Real Science Might Be Alive and Well

Sometimes I worry about the state of science today. The majority of students are woefully ignorant about even the most basic scientific concepts. More worrisome, however, ideology drives much of science. Evolution (in the ‘goo to you’ sense) is taught as fact, even though it is, at best, an unconfirmed hypothesis. In an attempt to promulgate this myth, many scientific journals refuse to publish anything that challenges the dogma of evolution.

And if any journal dares to publish a heretical paper, heads must role. For example, when Stephen Meyer sent a paper entitled “The Origin of Biological Information and the Higher Taxonomic Categories” to the small journal called Proceedings of the Biological Society of Washington, the editor (Dr. Richard Sternberg), sent it out for peer review. It passed peer review, and it was published. Then, a firestorm occurred. As the Washington Post says

Within hours of publication, senior scientists at the Smithsonian Institution — which has helped fund and run the journal — lashed out at Sternberg as a shoddy scientist and a closet Bible thumper.

Why did the firestorm occur? Because the paper discussed intelligent design in a positive manner. It doesn’t matter that the paper passed peer review. It doesn’t matter that the reviewers who didn’t even agree with intelligent designed called it meritorious and worthy of publication. The fact that it dared to question the dogma of the day was enough. Sternberg faced retaliation, defamation, and harassment because he allowed heresy to creep into the biological literature.

This is very worrisome, because science is built on debate and disagreement. Without an open debate on what the data mean, scientific progress is slowed. This debate, of course, needs to take place in the scientific literature, so that scientists can keep abreast of not only the data, but the leading interpretations of those data. In most fields, this happens regularly. In the field of biology, however, debate is usually squashed so that the reigning dogma of the day is not challenged.

However, there is hope. There are some peer-reviewed journals that publish scientific heresy. The CRS Quarterly is one such example. The online journal Answers Research Journal is another. However, this is not the ideal situation. Unfortunately, there is little genuine debate in the scientific literature related to biology, since the journals that are approved by the high priests of science expouse only the accepted scientific dogma, and the alternate journals expouse only scientific heresy. The ideal journal would present all views that are backed by the data.

Well, it may be that the ideal biology journal has finally come along. This new online peer-reviewed journal is called BIO-Complexity, and according to its stated purpose and scope:

BIO-Complexity is a peer-reviewed scientific journal with a unique goal. It aims to be the leading forum for testing the scientific merit of the claim that intelligent design (ID) is a credible explanation for life…To achieve its aim, BIO-Complexity is founded on the principle of critical exchange that makes science work. Specifically, the journal enlists editors and reviewers with scientific expertise in relevant fields who hold a wide range of views on the merit of ID, but who agree on the importance of science for resolving controversies of this kind.

If the journal lives up to this goal (and that’s a big IF), it will be at the forefront of biology. So far, the two initial papers are pretty much pro-ID. One is a report on original research following several populations of bacteria that had a doubly-mutated gene for the production of tryptophan, one of the 20 amino acids found in living organisms. They were hoping to see one of the populations evolve in a way that would “fix” the two mutations. They called this a “constructive” approach that would use “recruitment” of a nonfunctional gene to produce a functional gene that would be able to produce tryptophan. However, that never happened. Instead, the bacteria continued to acquire mutations that reduced the expression of the mutated gene, thereby increasing their metabolic efficiency. The authors called this a “reductive” approach to the problem. As they note:

If reductive, cost-cutting mutations are more abundant than mutations that convert or improve function, recruitment may be unlikely even in cases where a short adaptive path to a new function exists.

The results are clearly not what one would hope if one were promoting evolution, and I recognize one of the authors, Ralph Seelke. He was mentioned in the documentary Expelled because an evolutionary biologist at Stanford invited him to spend his sabbatical time doing some collaborative research, until the biologist found out he was pro-ID. The biologist then rescinded his invitation. Nevertheless, Seelke was able to spend his sabbatical at Stanford, working for a microbiologist who was more interested in science than in dogma.

The other article is a review article by a strong ID proponent, Douglas D. Axe. It discusses the difficulties protein folding presents to any evolutionary scenario.

So I would put both of these articles in the “pro-ID” camp. Hopefully, some “anti-ID” articles will be published so that some real science can happen. I guess we will just have to wait and see.

32 Comments

  1. Grant C says:

    Oh good grief.

    Dr. Wile, you may very well be extremely competent in your chosen field… but reading your opening paragraph where in only a few short sentences you move from bemoaning ignorance of science to demonstrating a sterling example of it I find myself coming to the conclusion that either that you have never applied that general scientific expertise in any way to a study of evolution, or you are deliberately misrepresenting the facts for religious purposes.

    I am referring specifically to this bit of nonsense:

    “Evolution (in the ‘goo to you’ sense) is taught as fact, even though it is, at best, an unconfirmed hypothesis.”

    Is that so? So, the nested hierarchical endogenous retroviral insertion pattern in the primate genome is what… a coincidence?

    The fact that evolutionary theory predicted in advance the existence and location of the GULO pseudogene in humans based on its placement in mammals capable of ascorbic acid synthesis was… pure luck?

    The fact that human chromosome 2 is a crystal clear fusion of chimp chromosomes 2p and 2q is… irrelevent?

    The entirety of all life on earth falling into a nested hierarchical structure of genetic traits, which is turn overlays the nested hierarchical structure of the fossil record both morphologically and geographically while the fossil record itself is littered with clear transitional evolutionary sequences is… all in our imagination perhaps?

    That phylogenetic analysis is capable of reconstructing ancestral relationships to astounding degrees of accuracy and constantly confirms the evolutionary relationships of all living things… is just some kind of magic trick with numbers? Mathematical sleight of hand?

    All of this is just a silly “unconfirmed hypothesis” that just happens to fully account for the entirety of available observational data in biology, has had it’s every tested prediction confirmed, and has survived every attempt at falsification for over 150 years? A “myth” is doing all that?

    Neat trick.

    Tell me… how exactly would you claim we go about confirming this hypothesis, since apparently the MASSIVE amount of testing already completed simply doesn’t count?

    1. jlwile says:

      Grant, I am afraid that you are the one demonstrating scientific ignorance, since you seem to be trapped in the long-debunked notion that ERVs are nonfunctional. Of course they are not. Back in 2006, Thornburg and his colleagues showed that transposable elements like ERVs influence development in mice (Thornburg, B.G., Gotea V., and Makałowski W., “Transposable elements as a significant
      source of transcription regulating signals,” Gene 365:104–110, 2006). In 2008, Conley and his colleagues showed that they can act as promoter sequences in humans (Conley, A.B., Piriyapongsa, J. and Jordan, I.K., “Retroviral promoters in the human genome,” Bioinformatics 24:1563–1567, 2008). So the ERVs are not the result of coincidence. They are functional part of the genome that come from design.

      The prediction of the GULO pseudogene position in humans was not pure luck. It was based on the fact that this once-functional gene would be similar in species that have similar biochemistry. That’s not evolutionary reasoning. It simple reasoning by analogy. Since you mention the GULO pseudogene, however, I might point out that it is one of the many failed predictions of the evolutionary hypothesis. After all, evolution would predict that there would be very few “shared mistakes” in the guinea pig GULO pseudogene and the human GULO pseudogene, since they are not closely related. However, Inai and colleagues found remarkable similarity (Inai, Y., Ohta, Y. and Nishikimi, M., “The whole structure of the human non-functional L-gulono-γ-lactone oxidase gene—the gene responsible for scurvy—and the evolution of repetitive sequences thereon,” J. Nutritional Science and Vitaminology 49:315–319, 2003). This, of course, points to a mutational hotspot explanation for the “shared mistakes,” not a common ancestry explanation.

      Human chromosome 2 is definitely not a “crystal clear fusion of chimp chromosomes 2p and 2q.” It does look like two chromosomes that are fused, but it doesn’t imply common ancestry with apes. Chromosome fusion events happen today in humans. All chromosome 2 tells us is that our human ancestors probably had 48 chromosomes, but then a genetic bottleneck (like a worldwide Flood) occurred, and the genome that survived came from humans who had two fused chromosomes.

      The fact is that life on earth does NOT fall into a nested hierarchical structure that overlays the fossil record. Indeed, evolutionists can’t even AGREE on this supposed nested hierarchical structure, as the structure one gets from morphology doesn’t agree with the structure one gets from molecular evidence. And, of course, there are no transitional sequences in the fossil record. Indeed, the fossil record is the biggest falsifier of evolution, as it is so lacking in transitional forms that evolutionists must come up with crazy ideas like punctuated equilibrium and evo devo to “explain away” the myriad of transitional forms that evolution predicts should exist.

      Phylogenetic analysis is not capable of reconstructing ancestral relationships. There are constant battles in the literature in which proponents of one phylogenetic analysis try to convince the reader that theirs is better than another one that says something completely different.

      The reason evolution is, indeed, an unconfirmed hypothesis is specifically because the data do not support it. It has been falsified by the data time and time again.

      Since you ask me how to go about confirming the evolutionary hypothesis, I will tell you. Demonstrate that it happened by simply showing me the fossils that trace exactly how one basic type of organism (like a fish) evolved into another (like an amphibian). Show each fossil in the line of descent. You only have to do that for one transition between two basic types of organisms, and I would be totally convinced. The other thing you could do is simply provide a mechanism that can show, step-by-step, how such a transition would occur. Demonstrate that each hypothetical step is consistent with our current understanding of biology, chemistry, and physics, and while that would be confirming evidence, it would at least move evolution out of the realm of religion and into the realm of science.

  2. Ben Michael Fournier says:

    Dr. Wile, slight errata in the first sentence of the second paragraph, unless you’re referring to some people taking upon themselves the role of a scapegoat, I think you would otherwise be making an allusion to heads rolling as from the action of a guillotine. Also the fourth sentence of the third paragraph has -ed suffixed to design. But enough with me being a grammar Nazi.

    It would be good to see a more balanced journal. I think moderators would be a necessity though, as usually militant atheists and other people with vested interest tend to quickly turn forums into flame wars. You know, they are usually trollish enough as it is, being like a flamethrower already, but after anything against evolution is mentioned then it is like spraying liquid oxygen on the situation. …

    You mentioned that it is primarily in biology where there isn’t a lot of criticism permitted, so would it be correct to assume that in areas of chemistry and physics scientists tend to be somewhat more open-minded and willing to accept criticism?

    1. jlwile says:

      Ben, thanks for the grammar comments. While I will probably not change the current post, I will try to be more careful in future ones.

      Interestingly enough, the chemistry and physics journals do tend to be more balanced, unless the subject of origins comes up. At that point, they genuflect at the altar of evolution.

  3. Josiah says:

    What would happen for example if somebody published a piece of evidence in physics or chemistry that effectively rendered an atheistic origin of life through evolution impossible? Would it be gunned down in the same way, and if so, by which field?

    1. jlwile says:

      Josiah, I am not good at “what ifs?” I would think a lot of it would rest on the nature of the evidence. Dr. Anthony Flew was convinced by the evidence at hand that the origin of life without God was impossible. Some people will cling to their atheistic faith so strongly that no amount of evidence would change their mind.

  4. Ben Michael Fournier says:

    Josiah, biology professors would probably do most of the squawking.

  5. This is a shocker: “So far, the two initial papers are pretty much pro-ID.”

    What did you expect with the lesser-known ID proponents on its editorial board? Or the fact that the Biologic Institute provides “institutional support”? So it’s an offshoot of the Discovery Institute. Really shocking, no? I wonder if they’ve learned their lesson from the Wedge document?

    If you want to surprise me, let me know when they publish a non-creationist (just to be clear, ID is a subset of creationism – see Dover case).

  6. Actually, I’d be surprised if they publish someone not on the Editorial Board.

  7. Okay, I am riled up now! Fun stuff, poking around on the internet. Going through the professors on the Editorial Board. Walter Bradley is mentioned on an old Panda’s Thumb post:

    “One questioner pointed out that evolution isn’t about the origin of life, but rather about what happened after the first life began. Bradley answered this question quite fairly, making the legitimate distinction between biological evolution (after the process of replication and natural selection began) and the chemical evolution of life from nonliving chemicals (although he also then implied that something other than natural selection must have guided this process.)”

    Legitimate distinction, eh?

    “The larger point here is the one that Bradley hinted at throughout his talk – that the belief that there is a naturalistic explanation for the chemical evolution of life, given the interrelated complexities of life, is a metaphysical assumption, not a scientific one. A thorough response to this point is beyond the scope of this post. Let me say merely that given that the success that searching for naturalistic explanations has had, and the lack of success in finding (or even articulating in a testable fashion) explanations which invoke “intelligent design”, and given the ongoing scientific research in origins of life issues (and corresponding lack of ID research), I think that a belief in searching for a scientific explanation in terms of natural chemical events is a practical and pragmatic belief.

    Science searches for “naturalistic” explanations because that has worked time and time again. It’s an inductive position about the utility of the scientific approach, not a metaphysical bias, that causes scientists to believe that the effort to understand the origins of life will pay off.”

    That is a large point. It is such a pleasure to read such a precise answer on this issue, rather than the warbling of creationists. But your particular bloviations are so addicting!

    1. jlwile says:

      Shooter, I have already demonstrated to you that the origin of life is not distinct from evolution. I know you need to try to ignore this fact because you have to cling to your faith, but all you have to do is look at how terribly you lost that argument to see that there is no legitimate distinction.

      I think you also need to re-read the discussion of Science’s Blind Spot (part 1 and part 2) as well as the ones on Seeking God in Science (part 1 and part 2) in order to see how the comment about science’s search for “naturalistic” explanations is fantastically incorrect.

      It is not surprising that you would think that such incorrect statements make up a “precise answer.” After all, if it confirms your preconceived notions, you think it is good. If it disagrees with them, you think it is bad. It is unfortunate that you aren’t willing to think about what you read!

  8. Regarding your comment to Josiah, this atheist would very easily give up my “worldview” if Jesus would once again walk the earth (or any other mode of transportation on or near the earth). Until that day comes, I’ll stick with naturalistic explanation.

    What of my comments at 3:36 pm?

    PS, Walter Bradley is a mechanical engineer, fancy that! What exactly is his expertise in Origin of Life, his listing on the Editorial Board?

    The list goes on… Stuart Burgess, another mechanical engineer, will miracles never cease! (actually, like I said, just one would be enough to convince me).

    Russell Carlson is at least close, a biochemist / molecular biologist, but his research is on “characterizing the molecular basis for the interaction between a bacterium and a plant or animal host cell.” That’s quite a bit after the origin of life, don’t you think? Cross-examination at Kansas science hearings. This question is classic.

    Marcos Eberlin, not much info in English, but he works with mass spectrometry.

    Oooh! Charles Garner is a prebiotic chemist! Unfortunately, I’ll have to wait til tomorrow to dig in to that.

    1. jlwile says:

      Shooter, I seriously doubt that you would give up your atheistic faith even if Jesus were to walk again on the earth. You can stick to the naturalistic explanation if you want. It just goes against the data. Of course, your entire worldview goes against the data.

      Unlike most of your comments, your comment from 3:36 is actually reasonable. If the board members are all pro-ID, then most likely, this journal will not be any different from the other journals that deal with scientific heresy. It will still be useful as a means of promoting the discussion. I just won’t be as useful as it would be if the journal actually lives up to its stated goal. As I said in the post, though, we will just have to wait and see.

  9. Ben Michael Fournier says:

    Norwegian Shooter, you don’t exist and you cannot prove me wrong.

  10. Grant C says:

    I’m sorry Dr. Wile, but your argument is nonsensical. Whether ERVs are non-functional or have some effect or not is of almost no relevance to their evidentiary value.

    Retroviral insertions happen at *random* points in the DNA of the infected host. The ERVs that have been mapped in the primate genomes are in identical locations… AND occur in a nested hierarchical pattern. I guarantee you have no rational explanation for that besides inheritance from common ancestry. Arguing *a viral infection* was designed is just ludicrous.

    The odds of two different species getting infected by the same retrovirus, in the SAME location in the billions of base pairs of their DNA… are not good. The human genome is a little over 3 billion base pairs. The chimp genome is of a similar size. The odds of a single ERV infecting both species in the exact same location is 1 in 9E18.

    Of course the odds of both species getting infected with a HERITABLE copy of the same retrovirus in the exact same location are a bit better than that, since no infection that occurs in the middle of a critical functional gene is getting passed on. But even if we eliminate ALL coding genes (even ones it would be questionable at best to call “critical”) and limited the infection cites to non-coding areas that still leaves us with the odds not very much improved since only about 2% of the genome is finctional genes. And yes, I’m aware you’ll want to argue that “junk DNA” isn’t actually junk and there’s evidence it serves certain regulatory functions…. another irrelevency. It can still be an infection site.

    Now… that’s the odds of ONE common retroviral infection. Between just a *single individual* in two species.

    Then there’s the odds both those infected individuals would independently be the jumping off point for a spread of that infection (or it’s de-activated remnant) through subsequent generations until it reached fixation in the entire species. The odds of that happening are incalculable.

    Then there’s the odds of that happening for multiple infections. Across significantly more than two species. AND it happening in a nested hierarchical pattern that just coincidentally happens to be THE signature of inheritance through common descent.

    You do not have a leg to stand on here. There is exactly one plausible explanation for that data.

    Regarding the GULO pseudogene… your argument makes no sense. The “animals with similar biochemistry” you’re speakng of are NOT similar in this respect. They synthesize ascorbic acid. We Do Not. Expecting to find the gene for ascorbic acid synthesis in US based on its presence in THEM cannot come from a “common biochemical design” argument if this particular feature isn’t commmon!

    That’s like saying you expect to find the (disconnected and not functioning) blade from a lawnmower in your car because they both have four wheels… and they both have motors… and they were both made by Honda after all.

    And then there’s the tiny little detail that the GULO pseudogene is, once again, found deactivated in the other primates. And it’s been deactivated in The Same Way. So now we’re dealing with you having to claim that in all the primate species the GULO gene was deactivated by a frame shift mutation *independently*. AND that that gene de-activating mutation *independently* reached fixation in all those different species populations. Which is so far beyond absurd I’m having difficulty describing it.

    And you’re glossing over the chromosome 2 implications. It does not just tell us that our ancestors probably had 48 chromosomes. It tells us our ancestors probably had 48 chromosomes that look a *lot more* like chimp chromosomes than what we have now. The two halves of chromosome 2 are darn near perfect matches with chimp chromosomes 2p and 2q.

    and as for your claim that phylogenetic analysis is incapable of reconstructing ancestral relationships, tell that to these guys: http://mbe.oxfordjournals.org/cgi/reprint/19/2/170.pdf

    Did they reproduce the correct phylogeny by luck? Not only the correct phylogeny, but also the correct *branch length* between every single divergence to within the calculated margin of error except for the single branch between population 2.2 and 3.3… which they missed by a single mutation? Would you care to share the odds of that being a fluke?

    As for your claim that life doesn’t fall into a nested hierarchy, don’t be ridiculous. And yes, there are some relatively *minor* disagreements between hieracrchies constructed morphologically and those constructed genetically but that’s only to be expected since doing the analysis morphologically is doing it using secondary indicators of inheritance that have to be interpreted whioe doing it genetically is working directly with the mechanisms of inheritance.

    Nobody is concerned about that fact except people desperate to cast doubt on the process.

    I am currently wading through your “time and time again” falsification link. Thus far I have not found any actual falsifications but I’m not finished reading yet so maybe I’ll be surprised before I reach the end.

    As for your demonstration criteria, I am quite confident you are familiar with the transitional vertebrate fossil FAQ at talk.origins and so I consider your claim that you would find a single transitional fossil sequence ot be the piece of evidence that would convince you to be questionable. I also find it curious coming from someone who presents themselves as knowledgeable about the subject matter since I cannot fathom how anyone who really understood evolution could possibly find fossil evidence more convincing than the genetic evidence. That’s like saying if you were on the jury in a murder trial you wouldn’t be swayed by the fingerprints on the murder weapon and the DNA match between the accused and blood spatter found on the victim… but if only someone could show you something really definitive… like a shoe print somewhere near the crime scene… THEN you could convict.

    1. jlwile says:

      Sorry, Grant, but it’s YOUR argument that is nonsensical. The functionality of ERVs is absolutely important to the argument. If they are functional and serve a purpose, they do not appear in RANDOM points in the DNA and are probably not the result of viral infection. You are ASSUMING they are the result of a viral infection because you WANT them to be. However, if they are functional, they are almost certainly NOT a result of a viral infection. You are assuming that because they appear similar to retrovirus sequences, they must be from retroviruses, and that is just an assumption. If the genes were nonfunctional, that would be evidence for your assumption. However, since they are functional, that is evidence against your assumption. Thus, you are the one who does not have a leg to stand on. The data simply do not support your assertions.

      You are still wrong about the GULO pseudogene as well. We don’t produce ascorbic acid because the gene that we were designed with has mutated to the point where it is nonfunctional. Given that humans and chimps have similar biochemistry, you would expect that the Designer gave us similar genes. Thus, simple analogy leads to the assumption that there should be a gene for ascorbic acid synthesis in humans as well. Unfortunately, mutations have caused that gene to be nonfunctional. The idea that the gene could become nonfunctional in several different organisms independently with similar mutations is not “beyond absurd.” In fact, it is supported by the study (which you conveniently ignore) that shows a high level of shared mutations in the guinea pig and human GULO pseudogene.

      I am certainly not glossing over the chromosome 2 implications. There are many similarities between human and chimp chromosomes, due to the fact that we have similar biochemistry. Thus, it is not surprising that the two human chromosomes that fused look a lot like chimp chromosomes. Indeed, you expect that based solely on functionality.

      Your example of the success of phylogenetic analysis is typical of the “bait and switch” that most evolutionary evangelists engage in. Of course those guys produced a good phylogeny, as it simply tracked evolution within a genome, which is easily understood. It did not track evolution from one type of genome to another, which is the kind of phylogenetic analysis needed for “goo to you” evolution. Remember, you want phylogenetic analysis to be evidence for that kind of evolution, and all you show me is that phylogenetic analysis can accurately analyze the kind of changes that occur in very simple microevolutionary scenarios.

      Of course I am not being “ridiculous” when I say that life doesn’t fall into a nested hierarchy. It doesn’t. The disagreements you call “minor” are anything but minor. Indeed, some are suggesting to do away with the “tree” view of life altogether. That is not minor. It is major. The fact that you want to call these “minor” disagreements tells a lot about your inability to see the data for what they are. Of course, since you seem incapable of seeing the data for what they are, it is not surprising that you claim to have “not found any actual falsifications” in Dr. Hunter’s document. In fact, the document is full of them to anyone who wants to rely on data rather than preconceived notions.

      Of course I am familiar with the incredibly deceptive talkorigins vertebrate fossil FAQ. That’s why I can state so strongly that the fossil record is such a major falsifier of evolution. Even deceptive evolutionary evangelists cannot produce ONE series of transitions between different types of organisms. That shows just how poorly evolution stacks up against the data.

      I don’t know why you think I find fossil evidence more convincing than genetic evidence. Of course, since you are an evolutionist, I suspect that you jump to conclusions all the time. The fact is that I don’t know of enough preserved DNA from extinct creatures that would allow us to track the process of evolution genetically. Thus, fossils seem to be the more likely scenario for confirmation of the macroevolutionary hypothesis. Of course if you could present genetic data that showed macroevolution, that would be convincing as well. However, our current understanding of genetics speaks strongly against evolution as well. Indeed, given that the best you can come up with are ERVs, the GULO pseudogene, chromosome 2 in humans, and molecular phylogenies that don’t match up with morphological phylogenies, genetics is clearly not a field supportive of “goo to you” evolution!

  11. Grant C – loved the shoe print line!

  12. Grant C says:

    You accuse me of ignoring studies while clearly either not reading or deliberately representing the studies you cited as supporting your position while likely banking on me not reading them and catching you at it.

    For example, the “Retroviral promoters in the human genome” study you cited as evidence that ERVs have function also specifically point out that yes, they ARE viral infection remnants. So you then turning around and saying that if they possess some function that means they weren’t the result of retroviral infections is blatantly dishonestly representing the data. The line of reasoning you appear to expect us to follow is:

    1. They’ve studied retroviral infection remansts.
    2. They’ve found they are having some effect on gene expression.
    3 Therefore they are NOT retroviral infection remnants.

    How you make the logical leap across the gaping chasm that lies between step 2 and step 3, or reasonably expect anyone to follow you across it, escapes my comprehension.

    You are similarly misreprenseting the situation with the GULO gene. For one thing, unless we are to expect that the Designer gave both us and the other primates similar NON-FUNCTIONAL genes for some unfathomable reason your comment about humans and chimps being similar makes absolutely no sense. what does human and chimps being “designed” with the same GULO gene sequences have to do with them both having been disabled by *the same mutation*?

    As for the GULO gene in Guinea pigs… yes it’s disabled, no it is NOT disabled by the same mutation and no the human and Gulo genese do not have a high level of shared mutations. The Nishikimi paper from 2003 that compared human, Guinea Pig and Rat GULO sequences erroneously jumped to the conclusion that the places where the human and Guniea Pig sequences had common differences from the Rat were examples of shared mutations in humans and Guuinea Pigs. They were nothing of the kind. They were in fact, and this has been made abundantly clear since with analysis of a wider sample of GULO sequences from other species:

    http://pandasthumb.org/archives/2008/05/24/images/GULO_CLUSTAL_ALIGN_V2.jpg

    … single mutations of the RAT GULO gene.

    And define “evolution within a genome” a little more rigorously for me if you wouldn’t mind, and point out for me the *mathematical* complicating factor that makes analysing that different from analyzing relationships between genomes. Otherwise you are simply handwaving off evidence you can’t deal with.

    And would you mind pointing me at who exactly is proposing doing away with the “tree” and the details of exactly how and why they are proposing such?

    The only thing your link to how talk.origins is “incredibly deceptive” says about the transitional fossil sequences is to declare in a pair of sentences that the transitional fossils are “highly suspect” and controversial… without backing that up in any way… and to claim that “the establishment” are invested in protecting their view “at all costs”, which is pretty standard conspiracy theorist boilerplater. Which is about on par with the quality of the substance of the rest of its claims. Do better.

    And I thought you considered the fossil evidence most important because when asked what you wanted to see that would demonstrate evolution was true you singled out that it was fossil evidence you wanted to see. If you think genetic evidence is more important, which I would expect anyone who kows what they’re talking about to think, then change your answer and tell me what genetic evidence you need to see. Saying we need intact DNA from extinct creatures only demonstrates ignorance of how genetic analysis works.

    1. jlwile says:

      Grant, I have, indeed, read the study and I am not misrepresenting it. The study presents strong evidence for function of ERVs. It does not present strong evidence that the ERVs are viral infection remnants. You are making the common mistake that many evolutionists make. You assume that since ERVs are very similar to retroviral sequences, they must come from retroviruses. That, of course, is not necessarily a valid assumption, and the fact that they have function indicates it is an incorrect assumption. It is more reasonable to assume that since they have function, they do not come from retroviruses and that the similarity to retroviral sequences is due to the nature of that function. For example, the study shows that ERVs act as transcription initiators. Well…if a retrovirus is going to insert something into a cell’s genome, that something is going to need to tell the cell to start transcription. Thus, the similarity is there not because the sequences came from retroviruses, but because the function is similar.

      I am certainly not misrepresenting the GULO pseudogene study, either. However, you ARE misrepresenting my view. The Designer did not give chimps and humans nonfunctional GULO genes. He gave us FUNCTIONAL genes that lost their function due to mutations. These mutations occur at hotspots, so the similarities are representative of the hotspots, not of common ancestry. Mutational hotspots will be similar in organisms with similar biochemistry. I have not seen the study that reports the Nishikimi paper (more properly called the Inai paper) is incorrect in its analysis. I will need more than a link to a figure from the panda’s thumb website.

      Evolution within a genome means that the genome’s structure has not been fundamentally changed. Comparisons between two genomes of the same structure are very easy – like comparing blueprints based on the same basic design. When you have to compare one genome to a genome with a fundamentally different structure, then all sorts of assumptions have to be made. These assumptions produce errors, and the more incorrect the assumptions, the more serious the errors.

      I don’t have to do better than the talkorigins link, as it clearly shows how deceptive talkorigins is. You don’t want to accept that, so you tray to handwave the evidence away. I won’t let you do that here. Talkorigins is a very deceptive website, as the link I gave you clearly demonstrates. Even given their level of deceptiveness, however, they still can’t produce a fossil series showing transition from one basic type of organisms to another. Once again, that demonstrates just how strongly the fossil record has falsified evolution.

      Your comments indicate your lack of understanding of how genetic analysis works. If you want to use PRESENT DAY genomes to try to develop evidence for evolution, it won’t work – not at our current level of understanding of genetics. The ERV issue is a clear example. You ASSUME that ERVs are remnants of retrovirus infection and then start making deductions based on that. However, the data indicate that your assumption is wrong, so your conclusions are wrong. Until we truly understand genetics, there is no way to flesh out evolutionary relationships using CURRENT genomes. Finding DNA from supposed transitional forms would be the only way to confirm evolution via genetics with our currently level of understanding of genetics.

      ADDED LATER:I decided to make a post to answer your question about why biologists are abandoning the “tree of life” approach, as it will be informative for many.

  13. The only thing your link to how talk.origins is “incredibly deceptive” says about the transitional fossil sequences is to declare in a pair of sentences that the transitional fossils are “highly suspect” and controversial… without backing that up in any way… and to claim that “the establishment” are invested in protecting their view “at all costs”, which is pretty standard conspiracy theorist boilerplater. Which is about on par with the quality of the substance of the rest of its claims. Do better.

    Grant, sadly, your exhortation will not happen. Simply declaring things without any support is how blogging creationists get through the day. I think divine revelation is so ingrained in their thought processes that they think saying something makes it so.

    However, keep it up, I’m enjoying your comments, but just give up on the notion that creationists can be persuaded through rational argument.

  14. Back to the editorial board. Charles Garner is certainly one of the bigger names on the list. He was one of three creationists appointed by Christian fundamentalists to the Texas science curriculum review, along with Steven Meyer and Ralph Seelke. He has a real science professor job and has published in biochemistry (notice that’s not pre-biotic chemistry). He is very likely to be one of the next authors for BIO-Complexity.

    Also notice that the Baylor Chemistry and Biochemistry Department added a Statement on Evolution after Garner’s testimony for the Texas science review. Source It states:

    Evolution, a foundational principle of modern biological sciences, is supported by overwhelming scientific evidence. It is fundamental to the understanding of modern biochemistry, and our faculty incorporate the principle of evolution throughout the biochemistry curriculum. We are a science department, and we do not teach alternative hypotheses or philosophically deduced theories that cannot be tested rigorously.Translated from academicese – ID is BS. Oh, snap!

  15. Ben Michael Fournier says:

    “I hear nothing, I see nothing, I know nothing! Nothing!!!”

    -Sergeant Schultz from Hogan’s Heroes.

  16. Last sentence is mine.

    Loren Haarsma – a good Scandinavian name, so I’ll go easy on him. Actually, I’ll go easy on him because he seems pretty reasonable in comparison to others.

    He wrote an article for TalkOrigins, seems to stick to NOMA platitudes, and doesn’t go out on any limbs.

    In fact, he might even be neutral to ID. However, his research record is shallow (one paper since 2001) and not on topic (electrophysiology). He teaches Intro to Physics and Quantum Mechanics. BTW, biophysics appears once on his CV, for a conference his own school put on. I’m beginning to feel like BIO-Complexity is stretching the truth.

  17. Ben Michael Fournier says:

    It’s rather sad that you evos spend so much time trying to argue by character assassination, in one form or another.

  18. Ben, quote me one thing I’ve said that is character assassination.

  19. Ben Michael Fournier says:

    In general, it is express as a concern over who is speaking rather than the content of what is spoken. Although you do sometimes address some random part of the content, it is usually the weaker parts only while the main is left unscathed due to some bizarre concept that nitpicking entails victory.

  20. Ben, I discuss who is speaking – as in what is their scientific background and production. Not the content of their character. Jay’s point about BIO-Complexity was that it would present both sides of the ID “debate”. I think that’s not correct and I need to look who is on the Editorial Board to support my contention.

    Jay, I found a great Antony Flew article for you.

    1. jlwile says:

      Shooter, you do engage in character assassination on a regular basis. Indeed, instead of concentrating on arguments, you usually try to tear down the person making the arguments. This is understandable, because your views cannot be supported by evidence. Thus, you have to resort to tearing people down. I don’t mind it, because it demonstrates how weak your arguments really are.

      Your Antony Flew article is a great example of this. The article tries to say that Flew was a doddering old man whose mind changed him. However, when atheists who cannot make good arguments floated this idea when his book came out, Flew himself shot it down:

      “My name is on the book and it represents exactly my opinions. I would not have a book issued in my name that I do not 100 percent agree with. I needed someone to do the actual writing because I’m 84 and that was Roy Varghese’s role. The idea that someone manipulated me because I’m old is exactly wrong. I may be old but it is hard to manipulate me. This is my book and it represents my thinking.”

      So rather than picking on old people and trying to tear down the people who present evidence that makes you uncomfortable, why don’t you actually try to use a bit of evidence in your comments? It would be something new for you.

      Now I do admit that most of what you have found out about the editorial board of BIO-Complexity is disappointing. As I said in this post, we will have to wait and see whether or not it lives up to its stated goal. Based on what you have learned about the editorial board, however, it doesn’t look like that will be the case, unless Loren Haarsma turns out to be a strong voice.

  21. This is the classic question for Dr. Carlson.

    Peter Imming is a German professor of pharmaceutical chemistry, so it’s hard to get facts, but I found this. He’s also involved with Wort und Wissen, funny coincidence. Wrote an article called “Monkeys are different – but how?” (third in link). I wonder what a pharmacologist would say about that?

    Wow! Just found this via the Imming search: Seer Reviewed, or I’ll take ‘Bar Trivia’ for $500, Alex. Awesome!

  22. Okay, this is getting tiresome. James Keener is a member of ISCID. ’nuff said. At least his area is correct.

    David Keller, spoke at “Grill the ID Scientist” and is one of the “People” at the Biologic Institute. At least this list takes Matti Leisola, Editor in Chief, and Colin Reeves off the research list. And obviously, I am omitting Douglas Axe, Michael Behe, William Dembski, Ralph Seelke, Richard Sternberg and Jonathan Wells – all very pro-ID.

    This is it for Branko Kozulic. That’s scraping the bottom of the barrel, don’t you think?

  23. Check your latest Antony Flew link.

    1. jlwile says:

      Thanks for noting that the link was bad. I fixed it.

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