April 26, 2009 by Dr. Mc.

[Don,]
I guess I missed your “evidence” for the creationist/Id explanation of the Cambrian explosion.

I guess I missed the part where I denied evidence, simply because you have not presented any evidence.

I guess I missed the fact that I denied any cracks in the dike. On the contrary, I fully understand that evolutionary theory has plenty of unresolved issues. I understand that it probably will, like all theories, be discarded someday in favor of a better one. Unlike you, I also understand that cracks in this theory are absolutely not the same thing as evidence for your theory. Evidence for your theory will require hypotheses (of which you have none), predictions (again, none), and new observations (again, none)

I guess you missed the part where the folks in those papers I cited had hypotheses, stated those hypotheses, tested those hypotheses, and found new evidence that supported the theory of evolution. Too bad.

You have a very different view of evidence from me. You have an idiosyncratic definition of information. I have pointed those facts out to you, but I see no evidence that you wish to recognize those problems with your positions.

From another form, discussing ID/creationists, here is a statement that resonates for me:

they just can’t accept that their core organizing belief does not and cannot contribute to a scientific understanding of the world - and take that to mean that science is an enemy of that belief.

Think about it. Just because your worldview is incapable of doing what science can do (you know, generate testable hypotheses and get new observations and accept or refute the hypothesis), that is not a good reason to rail against science.

cheers

Mark*
- - - - -
Mark,
You have the last word.
Don Mc
- - - - -
[Don]
I have no delusions that is true
cheers
Mark

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April 19, 2009 by Dr. Mc.

Mark,
You have given me examples of phenotypical changes that are useful to the organism and seem to be traceable back to random mutations. I appreciate that, and will enjoy looking into them over the next weeks. Still, I find you have stated no hypotheses, and I do not see any construct validity for how randomness can produce increased information. Information is fundamental, not only for simple change or even usefulness, but also as the whole basis of DNA.
I’m afraid I don’t see how white noise contains more information than a Beethoven sonata. There may be more data, depending on the length, but the difference between data and information is some discernable meaning in some identifiable context. By meaning I mean a consistent, logical interpretation into an application, as is the case with a sonata or DNA.
I also consider logic to be fundamental behind an hypothesis. Examples of change are nice, but the absence of construct validity is where “no hypothesis can stand.” After the logic behind the construct comes examples, or the examples themselves have no meaning–application to theory.
I see no reason to present further arguments. The ones I have presented you have disqualified, ignored, or pooh-poohed, but you have offered no logical rebuttals for any of them.
To date I am not convinced that evolution occurs beyond natural selection of pre-existing information or rearrangements of pre-existing information. That said, I believe, scientifically speaking, there is no reason why Darwinian (tree of life) evolution and design could not occur in the same universe. Said another way, everything need not be explained by one over the other. This apparently is not your position.
There is evidence for evolution, for gradual decent. I find it neither compelling nor up to the level of evidence for design, but I do not find it difficult to admit. It is there, and I can understand how a person could buy it, especially in the absence of any alternative presentation of fact, theory or hypothesis. After all, I was there once.
What I find more difficult to understand is complete denial of any evidence for alternative interpretations. I have attempted, with some effort at logic, to make the alternatives clear, pushed by curiosity to find what it might take to gain consideration. In this I have utterly failed.
Your reasons for rejecting my evidence include it’s too old (older than Darwin), it’s not my field (and no one should look outside their field), it’s too negative (viewing it for how it DOESN’T support evolution instead of how it DOES support design), and the most lame of all, it’s not about the Cambrian Explosion (as if the Cambrian were the real issue).
You are offended at the idea that evolutionary scientists might be wearing blinders, while illustrating the point perfectly. The fact that you are so intelligent, so well educated, and so highly positioned in your field make the point even stronger, that people can’t get that way by themselves. It takes a total culture of total denial to make it possible. The fact that any crack in the dike is intolerable says to me that denial itself is the last stronghold.
If you cannot admit that there is evidence on both sides of any argument, then you will never find the truth. I could have never written a scenario like the one you and I have constructed. I would not have considered the prose plausible. Thank you for an education in this area.
We can both stop here and consider ourselves to have won. My perceived victory is in being able to weigh evidence that alludes a very intelligent and educated mind. It looks to me like your perceived victory is in winning an argument over an “uncluttered” mind that “lacks understanding.”
Don Mc

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April 13, 2009 by Dr. Mc.

[Don,]
We may be getting toward the end of our discussion.
Yes, it would appear to be the case, since you have not managed to propose a single scientific hypothesis based on what you hope/wish is a powerful scientific approach. But I’m willing to be patient.
If I responded to your request for an hypothesis at any time with a list of topics, books, and referred articles, you would have rejected it.
I’m not sure I would have rejected it, since I haven’t seen them. I can tell you that I have yet to see a scientific hypothesis based on ID that would lead to a testable prediction unexplainable by current evolutionary theory. That was true before we started this conversation, and I have read additional ID and creationist materials since then, yet it remains true. I merely thought that since you broached the subject of the Cambrian explosion, you would have a ready explanation for it, based on your perspective. I guess that was a premature expectation.

Your example of nylonase in bacteria was better.
This is such a remarkably incorrect perversion of what we know that I don’t know where to start. But rather than get sidetracked on those issues (and further away from hearing a single hypothesis from you), I’ll merely point out that if you had read anything in Carroll’s book, or any of a number of other primary sources, you would not say that “loss of complexity” or “a degenerated mechanism” is the explanation. As pointed out before, you will need a significantly deeper understanding of genetic control mechanisms to proceed toward an understanding of why the entire paragraph above is simply wrong. Clearly you don’t have that understanding.

I think complexity is a legitimate term in biology,
I was asking simply because I had no idea what YOU meant by the word “complexity”. And now that I have that information, I have to point out to you (again) that your understanding is quite superficial. Increases in information are not the same thing as increases in complexity. Some well-accepted definitions of information would posit that there is more information in white noise than in a Beethoven sonata of the same length. Is white noise more “complex” than a Beethoven sonata? Most folks would say no. Others would posit that mere duplication of information is an increase in complexity; two copies of War and Peace is more complex than one. Yet there is no more information in two copies compared to one. At the biological level this conflation is also obvious. A duplicated gene has no more information content than the original gene, yet it can lead to increases in the “complexity” of the organism’s metabolism, structure, etc. See methotrexate resistance in human cancers, for one non-trivial example. A genetic control element moved to a novel chromosomal environment has no new information, but it can (as you would know if you read Carroll and others) lead to new structures which most people would describe as an increase in “complexity”.
So until you understand the fact that information and complexity are different things, we can’t really get much further.

I need nothing about natural selection.
Yet you deny those mechanisms. Gene duplication gives rise to new possibilities for selection to act upon. There are innumerable examples (antifreeze proteins in Antarctic icefish, for one) of duplicated genes giving rise to proteins with novel structure. Is an icefish with antifreeze proteins more “complex” than a related fish without those proteins? I happen to think so, but I can’t really figure out where you would stand on that question. Mutations that result in novel protein-protein interactions, for example in the Vpu gene in human immunodeficiency virus I (the virus that causes AIDS), can give “more complex alternatives” from which nature selects more lethal viruses (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=8794357&ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum%E2%80%9D). The literature is replete with the examples that you seek. Read about them, please. But don’t let it distract you from formulating your hypothesis about the Cambrian explosion, please.
So, more important than examples of change or defense of natural selection, I would like to see a logical argument supporting an hypothesis pertaining to increased complexity by random mutation.
Let me just say, then, that “where you come from” is a place that is remarkably uncluttered by the results of scientific research of the past 60 years. In addition, that place supports a definition of “complexity” (information = complexity, NOT) that fails to conform to standard usage. See http://pandasthumb.org/archives/2008/06/more-on-the-ori.html for a discussion of new genes in fruit flies, or http://pandasthumb.org/archives/2008/06/de-novo-origina.html for a discussion of the origin of a new gene in yeast. It is simply not true that “no hypothesis can stand” in this arena.

I believe I can give an example of an hypothesis supporting design
Let’s just hear the hypothesis, please.
Thanks

Mark

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April 1, 2009 by Dr. Mc.

Mark,
We may be getting toward the end of our discussion.
If I responded to your request for an hypothesis at any time with a list of topics, books, and referred articles, you would have rejected it. I could list for you example referred publications defending ID, communism or any number of topics, but I will respond:
Your example of nylonase in bacteria was better. At least it still holds more mystery in its cause. The research I have read on duplication of organs seems pretty straightforward. All organic processes begin and end with a molecular “command.” Simply looking at the chemical reactions, something starts to reproduce and grow because a molecular signal is given to begin. Likewise, other than by simply running out of raw materials, the process stops because a molecular command is given to stop. The same is true in my Excel programs. The program loops while it continually checks for some condition. When that certain level of computation is reached in a “compute” loop, the loop is sidetracked by an alternative “stop” command. If the beginning command does not occur in an organism, there is no continuation of life. If the ending command does not kick in at all, well we usually call that cancer. Sometimes the stop command looses function only partially, so that replication continues to abnormal size in an organ, or an organ is produced where it did not occur at all in previous generations. It is not new information; it is replication of old information by a degenerated mechanism. This explains fruit flies with extra wings, sticklebacks with extra fins, and freak shows where animals have too many legs. In any case, it can be explained by the loss of complexity, not the gain.
I think complexity is a legitimate term in biology, since one of your example answers was Carroll’s book, The Making and Evolution of Complexity. Modern technology has taken us to the molecular level, and demonstrated that information is stored there, something Darwin could not have imagined. Therefore, by increased complexity I mean there occurs (for whatever reason) more information at the molecular level than was present in the predecessor molecules. What I’d like to see is something pertaining to an increase in complexity.
I need nothing about natural selection. No one argues against natural selection’s power to eliminate the less competitive organisms, and thus the molecules that gave them rise. That is logical, and it is demonstrated daily. The part I need help with is the power of chance to mutate more complex alternatives from which nature is then to select.
So, more important than examples of change or defense of natural selection, I would like to see a logical argument supporting an hypothesis pertaining to increased complexity by random mutation. Where I come from, no hypothesis can stand, regardless of what it predicts or what is observed, without a logical, step-by-step explanation for why the observation supports the conclusion, and only that conclusion. I’m guessing you call that construct validity, just as I do.
I believe I can give an example of an hypothesis supporting design and based on the probable cause of the stickleback condition (and thus pertaining to the Cambrian issue), but I should wait for your example of validity and hypothesis on some aspect of increased complexity. Otherwise, I’m confident it will not meet your standard.
Don

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