Posted on 12/30/2001 2:08:09 PM PST by Exnihilo
I hope we all remember this. It is the atheists who are on the defensive. Those of us who are theistic have nothing to concern ourselves with, other than destroying materialism, which is of course, all but done at this point.
To jlogajan:
So, really, what's your story?
Why do the paintings of Salvador Dali look like they were painted by..... Salvador Dali? Did all evolve from one painting, or were all just created by the same artist?
Arguments may be made for evolution, but this is surely not one of its stronger arguments.
Information generation has no intrinsic mathematical or scientific relationship to biology any more than there is a theoretical model for gravitation in a ham sandwich. To assert otherwise is sheer cluelessness. Therefore, I will attempt to narrow down exactly what you mean by "informational generation".
It is questionable what you mean by "information generation" since "information" is a suitcase term that has very specific mathematical definitions that are quite different than many common definitions. If we were talking about something as simple as, say, concept formation in the brain (i.e. the process of thinking) you would be wrong to assert that there is informational generation that violates thermodynamics, as the processes create a net increase in entropy that is roughly 10^8 times greater than the decrease in entropy due to concept/thought creation. The DNA in living things behaves exactly like any other molecule, requiring an entropy/enthalpy gradient to execute its complex behaviors. Lacking an external gradient, the process stops.
The bottom line is that information creation is perfectly permissible with the caveat that the net entropy of the system is always increasing. Biological systems create vast quantities of entropy in their reproductive and complexity building processes, and the only reason it has been sustainable is that the solar system has a very large enthalpy gradient (from the sun mostly) that is being used up and converted into entropy as rapidly as possible in the process of building complex biological systems and organisms. If the sun went dark tomorrow, the process of "informational generation" would grind to a halt as it is an endothermic process ultimately. Which is all exactly what basic thermodynamics predicts (2nd Law and all that).
Does this answer the question?
Amino acids & nucleic acids spontaneously link & form longer & longer chains on the surfaces of minerals, even up to lengths where functional proteins & RNA start to be found.
Dear god.. you actually believe that? LOL!
The mineral surfaces are catalysts. Catalysts are substances that do great damage to creationist impossible odds arguments.
Most theories of the origin of biological organization assume that polymers with lengths in the range of 30-60 monomers are needed to make a genetic system viable. But it has not proved possible to synthesize plausibly prebiotic polymers this long by condensation in aqueous solution, because hydrolysis competes with polymerization. The potential of mineral surfaces to facilitate prebiotic polymerization was pointed out long ago. Here we describe a system that models prebiotic polymerization by the oligomerization of activated monomers--both nucleotides and amino acids. We find that whereas the reactions in solution produce only short oligomers (the longest typically being a 10-mer), the presence of mineral surfaces (montmorillonite for nucleotides, illite and hydroxylapatite for amino acids) induces the formation of oligomers up to 55 monomers long. These are formed by successive 'feedings' with the monomers; polymerization takes place on the mineral surfaces in a manner akin to solid-phase synthesis of biopolymers.
Ferris, Hill, Liu, & Orgel. 1996 May 2. Synthesis of long prebiotic oligomers on mineral surfaces. Nature, 381, 59-61.
What part of this study do you laugh at? And if you say it's the fact that it's a human-designed experiment, you lose. :-)
Ah, but bacteria that were cloned from a single initial bacterium also develop antibiotic resistance! IOW, if you take a single bacterium & place it into a nutrient solution that has first been sterilized in an autoclave, and let it split into a new colony of clones of itself, and then apply selective pressure to this colony over many generations, it will still eventually "adapt" to thrive in the new environment.
This is due to brand-new mutations appearing in the colony and getting selected for/against. The "inherent ability to adapt" in your sense was not there initially.
Bacteria are easy to study. This is an advantage in evolutionary studies because we can see evolution happening in the laboratory. There is a standard experiment in which the experimenter begins with a single bacterium and lets it reproduce in a controlled environment. Since bacteria reproduce asexually all of its descendents are clones. Since reproduction is not perfect mutations happen. The experimenter can set the environment so that mutations for a particular attribute are selected. The experimenter knows both that the mutation was not present originally and, hence, when it occurred.
Richard Harter, Are Mutations Harmful?, TalkOrigins
Playing the Devil's Advocate here, I can set the environment for changing a solid into a liquid and then back again in my kitchen using simple plastic trays; isn't the keyword in this and all such experiments the reliance on a suitable chance environment for the natural world to be so explained?
OK, this article says "Yes, there's what looks like evidence from multiple lines of evidence for common descent. However, you can in every case explain the same thing by the intervention of My Invisible Buddy."
True, you can explain anything you see in terms of magic or Goddidit. That's one sign of a totally useless theory. And why then does the evidence also fit evolution? Fitting evolution's a lot harder. One rabbit fossil in the Precambrian, etc., etc. And why do we need supernatural explanations at all, much less why should they be the default? And what's the evidence for supernatural explanations?
This is an old debate on FR. It took me a while, but I finally found Miller's (longer) online version of his book chapter, where he goes into detail about the blood clotting cascade.
Here's Behe's critique of Miller's original published description of blood clotting evolution. He complains that Doolittle's model (by way of Miller) doesn't take into account the evolution of regulatory methods, the lack of which in a modern mammal would kill it.
Here's Miller's response to Behe's critique. Here's Miller's original draft of the part of the IC chapter concerning blood clotting. As I suspected, Behe's complaints about lack of regulation destroying the organism before the new clotting steps could get refined are based on what would happen in a modern, high-blood pressure organism like humans, instead of the more realistic low blood pressure organism where the evolution of blood clotting really got started.
IOW, Behe's critique of Miller/Doolittle is an airball. It tries to cut off evolution at the start - in a small ancestor organism 600 million years ago - but does so by judging it according to the conditions of a wholly different organism!
Or as Miller puts it...
Behe asserts that the targeting of a protease, a digestive enzyme, to the bloodstream is a "potentially deadly situation," and tells the readers of his web document that we can tell how deadly this might be by looking at situations "where regulatory proteins are missing from modern organisms." In other words, Behe wants us to look at what happens when the highly-regulated current versions of clotting proteases are missing their regulatory factors. Despite this bluster, however, Behe has no evidence that the mistargeting of an inactive protease to the bloodstream would cause harm. Indeed, the recent discovery that antifreeze protein genes in fish arose from exactly such a mistargeting of proteases into the bloodstream (Chen, L., DeVries, A. L. & Cheng, C.- H. C. Proc. Natl Acad. Sci. USA 94, 38113816 (1997); and Chen, L., DeVries, A. L. & Cheng, C.-H. C. Proc. Natl Acad. Sci. USA 94, 38173822 (1997)) suggests that exactly the opposite is true.
Having made unsupported claims about the "danger" of such a mutation, Behe says that it would be difficult to see what "advantage" this would present to the organism. The answer, of course, is that it would provide a slight improvement in the organism's ability to clot blood - and that's the point. The clotting system doesn't have to work full-blast right away. In a primitive vertebrate with a low-pressure circulatory system, a very slight improvement in clotting would be advantageous, and would be favored by natural selection.
Behe then wonders how the circulating protease could become localized at the site of a clot, as if this were an insurmountable difficulty. It's not. As I suggested in my original draft on the evolution of clotting, a well-understood process called exon shuffling could have placed an "EGF domain" onto the protease sequence, and the "problem" that Behe puzzles over is solved in a flash.
Finally, Behe emphasizes that the real problem is not to generate a clot - it is to "regulate" that clot by means of an inhibitor of the protease so that it doesn't become destructive. But that's not a problem for evolution, either. As usual, Behe envisions a clotting protease that is just as powerful as the fully-evolved proteases in modern vertebrates. However, remember that this is the same guy who fretted a moment or two ago that the protease would not be strong enough to clot effectively. He wants to have it both ways. The answer to his objection is just what I wrote in the draft:
" ... a primitive clotting system, adequate for an animal with low blood pressure and minimal blood flow, doesn't have the clotting capacity to present this kind of a threat. But just as soon as the occasional clot becomes large enough to present health risks, natural selection would favor the evolution of systems to keep clot formation in check. And where would these systems come from? From pre-existing proteins, of course, duplicated and modified. The tissues of the body produce a protein known as alpha-1-antitrypsin which binds to the active site of serine proteases found in tissues and keeps them in check. So, just as soon as clotting systems became strong enough, gene duplication would have presented natural selection with a working protease inhibitor that could then evolve into antithrombin, a similar inhibitor that today blocks the action of the primary fibrinogen-cleaving protease, thrombin."
In short, none of the points raised by Behe are adequate to explain why the vertebrate clotting system could not have evolved. Furthermore, as Doolittle's work has shown clearly, the hypothesis of evolution makes testable predictions with respect to the DNA sequences of clotting proteins, and these predictions have turned out to be correct time and time again.
Why has Behe's "Biochemical Challenge to Evolution" met with so little support within the scientific community? I would suggest that the reason is simple. His hypothesis is wrong. The complex biochemical systems of living organisms, including the vertebrate clotting cascade, are fully understandable in terms of Darwinian evolution.
Here's the total response Behe had to say about that...
Kenneth Miller, Brown University Professor of Biology and author of Finding Darwin's God, has posted a response to my essays: http://biocrs.biomed.brown.edu/Darwin/DI/Design.html Overall I'm satisfied with his reply because, although he continues to defend his position, from the substance of his writing I think it should be plain to most open-minded readers that he is struggling to fend off examples that weigh heavily against Darwinism. So, for the most part, I am content to let the exchange end here. I simply urge all who are interested to read my essays as well as his response and come to their own conclusions.
Behe did respond to other points Miller has made, but I haven't followed those so I don't know if he scored points or not. But as for the blood clotting cascade, Behe clearly has pleaded no contest.
Yes, but the question at issue is, "what's plausible in the natural world & what's not?" In an experiment you'd purposefully change the temperature up or down, but that's perfectly valid as long as temperatures go up & down in nature.
As for the bacteria, the question was, "where does the ability to survive in the face of antibiotics come from?" You can't answer this as definitively in the wild as you could in an isolated lab environment, since you could never be sure it was the test bacteria that evolved, nor could you be sure that some kind of lateral DNA transfer hadn't occurred from another species of bacteria, etc. That's why the lab experiment is so powerful.
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