gradualism and assume that is it. But there are others who publish and Allen MacNeill obviously has access to this type of thinking no matter what you personally think of him. Cornell is not some backwater university and he teaches evolutionary biology there and has a published course on evolution at the Modern Scholar. So he is knowledgeable. Those who defend the punctuated equilibrium scenario point to another origin of alleles. It is the slow mutation of non-coding, non functional regions of the genome. Various parts of this very large area is mutating away in all the individuals of a population and over time they claim that a new allele will arise. So essentially they are challenging Axe and Durston. And this is testable. If such a process is happening then it will arise throughout the species not just in one small sub-population. When a separated population develops the new allele, there will be parts of this coding sequence in other parts of the parent population. However, these sequences will not be functional. So for every unique coding sequence there will be evidence of it not succeeding in similar species. These make testable hypothesis.jerry
April 23, 2014
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I lost my internet connection. Have to use the 3G connection on my iPhone to read this. Gpuccio, I read your reply to Allen though on an iPhone it is difficult. Generally agree with all of it except I believe you are reading Allen a little wrong. This is a complicated issue. My connection just returned.jerry
April 23, 2014
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jerry: In this thread: https://uncommondescent.com/news/1177-human-orphan-genes-removed-by-evolutionists-from-databases/#comments Allen MacNeill posted at #100 what you quote at #28 here. I answered with some detail in post #111. He has not answered. You can give a look at my post, if you like. I remain of the same opinion.gpuccio
April 23, 2014
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It does? In what way?
You said "No, the whole debate is about what is the cause of design in nature/ biology" I am not sure what this means because it is too vague or broad. But it sounds like those who object to ID because no one can point to a specific designer and what methods they used. They will say it is nature because there never was a designer. Richard Dawkins would except ID if there was someone who he could point to as long as it was not God. The debate has always been about the origin of new alleles. Meyer makes that point in his book but he use the term "information" which essentially means the same thing. Meyer goes on to point out that it is much more than alleles by talking about body plans but until now the debate was over new coding regions or alleles leading to proteins. This is what Axe and Durston's work is all about, the impossibility of new alleles arising naturally. The debate is now expanding to the origin of regulatory system as well as coding regions or body plan information. Again the origin of new functional information.jerry
April 23, 2014
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Mr. Coder wrote: So much for “free peer review”.
Well, let's see what the reviewers have to say about this question: https://uncommondescent.com/genetics/if-most-molecular-evolution-is-non-darwinian-how-can-codon-bias-and-duon-codes-evolve/scordova
April 23, 2014
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Jerry, Allen's is not in any peer-review journal. As a matter of fact there isn't any theory of evolution in a peer-review journalJoe
April 23, 2014
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Really? Where are the testable hypotheses for blind and undirected processes producing genomes?
They will be in the genomes of supposedly related species.
That doesn't even make any sense.Joe
April 23, 2014
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No, the whole debate is about what is the cause of design in nature/ biology
This sounds like those who object to ID because we cannot identify the designer and how the designer did it.
It does? In what way?Joe
April 23, 2014
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Cost of Maintenance: associated with Nachman's Paradox and Poisson distributions as discussed in Fixation rate, what about breaking rate Cost of Construction: associated with Haldane's Dilemma Larry and PZ's solution, "molecular evolution is mostly free of selection, therefore no cost, evolution comes free of charge, what a deal!"scordova
April 23, 2014
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No, the whole debate is about what is the cause of design in nature/ biology
This sounds like those who object to ID because we cannot identify the designer and how the designer did it. Before one can get to design, the EF requires one to eliminate natural origins of the entities. I just provided a way to do that which eliminates nearly every way the naturalist proposes. When these processes are eliminated, I am sure they will have new ones.jerry
April 23, 2014
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When Allen comes up with his theory I will listen. Until then NS is a proposed designer mimic.
I guess you didn't read the comments I referenced by Allen. Here they are in entirety. from 5 years ago
“Natural selection, though, adds no information. It only EVER reduces it. If you are trying to invoke mutations, then all known ones are (again) a loss of information.”
This quote demonstrates a basic misunderstanding of the process of natural selection. According to Darwin (and virtually all evolutionary biologists), natural selection has three prerequisites: 1) Variety (generated by the “engines of variation” 2) Heredity (mediated by the transfer of genetic material, either vertically – from parents to offspring – or horizontally – via viral transduction, retrotranscription, etc.) 3) Fecundity (reproduction, usually at a rate that exceeds replacement). Given these three prerequisites, the following outcome obtains: 4) Demography: some individuals survive and reproduce more often than others. Ergo, the heritable variations of such individuals become more common over time in populations of those organisms. Natural selection is synonymous with #4; it is an outcome of the three processes listed first, not a “mechanism” in and of itself. Ergo, the real dispute here is not over natural selection per se, but rather the properties and capabilities of the “engines of variation”. I have written extensively about these here: http://evolutionlist.blogspot......ution.html and here: http://evolutionlist.blogspot......awman.html Yes, natural selection (i.e. #4, above) is conservative not creative. It produces no new genetic nor phenotypic information, which is why Darwin eventually came to prefer the term “natural preservation” rather than “natural selection”. However, it is also abundantly clear that the “engines of variation” – that is, the processes the produce phenotypic variation among the members of populations of living organisms – are both extraordinarily creative and extraordinarily fecund. The real problem in biology is not producing new variation, but rather limiting the production of new variation to the point that the “engines of variation” do not cause the rapid disintegration of living systems. As just one example of this problem, the genetic elements known as transposons generate a huge amount of new genetic variation, much of which is either phenotypically neutral or deleterious to the organism. There are biochemical mechanisms by which cells can monitor the incidence of transposition in themselves, and limit its consequences (up to and including the active self-destruction of the cell via apoptosis). At the same time, there is very good evidence in the genomes of many organisms that retrotransposition events mediated by transposons have produced genetic changes that have resulted in increased survival and reproduction of the organisms in which such events have taken place. There is a large and growing literature on this phenomenon, all of which points to the inference that retrotransposition via transposons both creates new genetic and phenotypic variation, and that in some cases such variation can provide the raw material for evolutionary adaptations, which are preserved via natural selection. So, if you really want to find out where the “intelligent designer” might create new variations, you should follow the lead of Darwin’s good friend, Asa Gray, and look for the telltale evidence for such intervention in the “engines of variation”. Of course, you will have to show pretty conclusively, using empirical investigations and statistical analysis, that such “creation events” are not the result of purely natural, unguided processes. If you can do this, you will undoubtedly win a Nobel Prize and a Crafoord Prize (plus a MacArthur or two). Notice that this will involve looking carefully into the mechanisms by which new variations are produced, rather than pointing to the outcomes of such processes (i.e. natural selection) and simply asserting that “you can’t get here from there”. Simply asserting (without empirical evidence) that something can’t happen isn’t “doing science” at all. In fact, it’s doing just the opposite…
From last week
Long repetitive sequences (LINEs and SINEs) clearly do not have a coding function, as they lack promoter sequences (which are absolutely necessary for a sequence to be transcribed and subsequently translated). However, they may have other biological functions. For example, the coding sequences in eukaryotic DNA are not entirely randomly located. Rather, they are located in parts of the genome that allow them to be associated with the histone proteins in nucleosomes. This is because modification of DNA binding to histones is an important mechanism of gene regulation in eukaryotes. Therefore, the “spacer” non-coding DNA such as LINEs and SINEs could still influence the expression of genes located at significant distances away by modifying their binding to histones in nucleosomes. As for the “engines of variation,” I would like to emphasize that the kind of variation I have written about is both genetic and phenotypic variation. Indeed, the majority of the mechanisms I listed in my “engines of variation” posts at The Evolution List are mechanisms that primarily affect gene expression, rather than gene sequence. Regulation of gene expression in eukaryotes is both complex and massive (I know, I’m teaching a course in it right now). Simply knowing the number of coding sequences in the genome of a multicellular eukaryote (especially an animal), for example by knowing the number and location of promoter sequences, tells you almost nothing about how the coding sequences (i.e. “genes”) are expressed and regulated. There are hierarchical biochemical systems involving anti-sense RNAs, small polypeptides, proteins, and non-coding sequences in DNA that all interact to produce the components of the phenotype. Increasingly fine-grained analyses of these systems has revealed that many of them are “kludges;” that is, they work, but not well and not always consistently. This “kludginess” of gene expression/regulation in eukaryotic cells is an apparently inescapable concomitant of both the complexity of the systems involved and the history of their implementation Think about how kludgy a huge OS like Windows has become; it’s essentially a small core of original integrated code, massively modified by an almost uncountable patchwork of “bug fixes” and “extensions.” The surprising thing about such systems is not that they don’t work well (they don’t), but rather that they work at all. It is becoming clear that the “software” of a typical eukaryotic cell is really mostly “kludgeware.” It generally works “just good enough” to not self-destruct. And, as it is replicated and modified (and especially as “foreign” sequences are introduced into it or removed from it by retrotranspositions, transposons, retroviral insertions, polymerase “skip-copying” and other “noise” events), it stumbles along in much the way that “Mendel’s Accountant” and the nearly-neutral theories predict that it should. This is one of the main reason that germ cells are set aside very early in embryonic development in eukaryotes. The less often the genome is replicated, the fewer mistakes it accumulates. This is part of what is wrong with “Mendel’s Accountant:” it doesn’t take into account the particular kinds of cells that actually constitute the ongoing phylogenetic lines it purports to describe. THe MA model assumes that all cells change randomly at approximately constant rates, yet germ cells don’t change at anything like the same rates as most cells, primarily because they don’t undergo mitotic divisions at anything like the rates of most other cells. And may I say that gpuccio is entirely correct about the idea that homologies (combined with shared derived sequences) are indeed very strong evidence for common descent. This is especially the case for non-coding sequences that have little or no effect on phenotypes. There are a multitude of examples of homologous sequences that either have no effect on phenotypes or have surprisingly different effects in different organisms as a result of modified gene expression in diverging phylogenetic lines. The assertion that the origin of such homologies is the result of the intervention of an intelligent designer, however, is not empirically verifiable or falsifiable, and so I won’t address it. As for how functional orphans can arise from non-coding sequences, one first has to specify what kind of non-coding sequences one is referring to. If one means LINEs and SINEs, then I agree completely. Transforming a very long sequences of repeated tandem repeats into a coding sequence, complete with a promoter, terminator, and enhancing sequences would indeed be miraculous. However, a significant fraction of the non-coding sequences in eukaryotes consist of sequences that were once viable coding sequences. These either were corrupted and thereby inactivated by mis-replication of their promoters/enhancers or (more commonly) were inserted into the genome as the result of retrotransposition, reverse transcription, transposon insertion, and similar processes, in which coding sequences with functional promoters, terminators, and enhancers are inserted or removed from the genome. In a great many cases, such sequences are quickly identified and inactivated by “surveillance/editing” mechanisms, which identify and inactivate the “rogue” sequences by inactivating their promoters and/or enhancers. However, this means that “dead” former coding sequences are scattered throughout the genome and can be reactivated by inserting new, active promoters/enhancers that can reactivate part or all of the “dead” sequences. This has actually been accomplished in the laboratory, where a “dead” retroviral sequence estimated at being inactive for millions of generations was “resurrected” by providing it with an active promoter sequence. The “fossil” sequence then acted like a functional virus, infecting host cells and generally acting like “its old (now extinct) self.” So, can reactivation of non-coding sequences produce new, functional gene sequences? Yes, if the non-coding sequences were once active coding sequences that had been inactivated by modification of their promoters/enhancers.
jerry
April 23, 2014
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Really? Where are the testable hypotheses for blind and undirected processes producing genomes?
They will be in the genomes of supposedly related species. Any new coding region must have remnants in related species that never reached the point where they could code. They are either there or not there. As genomes of various species get published it will be easy to verify this one way or the other. If there is nothing this will indicate that the coding region appeared out of nowhere. If it appeared naturally there will be corresponding non-coding regions in other species that do not code for anything. As I said with current technology and the way it is headed getting these genomes will be fast and inexpensive. They now code a significant section of the human genome for about $10-$15. That is what it cost 23andme and Ancestry dot com to process samples sent in to them. The amount should increase with time and the cost should go down.jerry
April 23, 2014
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In my first post above (#1), the link to Dr. Moran's blog should have been here. I didn't realize it at first, but actually dates to before the ENCODE phase 2 announcement.JoeCoder
April 23, 2014
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BA77, These sorts of comments are welcome in the discussion.
“Although living things occupy a three-dimensional space, their internal physiology and anatomy operate as if they were four-dimensional. Quarter-power scaling laws are perhaps as universal and as uniquely biological as the biochemical pathways of metabolism, the structure and function of the genetic code and the process of natural selection.,,, The conclusion here is inescapable, that the driving force for these invariant scaling laws cannot have been natural selection.” Jerry Fodor and Massimo Piatelli-Palmarini, What Darwin Got Wrong (London: Profile Books, 2010), p. 78-79
Thank you for that.scordova
April 23, 2014
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There are very testable hypothesis on this.
Really? Where are the testable hypotheses for blind and undirected processes producing genomes? Are they locked up somewhere? They are definitely hidden from public view.
I don’t think naturalist like Allen MacNeill say it is a designer.
When Allen comes up with his theory I will listen. Until then NS is a proposed designer mimic.
The whole debate is over the origin of new alleles, not how they survive or get fixed.
No, the whole debate is about what is the cause of design in nature/ biologyJoe
April 23, 2014
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Even first year biology students know that natural selection is not dependent on the sacrifice of individual lives. It only requires an increased rate of reproduction as compared to those that lack the trait b
LOL! So individuals that lack a trait that reproduce at a lower rate in a limited population aren't essentially sacrificed according to you. The ones with excess reproductive rates essentially scarifice those with less. That was clearly the sense I was using it. You either fail basic math or you show yourself misrpresenting what I said. I said:
reproductive excess
So is most molecular evolution non-Darwinian or not?scordova
April 23, 2014
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"accusing someone of lying gets you no where" It is not an accusation but a documented fact! Sorry Sal, but I DO NOT LIKE BEING LIED TO! Especially in matters relating to scientific evidence. I will bother your post no more.bornagain77
April 23, 2014
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the fact that Sal couldn’t even bother to mention the possibility that most of the genome is junk,
Correction Nick, I pointed out the position of some of you guys:
“evolution is a random walk and we are obviously junkyards and you’re an IDiot if you think biological organisms are mostly functional.”
scordova
April 23, 2014
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You may consider such dishonesty a trivial matter, but I do not.
I do not consider it a trivial matter when someone lies. I have children who have done it many times with me and I have found it best to be polite about it when they are caught. It gets you much further. But on this topic under discussion we have no evidence yet of such and accusing someone of lying gets you no where. I would like Nick to answer some basic questions which he should be able to. I hope he does.jerry
April 23, 2014
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jerry, you never answered why I should take Nick’s claims for anything seriously since he has shown a willingness to lie in the past to protect a philosophical bias (which happens to be atheistic/materialistic). You may consider such dishonesty a trivial matter, but I do not.
Nick's personal beliefs as well as anyone else's aren't on topic unless they volunteer it in this discussion or it has relevance to the cost issue or function issue. Please drop it in this discussion. You can take issue with his scientific claims about junk. Sorry, Nick. Thanks for visiting.scordova
April 23, 2014
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Here are a couple posts by Allen MacNeill on the topic of NS and variation: https://uncommondescent.com/news/1177-human-orphan-genes-removed-by-evolutionists-from-databases/#comment-496789 https://uncommondescent.com/intelligent-design/microbe-evolution-virtually-finished-25by-ago/#comment-306698 Now MacNeill may vary from people like Nick Matzke but both are naturalist and we will have to see which of these view points NS lets survive. Maybe NS will eliminate both of them.jerry
April 23, 2014
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jerry, you never answered why I should take Nick's claims for anything seriously since he has shown a willingness to lie in the past to protect a philosophical bias (which happens to be atheistic/materialistic). You may consider such dishonesty a trivial matter, but I do not.bornagain77
April 23, 2014
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Natural selection has proven to be impotent as a designer mimic.
I don't think naturalist like Allen MacNeill say it is a designer. It is more like the explanatory filter which allows certain arguments to get through while rejecting other arguments. NS allows certain new variation to get through while rejecting others. It is not the source of variation. There is a similar problem with drift in the evolution debate in that it fixes already accepted variation and nothing else. The EF is not the source of arguments but the blessing of successful arguments. Neither the EF or NS create anything. So evolution is an after effect of the NS process which allowed some variation to survive while rejecting others. The whole debate is over the origin of new alleles, not how they survive or get fixed. We can now extend the allele argument to non-coding functional regions. How did they arrive?jerry
April 23, 2014
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