Behe Responds
by MikeGeneI hope Eric doesn't mind me forcing him to be a guest contributor, but I thought his announcement shouldn't be buried:
Eric:
FYI to all regarding The Edge of Evolution, Behe has begun to post some responses to reviews by prominent academic Darwinists at his Amazon blog.
He is starting with responses to the reviews by
Jerry Coyne (professor of evolutionary biology at the University of Chicago);
Sean Carroll (professor of developmental biology, University of Wisconsin); and
Michael Ruse (professor of philosophy at Florida State University).
After several other expected major reviews are published in the coming month, he plans to post a comprehensive response.
The blog also includes an early post that provides an interview style series of "Question & Answer With Michael J. Behe".
June 29th, 2007 at 1:08 am
Isn't the post-Wedge world great!
Comment by Salvador T. Cordova — June 29, 2007 @ 1:08 am
June 29th, 2007 at 1:33 am
And yet he was given honorary PhD's….
Comment by onething — June 29, 2007 @ 1:33 am
June 29th, 2007 at 1:54 am
I have two interesting interviews (well 25 interesting interviews, but 2 interesting and relevant interviews to the specific topic) coming up in "Darwin or Design ?" and audio book that is soon to be release.
I have an interview with Sean Carroll and it is interesting listening to his choice of language when talking about how EvoDevo works. Specifically in the way "toolkit" is used so easily and appropriately.
I also have one with Mike Behe, who is always interesting to talk to.
Stay tuned for July 15th
Jason
Comment by thesciphishow — June 29, 2007 @ 1:54 am
June 29th, 2007 at 6:52 am
From Ken Miller's Nature review of The Edge of Evolution:
Comment by keiths — June 29, 2007 @ 6:52 am
June 29th, 2007 at 7:06 am
Ken Miller:
So Miller's counter to the idea that "production of so much as a single new protein-to-protein binding site" is implausible amounts to what- homology based arguments? observing a new protein-to-protein binding site? or what?
Comment by Bradford — June 29, 2007 @ 7:06 am
June 29th, 2007 at 7:43 am
Bradford,
Literary critics don't rewrite the novels they review. Why should Miller rewrite Behe's book? Isn't it enough to point out Behe's egregious errors?
Comment by keiths — June 29, 2007 @ 7:43 am
June 29th, 2007 at 9:28 am
Before determining if something is an error, much less an egregious one, I want to know what the evidence for the production of new protein-to-protein binding sites is. It's a reasonable question. Did Miller observe it? Is it inferred through circumstantial evidence?
Comment by Bradford — June 29, 2007 @ 9:28 am
June 29th, 2007 at 9:40 am
Bradford,
In the review, Miller explains exactly why Behe is in error:
Which of Miller's points do you dispute, and why?
Comment by keiths — June 29, 2007 @ 9:40 am
June 29th, 2007 at 11:00 am
Before Keiths embraces Miller's buffoonery, he might familiarize himself with several areas where Miller erred. It was humorously bad. See: Ken Miller, an honest Darwinist
Furthermore, before Keiths asserts Behe was refuted, I would be interested to know if Keiths has Behe's book. He can a copy for a modest donation at ARN.
Comment by Salvador T. Cordova — June 29, 2007 @ 11:00 am
June 29th, 2007 at 11:14 am
Wow. Coyne, Carroll and Ruse are generally highly respectable. It is quite telling that they could barely form one relevant argument among the three of them.
I hate to say it, but so far Matzke's criticism (at PT) seems to be the only one that on it's face really addresses Behe's argument. (and perhaps Miller's – I haven't read it yet)
These three "giants" appear to have punted.
Comment by chunkdz — June 29, 2007 @ 11:14 am
June 29th, 2007 at 12:09 pm
Unfortunately that's the essence of most atheist critics. X or Y has published a critique of Behe, therefore Behe must be in error. There's no evidence Keiths has even critically analyzed Miller's supposed 'rebuttal', he accepts it blindly only because it is consistent with his preconveived ideas.
Comment by Jean — June 29, 2007 @ 12:09 pm
June 29th, 2007 at 12:30 pm
Keiths, when you wrote those words, was it penned wtih the first hand experience of actually having read Behe's book? Did you even have Behe's book when you wrote those words?
Comment by Salvador T. Cordova — June 29, 2007 @ 12:30 pm
June 29th, 2007 at 12:37 pm
Now Miller and then shortly Richard Dawkins. Who else do they have left? My bet is Dawkins (wisely so) will only focus on religion and metaphysics and not even try to touch upon the science or even literature bluff like Miller.
Comment by Salvador T. Cordova — June 29, 2007 @ 12:37 pm
June 29th, 2007 at 12:45 pm
Keiths, I have not read Behe's new book so I'll not comment further on these specifics other than to observe that when speaking of protein-to-protein new active sites, in general, it is something that is argued rather than directly observed. That has significance to me when evaluating statements of those who would use strong language like lies and egregious to describe Behe's position.
Comment by Bradford — June 29, 2007 @ 12:45 pm
June 29th, 2007 at 12:48 pm
keiths
Behe actually spends a lot of time discussing cumulative resistance, for example Malarial resistance to pyrimethamine.
What Miller doesn't say is that where a mutation at 220 is absent mutations at two other positions (144 and 160) are present, making it even less probable.
Furthermore, Behe's analysis is not just theoretical it is consistent with observations. If chloroquine resistance can be conferred by sequential mutation as Miller claims, where is the evidence? And given the astronomical numbers of organisms malaria represents, why doesn't chloroquine resistance independently arise more often?
Comment by Jehu — June 29, 2007 @ 12:48 pm
June 29th, 2007 at 1:27 pm
Jehu, I have a question. Does Behe or anyone else have a theory explainging why the ID carefully crafted drug resistant malaria parasites to kill millions of children? On another thread, Eric assumed this was a theological question, which is a strange assumption, because of course IDism isn't about religion at all. It sounds like the ID is engaging in biological warfare in Africa; what do you think?
Comment by Aagcobb — June 29, 2007 @ 1:27 pm
June 29th, 2007 at 1:35 pm
Aagcobb, those drug resistent parasites have information laden genomes that allow for adjustment to environmental conditions. Do you know of a law of physics that generates symbolic encoding systems?
Comment by Bradford — June 29, 2007 @ 1:35 pm
June 29th, 2007 at 1:36 pm
You are assuming that intelligence is an entity.
Many ID proponents see intelligence as an aspect of the universe, not some kind of external entity who deliberately genetically engineers malaria parasites. So your question really only addresses "externalist" flavors of ID, not EAM and the like.
Comment by mcromer — June 29, 2007 @ 1:36 pm
June 29th, 2007 at 1:41 pm
Aagcobb,
Your statement is a nonsequitor. "IDism isn't about religion" therefore Behe should explain why Malaria exists? That doesn't makes sense. If ID is not about religion then ID shouldn't concern itself with why Malaria exists, not the other way around.
Furthermore, do you posit that because Malaria kills children it must have evolved by RM+NS? Regardless of the huge mathematical barriers?
I could venture several good scenerious why Malaria exists but they would mostly be theological. ID is concerned with identifying design, not explaining who designed it or why.
Comment by Jehu — June 29, 2007 @ 1:41 pm
June 29th, 2007 at 2:10 pm
Hi Jehu,
No, if ID is science, and Behe has scientific evidence that the malaria parasites have been carefully designed to be drug resistent so they can kill more people, that isn't information you simply muse over. If Behe is right, he has identified a terrorist plot to wage biological warfare in Africa, and it is morally incumbent on him to help identify the perpetrators so that strategies to stop them can be developed. OTOH, if the point of ID is just to identify the hand of God at work, then ID critics were right all along.
I'm not aware an of any actual mathematical barriers. Behe's calculations are GIGO. And its not the fact that malaria kills people that leads one to conclude it evolved; its all the evidence that it, and life in general, evolves.
Comment by Aagcobb — June 29, 2007 @ 2:10 pm
June 29th, 2007 at 2:18 pm
No, we don't want to overlook this so let's give you the answer we get in response to the origin of life question. We'll get back to you when the motive is determined. It could take awhile as OOLers have shown.
Comment by Bradford — June 29, 2007 @ 2:18 pm
June 29th, 2007 at 2:38 pm
Aagacob,
Maybe but that is not an issue ID is concerned with.
Tee-hee! You are so clever!
The assumptions behind Behe's calculations are solid and well supported by evidence. If there is some error in them why hasn't anybody pointed them out by now?
Comment by Jehu — June 29, 2007 @ 2:38 pm
June 29th, 2007 at 2:49 pm
"ID is concerned with identifying design, not explaining who designed it or why."
If it has been designed, it was obviously designed to kill people.
As for motive, maybe Satan designed it.
Good as explanation as any other.
Comment by kornbelt888 — June 29, 2007 @ 2:49 pm
June 29th, 2007 at 2:54 pm
Hi Jehu,
Umh, they have. In lots of places.
Comment by Aagcobb — June 29, 2007 @ 2:54 pm
June 29th, 2007 at 2:59 pm
Hi Jehu,
So Behe can tell someone designed the malaria parasites to make them more effective child killers, but he is utterly incapable of developing a single shred of information to help authorities find or stop the terrorists behind it. And you wonder why scientists don't take IDism seriously.
Comment by Aagcobb — June 29, 2007 @ 2:59 pm
June 29th, 2007 at 3:16 pm
mcromer said:
Well, the universe definitely contains intelligence (us). And you can view the process of natural selection as a distributed design process, an intelligence that works by trying things (mutation) and picking out the ones that work (selection). So yes, the universe has an aspect of intelligent design, manifested as natural selection. If that's what you mean by ID then there is no quarrel between it and mainstream science.
Comment by mtraven — June 29, 2007 @ 3:16 pm
June 29th, 2007 at 3:18 pm
Behe should explain why gravity exists as it does too. After all, if you jump from a 10-story high building you're just as dead. Obviously, gravity kills people too, not just Malaria parasites! In fact the whole universe is hostile, radiation kills people, the vacuum of space kills people. Yep, plenty of killin' things out there!
Aagcobb, your non-sequiturs are hillarious!
Comment by Jean — June 29, 2007 @ 3:18 pm
June 29th, 2007 at 3:22 pm
In what way is "mutation" intelligent?
Comment by Jean — June 29, 2007 @ 3:22 pm
June 29th, 2007 at 3:36 pm
Jean:
and then:
Oh the irony! It hurts.
Comment by Raevmo — June 29, 2007 @ 3:36 pm
June 29th, 2007 at 3:45 pm
Jean:
It's not. The combined process of mutation and selection can be thought of as intelligent, in a loose sort of way.
Comment by mtraven — June 29, 2007 @ 3:45 pm
June 29th, 2007 at 3:57 pm
This is very poor terminology.
Almost everyone here agrees that organisms "evolved", the question is whether or not the natural selection of random mutations is able to account for the designs that appear in the course of that evolution.
Comment by mcromer — June 29, 2007 @ 3:57 pm
June 29th, 2007 at 4:03 pm
This is where you take an utterly anthropomorphic viewpoint on what intelligence must be.
Comment by mcromer — June 29, 2007 @ 4:03 pm
June 29th, 2007 at 4:13 pm
The truth is, we have no good theories of what "intelligence" and "creativity" actually are (much less consciousness). If you study what some of the most gifted artists and scientists say, they will usually remark that some of their most brilliant work appeared in a "flash of insight" or even "came from something beyond myself". So it is entirely possible that creativity and insight come from "beyond" the individual, that the universe manifests creativity through the vehicle of individual people, but that the actual creativity and insight are not strictly speaking personal qualities (although certainly some people are better channels for creativity to flow through than others).
It is not a surprise that we have trouble understanding the intelligence in natural designs, since we do not understand how human intelligence and creativity works. So it is entirely possible that the intelligence and creativity that manifests itself through human beings and the intelligence and creativity that manifests through nature and biology have the same source, and that it is something more than simply natural selection of purely meaningless, random inputs.
Comment by mcromer — June 29, 2007 @ 4:13 pm
June 29th, 2007 at 4:32 pm
Hi All,
For what it is worth, of all of the leaders in the ID Movement, Behe is among those I feel somewhat neutral towards (verses distain). At least Behe is trying to be scientific.
He accepts mainstream evolutionary concepts to the point that it appears he is only arguing the details of the mechanisms. Arguing the details of the mechanisms is a major pastime of Evolutionary Biologists. Unfortunately for Behe, he appears to resist offering his own mechanism and the reviewers gleefully take him to task for it. An improbable explanation is better that an unknown (or unknowable) one. Of course it is a well-known secret that Behe probably favors an unstated mechanism.
Even if Behe doesn't have an unstated mechanism in mind, the "GodDidIt" mechanism ("IntelligentDesignerDidIt" mechanism if you prefer) will undoubtedly be assumed by most of the audience, proponents and critics alike. However, I feel that is a violation of NOMA principles. More specifically, it is using a metaphysical construct to try and solve a scientific puzzle. This is the same problem I have with the multi-world interpretation of quantum mechanics.
Obviously, I can't demand that Behe provide a scientifically consistent explanation (I wouldn't want to give Vivid too big of a club) but I can be curious as to why Behe doesn't avail himself of scientific ID hypotheses like EAM or the Penrose/Hameroff model.
He wouldn't even have to embrace them fully, just enough to take that obvious bit of ammunition out of his critic's hands. In case it isn't obvious, from what I can tell, Behe's arguments are very supportive of the Penrose/Hameroff quantum hypothesis.
Comment by Thought Provoker — June 29, 2007 @ 4:32 pm
June 29th, 2007 at 4:40 pm
I see you are citing Mark Chu-Carroll's Super Monkey Ball theory of dynamic fitness landscapes as a refutation of Behe's calculations.
Why is it only small time bloggers are raising the argument? Why do you think that Sean Carroll, Ken Miller, and Jerry Coyne failed to raise the issue? Could it be because Super Monkey Ball evolution is no better than a random walk?
Comment by Jehu — June 29, 2007 @ 4:40 pm
June 29th, 2007 at 5:45 pm
TP
Let me see if I follow you.
Behe's failure to endorse a mechanism will be interpreted as an endorsement of "Goddidit". And this is somehow Behe's problem? The violation of NOMA only seems to occur in the minds of those who would fill in the thought balloons for Behe. How is that his fault?
For one thing the title of the book is "The Edge of Evolution: Finding the Limits of Darwinism". It is not "The Mechanism of Evolution: Finding An Alternative to Darwinism".
Furthermore, do you really think that Behe would soften the critics by latching on to highly speculative hypotheses like EAM or Orch OR?
Comment by chunkdz — June 29, 2007 @ 5:45 pm
June 29th, 2007 at 6:04 pm
Hi Chunkdz,
You wrote…
Actually, I think it would dramatically increase the criticism and probably alienate a large percentage of his defenders.
But he would have me in his corner (and probably Joy).
How many other TTer's would like to see a true battle against that misuse of science from BOTH SIDES of the Culture War?
Comment by Thought Provoker — June 29, 2007 @ 6:04 pm
June 29th, 2007 at 6:11 pm
Aagcobb, to answer you question cleanly, in parts:
…so far so good…
…?? Not so good. I have not finished the book (on chapter 9), but perhaps you can show me where Behe argues this? The central argument of the book is that malarial drug resistance is dependant on Darwinian/unguided mechanisms, so we now have direct evidence of what those mechanisms are capable of. The empirical answer: not very much.
…that's where you really overstep. Behe does not argue malaria were designed to "kill more people."
It is easy to break something; it is a lot harder to fix something. There are many ways to do the first, but only a few ways of doing the latter. Perhaps malaria is something that was not designed to "break" humans, but since there are so many ways to do so, it may have become "broken" itself, and now "breaks" humans. (An out of control process, if you will)
Comment by Atom — June 29, 2007 @ 6:11 pm
June 29th, 2007 at 6:15 pm
Chunkdz:
I can quite firmly say that I would.
Comment by bj — June 29, 2007 @ 6:15 pm
June 29th, 2007 at 6:17 pm
Sorry, previous comment needs to be addressed to TP
Comment by bj — June 29, 2007 @ 6:17 pm
June 29th, 2007 at 6:20 pm
Addendum/Clarification:
"The central argument of the book is that malarial drug resistance is dependant on Darwinian/unguided mechanisms" – so that aspect of their form (the drug resistance) is not the result of design. It is the result of unguided mechanisms at work, in all their (limited) glory.
Comment by Atom — June 29, 2007 @ 6:20 pm
June 29th, 2007 at 6:35 pm
I haven't read Behe's book, but perhaps the Behe-fans on this blog can explain to me how Behe reached this conclusion (from the Nature review):
How does he calculate that?
Comment by Raevmo — June 29, 2007 @ 6:35 pm
June 29th, 2007 at 6:51 pm
Just a guess but I suspect he identified the proteins involved and the codons in each. Knowing the end configuration of the proteins one would need to estimate the starting protein nucleotide configurations and assume the chance of a mutation was equally distributed throughout the proteins. Factor in human reproductive figures and there you go. These things are rough by nature but how would you approach it?
Comment by Bradford — June 29, 2007 @ 6:51 pm
June 29th, 2007 at 7:32 pm
Are you saying you did not notice I was being facetious?
That's not what you said above. And besides, I still don't see how a "combined process of mutation and selection" is "intelligent", even in a "loose sort of way". Define intelligence for us would ya?
I think you're really begging the question, again. You know the output of the evolutionary process, which are highly evolved complex organisms. You also "know" that a "combined process of mutation and selection" must be the cause. So that same "combined process of mutation and selection" _must_ be 'intelligent'. Because if it wasn't, we wouldn't be seeing complex organisms in the first place.
In short, you've simply assumed the truth of your proposition. Poor logic, shame on you.
Comment by Jean — June 29, 2007 @ 7:32 pm
June 29th, 2007 at 8:07 pm
This is an important point that seems to be missed regarding calculations of probabilities. These can be approached in two ways, theoretically and empirically.
It is almost always possible to question whether some mathematical model of reality is realistic. The acid test is to compare with the actual evidence offered by reality.
A major significance of Behe's book is to point out and highlight the objective, observable facts about how relatively little undirected processes have been able to accomplish in the trench warfare of life, such as with diseases like malaria.
Those who question Behe's calculations as being supposedly significantly wrong need to support their alternate claims with an examination of the empirical evidence.
Comment by eric — June 29, 2007 @ 8:07 pm
June 29th, 2007 at 8:33 pm
Aagcobb has repeatedly suggested that Behe's position implies the malaria parasites have been carefully designed to be drug resistent so they can kill more people.
and
Atom is on target. The whole point of The Edge of Evolution is to examine what undirected processes are capable of doing.
Notice that malaria (and therefore its earlier design) existed before the drugs to fight it. Those drugs may have been initially effective against that design. But if it only takes one simple substitution error to escape the effect of a heavily used drug, it becomes easy for that error to be propagated. That is an undirected process propagating an error in reproduction.
This undirected process is not unique or exclusive to any living organism. Darwinists know this, of course, but somehow it seems to be forgotten or assumed to not be true when discussing work such as Behe's.
Perhaps Aagcobb did not intend to create this impression, but his posts tend to give the impression that Behe suggests that the designer is engaging in ongoing re-engineering in order to counteract drugs. That would be a significant misunderstanding of Behe's position.
Someone else wondered about Behe's model. Behe leans toward a front loaded model for design. This was stated as far back as Darwin's Black Box. (The developments since then about the lossy nature of evolution are interesting in this regard.) He is not supposing design intervention at each change.
Comment by eric — June 29, 2007 @ 8:33 pm
June 29th, 2007 at 8:36 pm
This makes me wonder if Aagcobb has yet read through Behe's blog, which includes this relevant response:
p.s. To spell it out more explicitly, it is hugely important for science to gain an objective understanding of the true limits of evolution — an understanding that is not corrupted or distorted by ideological beliefs in what such processes ought to be able to do.
It is only by understanding what these processes can and cannot do that we will understand how to resist diseases like malaria effectively. Believing blindly that evolution can do anything we could hope or imagine or that it might "need" only blinds our own efforts to thwart its tendency to overcome our older approaches.
Comment by eric — June 29, 2007 @ 8:36 pm
June 29th, 2007 at 11:22 pm
Aagcobb wrote:
This is sheer nonsense. There are billions of ways to die. Were they all carefully designed with the intention of killing people? Don't be ridiculous. They are simply facts about the finitude of living organisms.
If I fly into the sun or swim in a shark-filled pool with a bleeding wound in my leg, I'll probably not live to tell the tale. On the other hand, Third World countries have large numbers of living people. And if we in the West were serious about following the teachings of Christ, far fewer of them would die as children.
Atom nailed it:
Comment by stunney — June 29, 2007 @ 11:22 pm
June 30th, 2007 at 12:17 am
Hi bj,
When I asked…
"How many other TTer's would like to see a true battle against that misuse of science from BOTH SIDES of the Culture War?"
You answered…
Thank you for the support.
It is unfortunate that we seem to be a very small minority.
Comment by Thought Provoker — June 30, 2007 @ 12:17 am
June 30th, 2007 at 7:53 am
Raevmo, to Jean:
Jean:
Ow! Ow! Ow!
Comment by keiths — June 30, 2007 @ 7:53 am
June 30th, 2007 at 9:43 am
keiths,
You have not responded to my simple questions.
You claimed Behe made egregious errors. And then I asked you a couple of opening question as part of making you defend your claim. Let me restate them (with a couple typos removed) in case you didn't comprehend:
Is that because you are you making claims about a book you haven't even read?
Comment by Salvador T. Cordova — June 30, 2007 @ 9:43 am
June 30th, 2007 at 12:37 pm
Salvador,
You never learn, do you?
Yes, I own and have read EoE, as well as DBB and the Proceedings of the Wethersfield Institute, not to mention my other ID books. I'm not thrilled about the idea of lining Behe's pockets (and Dembski's, Wells', Woodward's, etc.), but I do find it useful to have copies at hand. Indeed, judging from our past interactions, I've read and retained considerably more about ID than you have about information theory or computer science.
Nevertheless, I would have quoted Miller's review even had I not read EoE, as it fits perfectly with the topic of the thread. Anyone who thinks that Miller has distorted Behe's position is welcome to make a case. It's telling that you and others in this thread have chosen not to, for the most part attempting to draw attention away from Miller's criticisms rather than tackling them head-on.
Your UD post, for example, is an attempt to smear Miller as dishonest, yet you don't address his argument. Why is that, Salvador?
Comment by keiths — June 30, 2007 @ 12:37 pm
June 30th, 2007 at 12:57 pm
Behe writes (EoE, p. 237):
Yet he also writes (EoE, p. 47):
I wonder what Behe would consider to be a "fitting end" for the Agent who designed this agent of such human misery.
Comment by keiths — June 30, 2007 @ 12:57 pm
June 30th, 2007 at 1:05 pm
Well, excuse me, given your comments, I'll have to instead attribute your mis-statements to your inability understand and reluctance to accuretaly represent ID proponents.
Thanks, however, for contributing to the children of Michael Behe college fund.
I did address Miller's literature bluff. It was good for the gullible who have not read Behe's book. And since you have his book, you have even less excuse for repeating Miller's distortions and misrepresentations and outright falsehoods. I presumed you didn't have the books, otherwise you wouldn't have been complicit in promoting Miller's review as a good review. It appears my mistake was giving you too much credit.
Comment by Salvador T. Cordova — June 30, 2007 @ 1:05 pm
June 30th, 2007 at 1:27 pm
Salvador,
Can you refute Miller's argument?
Comment by keiths — June 30, 2007 @ 1:27 pm
June 30th, 2007 at 1:44 pm
Hi All,
I broke down and looked into two books of current interest, Behe's The Edge of Evolution and Paul Davis' Cosmic Jackpot. As unfair as it is, I will do a compare and contrast of these two starting with Paul Davies's book. And to add to the unfairness, I will also be referencing Penrose's Road to Reality intermittently.
If you are reading Cosmic Jackpot on your own and don't want me to spoil the ending, stop reading now because I am going to attempt to summarize Davies' conclusions and how he got there.
I can see why Cosmic Jackpot is popular. It is easy to understand yet deals with tough subjects. And Davies directly deals with them instead of just talking around them. I will have to do a reread, but at this point I don't think there is any hard scientific conflict between Davies and Penrose. In fact, I saw a lot of Penrose in Davies. For example, figure 2 shows how a portion of the Platonic World is projected into the physical world. This is just one leg of Penrose's three legged metaphysical loop. To me, Davies' ideas appear to be a subset of Penrose's ideas. Of course that is a biased point of view. A Davies' proponent would see it as Penrose using Davies' good ideas to promote a particular controversial hypothesis (Orch OR). I don't know what the Truth is so, at this point, I will just accept both viewpoints as multiple, contradictory Truths. Davies does mention Penrose twice in his book; once for Penrose's work (along with Stephen Hawking) on singularities, and a second time for Penrose's argument for the impossibility of computerized consciousness (via pure algorithmic processes). Davies appears to agree with Penrose by pointing out the uncomfortable ramifications if one assumes Penrose is incorrect (The Matrix is all but a certainty).
The concept that the ideas presented in the Cosmic Jackpot are a subset of those presented in Road to Reality isn't a surprise considering we are comparing a 269 page book to a 1100 page book. Also, Davies does something that Penrose does not. Davies gives a reasonably balanced treatment of various hypotheses, even those he disagrees with. I suspect most Intelligent Design proponents will like Chapter 9. They might even be comfortable with Chapter 10 until the bold-faced pronouncement "Quantum Mechanics Could Permit a Subtle Form of Teleology" on page 242. From here until the end of the book, Davies describes a quantum mechanical explanation for everything. It includes positive discussions about casual loops and how the retrocausual paradox isn't a problem in a universe that is internally consistent. In short, this part of the book is chock full of quoteminable material for a Quantum Quack like me.
I was partially inaccurate when I implied that the last 27 pages supported my pet hypothesis. Davies did something I find admirable. He attempted to clearly separate his analysis from his biased interpretation by adding a separate "Afterward:" at the end of his book. In case there is any doubt Davis was being biased here, he framed the discussion of the various positions by starting with "The Absurd Universe".
Here is a summary of everyone's position ala Davies"¦
A. The Absurd Universe "“ "There is no God, no designer, no teleological principle, no destiny. Life in general, and human beings in particular, are an irrelevant embellishment in a vast and meaningless cosmos, the existence of which is an unfathomable mystery."
B. The Unique Universe "“ "This point of view holds that there IS a deep underlying unity in physics, and there is a mathematical theory "out there" that will pull it all together if we are only smart enough to formulate it." (think String Theory)
C. The Multiverse "“ "Modern cosmological models point strongly to the existence of a multiplicity of cosmos domains"¦as a natural and generic feature in which the big band that gave birth to our universe is but one of many (probably an infinite number of) bangs generating a multiplicity of "universes".
D. Intelligent Design "“ "The traditional monotheistic view is that the universe is created by God and designed to be suitable for life because the emergence of sentient beings is part of God's plan."
E. The Life Principle "“ "In this theory, the bio-friendless of the universe arises from an overarching law of principle that constrains the universe/multiverse to evolve toward life and mind."
F. The Self-Explaining Universe "“ "All the forgoing options hit the tower-of-turtles with the exception of [a must-be-what-it-is variant of B], the Tegmark version of the multiverse [under C], and the existence of a necessary God [under D]. Something unexplained has to be accepted as given and the rest of the explanatory scheme constructed on that ad hoc foundation."
G. The Fake Universe "“ "We are living in a simulation, and what we take to be the real world is an ingeniously contrived virtual reality show."
H. None of the Above "“ "Did I leave anything out?"
Davies' inclinations ""¦lie in the directions of E and F, although there are many details to be worked out." Which is pretty closed to the Penrose/Hameroff position, IMO.
Now for Behe. While I was biased by the back and forth exchanges, Behe's book offered little in the way of surprises. Behe only mentions quantum mechanics in a passing reference to its appearance in the early 1900's. Of course there is no reference of Penrose. BTW, he did talk about the apparent malevolence of an Intelligent Designer who intentionally designed malaria. It is obvious he is looking at it from a religious outlook. He even mentions demons.
One thing did surprise me. Behe PROPOSED A MODEL!
It was The Truman Show. This would be Davies' "G. The Fake Universe".
Behe, of course, didn't explore the mechanistic details of this model. Like the location of God's hidden cameras, or who and what are God's employees creating reality.
Please don't go overboard in pointing out I am being unfair to Behe. I know that I am. But it was his choice to focus almost exclusively on limiting evolution without offering a realistic alternative. This is pretty much my complaint about the ID Movement's methods in general.
Davies, Penrose, Hameroff, Joy, tb, myself and others are suggesting we explore a third choice. One that truly follows the evidence yet doesn't try to impose a social preference.
P.S. I apologize to all EoE readers for whom I spoiled the ending.
Comment by Thought Provoker — June 30, 2007 @ 1:44 pm
June 30th, 2007 at 1:48 pm
Keiths, thank you for the reference. (I am on p. 206, so I haven't read that part yet.)
For some context, a little later in EOE on page 238:
So Behe acknowledges this as a philosophical/theological problem, not a scientific one. He also shows that it may be possible the design of the "horrible" feature is really a small part in a larger design, which would bring the greater good on balance (a philosophical answer).
For my part, I stick to my own philosophical answer to this question: it is entirely possible that malaria have become "broken" from their original design and now wreak havoc. For example, just because broken (cancerous) cells kill humans does not mean that our cells were intentionally designed to kill us. I think the same may be the case with malaria. (Or perhaps Behe is correct.)
And there is always the possibility of malevolent secondary designers "hacking" original designs for their own purposes.
Comment by Atom — June 30, 2007 @ 1:48 pm
June 30th, 2007 at 1:58 pm
Addendum:
Furthermore, Behe limits the design to the "molecular machinery with which the parasite invades red blood cells", not to the "drug resistance", as was claimed earlier by another poster. Furthermore, can we show conclusively that malaria were designed to: a) invade red blood cells specifically? b) invade human red blood cells? c) once in a cell, destroy it? d) destroy enough red blood cells to kill or permanently harm a human?
We would need solid evidence showing all points (a-d) were the specific result of intentional design, rather than the result of an out-of-control process, for the dilemma to have force.
Comment by Atom — June 30, 2007 @ 1:58 pm
June 30th, 2007 at 2:13 pm
New, functional protein-to-protein binding can be evolved in a couple of weeks. The source of genetic variation in this case is primarily recombination (not included in any of Behe's calculations), secondarily frameshifting (not included in any of Behe's calculations), and least of all point mutations (the slowest variation mechanism, and the only one that Behe considers).
I agree completely, and it is one that Behe doesn't address very well.
I'm sure that he has, as have you. Can you identify the system to which I refer? Remember, Behe's thesis in this book is not about selection, it's about generation of genetic variation (which was never a part of Darwin's theory, another egregious error by Behe).
Not in this case. The production of new, functional protein-to-protein binding sites can be observed, step-by-step, in real time and is well-understood through direct experimental manipulation of the components.
So can you figure out which system this is? Behe won't help.
No, each different allele makes it MORE probable, even if you assume without any evidence that they have to occur simultaneously.
No, Behe's MO is to list the observations and then ignore critical ones that he just listed in his calculations.
Behe notes the relevant observation that explains why on page 50-51, and then ignores this critical observation in his calculations. Ironically, it has to do with fitness landscapes changing over time.
Comment by JAM — June 30, 2007 @ 2:13 pm
June 30th, 2007 at 2:17 pm
Behe on the malignancy of a designed biosphere:
pp238-239
EoE
Comment by Pez — June 30, 2007 @ 2:17 pm
June 30th, 2007 at 2:49 pm
TP,
You are not being unfair to Behe, but that is only because whomever you are discussing it is not him.
The Truman Show is not his model, he does not propose a Fake Universe (although he dismisses it quite nicely from pages 224-227), he doesn't limit evolution and he does provide a realistic alternative to Darwinism.
Comment by Pez — June 30, 2007 @ 2:49 pm
June 30th, 2007 at 2:51 pm
Atom, Pez –
Behe is leaping to his desired conclusion about Darwin's reasons for denying a designer:
Darwin believed that the Ichneumonidae could not have been designed by a specifically "beneficent and omnipotent God" (note the adjectives), but there is nothing to suggest that he rejected the possibility of a designer altogether on that basis. After all, he had discovered a mechanism that made the designer superfluous, which was reason enough to jettison the idea.
Revulsion may not be a scientific argument, but the Origin certainly is.
Comment by keiths — June 30, 2007 @ 2:51 pm
June 30th, 2007 at 2:57 pm
Hi Pez,
You wrote…
Ok, I will bite. What is Behe's "realistic alternative"
Comment by Thought Provoker — June 30, 2007 @ 2:57 pm
June 30th, 2007 at 3:00 pm
Atom wrote:
Why Charles Darwin Wouldn't Have Done It That Way If He Was The Designer.
Uh-huh. Er, why, Chuck?
And what other, mathematically sound, and logically consistent pathway of generating viable big-but-finite-brained beings do you propose instead, that would rule out pathogens?
Comment by stunney — June 30, 2007 @ 3:00 pm
June 30th, 2007 at 3:02 pm
Atom,
Sorry, I didn't see that you had already referenced the Behe quote.
===
TP,
You may already have heard of it.
Purposeful design.
====
Keith,
Perhaps.
But if you are right that that was not Darwin's reason, Behe is selecting that that reason (whomever holds it) as the indefensible one.
As an indefensible rationale it ought not stand as evidence either, neither in an argument, nor a book which is an extended argument.
Comment by Pez — June 30, 2007 @ 3:02 pm
June 30th, 2007 at 3:11 pm
Hi Pez,
You wrote…
You get points in my book for using the word "Purposeful".
I had borrowed my copy of the Edge of Evolution so I don't have it handy. However, I can get it again.
Can you tell me some page numbers where Behe outlines his model for Purposeful Design? It was my recollection that Behe's explaination of this was towards the end of the book where he said something like…
"Truman knows something is not right, his gut instincts and the many little clues are contradictory." [paraphrased from memory]
Comment by Thought Provoker — June 30, 2007 @ 3:11 pm
June 30th, 2007 at 3:16 pm
Hi TP,
What can I buy with my points?
I didn't choose the word 'purposeful', that is how Behe discusses design.
And what do you mean by 'model'?
How does your term 'model' qualify the statement that Behe proposes a realistic alternative to Darwinism?
Comment by Pez — June 30, 2007 @ 3:16 pm
June 30th, 2007 at 3:24 pm
Quote-mining. It's a private letter, not a scientific argument. Darwin's thoughts are much more subtle than what Behe allows. And Behe misrepresents Darwin's conclusion.
So Darwin looks to laws designed by an omniscient Creator, considers his views not at all necessarily atheistical, thinks it may be too profound for the human intellect to understand, allows each man hope and believe what he can, and that he himself is bewildered by the contradictions in the human condition.
Comment by Zachriel — June 30, 2007 @ 3:24 pm
June 30th, 2007 at 3:37 pm
Hi Pez,
You asked…
What you might call Evolution's "just so" story is a model. It is internally consistent, even if the assumptions are incorrect and don't match the evidence.
"God Did It" is a model. God is the mechanism that explains everything since God is omnipotent by definition.
"The Matix" is a model. Nothing we call "real" is real. It is all computer-generated and we have no way of knowing what the REAL reality is like.
EAM is a model. Matter, itself, is conscious and manipulates reality.
Here is a model I offer as a possible ID alternative based on the Penrose/Hameroff model. All quantum effects (including those in microtubules) are interconnected in the space-time continuum forcing consistency.
Did you check the end of Behe's book where he talked about the Truman Show? My memory/understanding may be faulty. But it appeared to me that Behe was making some kind of attempt to provide a model.
The Truman Show had a Purposeful Designer that created and ran Truman's world.
Comment by Thought Provoker — June 30, 2007 @ 3:37 pm
June 30th, 2007 at 4:10 pm
Hi Zachriel,
Now why did you have to go a burst their bubble on that one?
Behe had to do something to not appear to embrace Darwin too much considering how Behe agreed with practically all of Darwin's theories, including Common Descent. Behe even wrote a paragraph acknowledging Darwin's positive contribution to science.
Darwin's statement
"...the more I think the more bewildered I become"brings up a conversation I just finished with my sixteen-year old son. My son had a straight-forward answer…"Don't ask the question in the first place!"
I had to admit that 99.9% of the population probably shares his attitude. However, we still managed to continue the conversation where he was impressed that these "simple" questions are tough even for his father and all the authors in these books I have been reading.
Paul Davies has two pictures of the turtles all the way down. My son already knew about the turtle dilemma from earlier conversations, so at one point he asked "Yes, but what is the last turtle standing on?" Paul Davies has a picture of the world on the back of an elephant on the back of turtles on the back of one giant SUPER TURTLE. He laughed. I think he might even read the book now.
Comment by Thought Provoker — June 30, 2007 @ 4:10 pm
June 30th, 2007 at 4:17 pm
So Darwin looks to laws designed by an omniscient Creator, considers his views not at all necessarily atheistical, thinks it may be too profound for the human intellect to understand, allows each man hope and believe what he can, and that he himself is bewildered by the contradictions in the human condition.–Comment by Zachriel
Darwin was a Creationist!? Whoa! The implications boggle!
Comment by Rock — June 30, 2007 @ 4:17 pm
June 30th, 2007 at 4:20 pm
New, functional protein-to-protein binding can be evolved in a couple of weeks. The source of genetic variation in this case is primarily recombination (not included in any of Behe's calculations), secondarily frameshifting (not included in any of Behe's calculations), and least of all point mutations (the slowest variation mechanism, and the only one that Behe considers).
I agree completely, and it is one that Behe doesn't address very well.
I'm sure that he has, as have you. Can you identify the system to which I refer? Remember, Behe's thesis in this book is not about selection, it's about generation of genetic variation (which was never a part of Darwin's theory, another egregious error by Behe).
Not in this case. The production of new, functional protein-to-protein binding sites can be observed, step-by-step, in real time and is well-understood through direct experimental manipulation of the components.
So can you figure out which system this is? Behe won't help.
No, each different allele makes it MORE probable, even if you assume without any evidence that they have to occur simultaneously.
p(A and B)=p(A) x p(B)
p(A or B)=p(A) + p(B)
No, Behe's MO is to list the observations and then ignore critical ones that he just listed in his calculations.
In the multiple resistant alleles that have been observed.
Behe notes the relevant observation that explains why on page 50-51, and then simply ignores this critical observation in his calculations. I don't know whether he was being negligent or deceptive in doing so. Ironically, it has to do with fitness landscapes dramatically changing over time, in this case mere weeks.
Jehu, do you realize that when Behe notes that CQ resistance has only arisen 10 times, he is equivocating? The number 10 refers to population events and he is presenting it as the number of genetic events.
Comment by JAM — June 30, 2007 @ 4:20 pm
June 30th, 2007 at 4:36 pm
TP,
Thanks for providing examples of what you consider to be models.
As I suspected, these ideas of 'model' do nothing to disqualify purposeful designl. At the same time, however, they do nothing to demonstrate what you mean by 'outlines his model' at the end of this chain:
TP: Behe provides no realistic alternative to evolution (sic).
Me: Yes he does, it is purposeful design.
TP: "Can you tell me some page numbers where Behe outlines his model for Purposeful Design?"
What is it that needs outlining?
Behe's model is one in which a mind, a purposeful, agent, has specified certain aspects of the universe/biosphere and that there are instances in which we can discern that this specification took place.
Yes, I read the entire book and no, the Truman Show is not Behe's model.
It is a metaphor for how contingency, chance and will can continue to act in a designed universe – how the raw observation of the design behind our universe need not impact the control we have over our daily lives.
Comment by Pez — June 30, 2007 @ 4:36 pm
June 30th, 2007 at 4:50 pm
Hi Pez,
I will certainly reread it now with this in mind.
I have to admit, I never considered that Behe was suggesting we have enough control and will to detect the Purposeful Designer's manipulation contrary to his/her intent to hide that from us.
However, you still haven't suggested a particular section of the book where Behe provides an alternative explaination beyond using the term "Purposeful Design". Would it help if I asked for mechanisms instead of a model?
Comment by Thought Provoker — June 30, 2007 @ 4:50 pm
June 30th, 2007 at 5:07 pm
No, I don't think so.
Having escaped the mechanistic/clockwork view of nature I think the word 'Mechanism' is an inappropriate word choice, and, at least, does nothing to clarify what you are asking.
It would help if you defined 'model' to demonstrate why your question has not been answered.
You provided examples of models – 'just so stories', 'God did it' and the 'Matrix'.
Purposeful design is a model in exactly the same way, but you still say I am not providing a model.
What is it you are looking for? What is it that you think will define science in this instance? Why is purposeful design not realistic? How does following the evidence where it leads independently of imposing a social preference disallow purposeful design from your category of 'model'?
Comment by Pez — June 30, 2007 @ 5:07 pm
June 30th, 2007 at 5:23 pm
TP,
ps.
What was this supposed to mean?
You aren't half as cute as you seem to think you are, so why not just try having a conversation?
Comment by Pez — June 30, 2007 @ 5:23 pm
June 30th, 2007 at 5:27 pm
Hi Pez,
I am sorry that my request was too confusing and/or too difficult.
Repeating a single phrase over and over does not help a reader understand how everything fits together. I call an explanation of how everything fits together, "a model".
The last chapter in EoE is titled "All the World's a Stage". This title suggests a model to me. (It was Shakespeare's model of reality).
link
The last chapter is where most scientific books summarize findings into a consistent model. That is what I understood Behe was doing in this chapter where he used The Truman Show as an explanatory vehicle.
However, I will reread that chapter with what you have said in mind.
Comment by Thought Provoker — June 30, 2007 @ 5:27 pm
June 30th, 2007 at 5:37 pm
Hi Pez,
You asked…
I thought we were.
A common description of me is "arrogant".
Comment by Thought Provoker — June 30, 2007 @ 5:37 pm
June 30th, 2007 at 5:41 pm
Your request isn't confusing or difficult because it isn't a request. It is a challenge for which there is no appropriate answer and for which you will accept no answer.
Now, when repeatedly asked what you mean by 'model', you give a version of a definition where before when I asked you gave some examples.
"An explanation of how everything fits together":
Let's limit this to biology, as per Behe.
Certain aspects of life are best explained by reference to purposeful design.
The purposeful design is the product of a willful agent making choices or specifications.
This is evidenced by the fact that the combination of chance and law do not provide good explanations for certain features whereas purposeful agents are known to have the ability to bring such features into being.
What's unrealistic about this?
Why isn't this a model?
Why do you require a 'mechanism'?
Comment by Pez — June 30, 2007 @ 5:41 pm
June 30th, 2007 at 5:45 pm
re: Your (self) description:
I know it is.
And it is nothing to be proud of or try to live up to.
Comment by Pez — June 30, 2007 @ 5:45 pm
June 30th, 2007 at 5:49 pm
It seems to me that JAM has done a convincing job in debunking Behe's analysis of plasmodium resistance, but I'm sure not all here will agree with my assessment. I asked before if a Behe-fan could provide me with the details of Behe's calculation of the crucial 10^-20 number and why this implies that it would take humans 10 million times 100 million years to evolve a comparable adaptation, but no luck so far. Anybody? Let's discuss the actual calculations and the underlying assumptions and population genetic models. In the mean time I've ordered the book myself (Behe's numerous kids have to eat too right?), but I'm impatient (it'll take at least a week for the book to arrive) and I want to know now.
Comment by Raevmo — June 30, 2007 @ 5:49 pm
June 30th, 2007 at 5:59 pm
TP,
The last chapter includes sections on consilience of results from various branches of science, Behe's reference to fine-tuning in laws, properties details and events, a reflection upon design and OOL, how deep design goes into the planning of life, a rejection of multi-world explanations, a discussion of whether or not the designer needs to be supernatural, whetehr or not the designer needs to 'intervene' to realize the purposes, demarcations of science, implications of inferring teleology, implications of inferring ateleology, the aforementioned rejection of the design inference because of squeamishness, and, finally, the implication of the design inference, re: The Truman Show (ie: are we just puppets?).
So, yes, it is a summary of Behe's findings. Your discussion thus far has been based upon the final page of the book.
Comment by Pez — June 30, 2007 @ 5:59 pm
June 30th, 2007 at 6:16 pm
Raevmo,
You'll be disappointed. Strangely, there's room for an entire page devoted to a callout box explaining scientific notation, but there's no step-by-step derivation of the 10E-20 number.
Therefore, I predict that you will be met with great reluctance to discuss the calculations among Behe's acolytes.
Pez, the term "findings" has a very clear meaning among scientists: it means data, and is never used to describe anyone's interpretation of the data, theirs or anyone else's. It doesn't refer to what you glean from other people's findings. So, to me, you are claiming that Behe published new data in this book, and I sure don't recall seeing anything of the sort. Is that what you mean?
Comment by JAM — June 30, 2007 @ 6:16 pm
June 30th, 2007 at 6:18 pm
Hi Pez,
You stated…
I requested that you point to page numbers in Behe's new book, Edge of Evolution, where Behe provides an alternative to what you and he refer to as "Darwinism".
It may be a "challenge" if it is not there. I think the last chapter is Behe's alternative model. You, apparently, are uncomfortable with that.
To this, you have offered that YOUR position is…
And then ask…
If I offered my opinon on these questions, I would expect (because it has happened before with other people) that you will ask why I "require" a mechanism and get indignant about my unreasonable "demands".
Therefore, I will cut this short by pointing to THIS LINK where I have offered my model complete with mechanisms. (see the six chapters in the comments).
If you want to point me to an alternative model that includes an equivalent amount of details, I will gladly read it.
"All the world's a stage,
And all the men and women merely players:
They have their exits and their entrances;"
While I think Behe's overall model a similar to Shakespeare's, I will reread the last chapter with what you have said in mind.
If you wish to discuss my Paul Davies review, I will gladly do that. Here is a link.
Comment by Thought Provoker — June 30, 2007 @ 6:18 pm
June 30th, 2007 at 6:20 pm
JAM,
His book is a popular treatment of the body of available evidence, not a scientific paper on a laboratory experiment.
Behe finds that by looking at the available information he can determine certain probabilites and make certain inferences. That is what he finds, and those are his findings.
Comment by Pez — June 30, 2007 @ 6:20 pm
June 30th, 2007 at 6:26 pm
Pez,
If it truly covers the body of available evidence on the generation of Darwinian variation, why did Behe choose Plasmodium, a system in which we are incapable of examining mutations immediately after they occur, because we have yet to figure out how to culture the sucker?
Why did Behe not explore the vast body of available evidence from far more tractable systems?
How do you know that he looked at all the available information and didn't cherry pick?
Would you be willing indulging Raevmo and going through the assumptions underlying Behe's alleged determination of the 10E-20 probability?
I don't think he merely found the data he chose to put in the book. I think he rejected enormous amounts of far more relevant data.
Comment by JAM — June 30, 2007 @ 6:26 pm
June 30th, 2007 at 6:29 pm
tp,
No, I am not.
What I told was that the last page (and a quarter, perhaps) did not contain his model.
If you accept model as you've described then the last chapter does, indeed, provide the model – but over several sections, and not in the Truman Show analogy.
Perhaps so.
Then again, perhaps your opinion is required if you are going to say that Behe doesn't offer a reasonable alternative.
I am not particularly interested in your review of Davies or Penrose, or even Wheeler, whose retrocausation Davies was discussing in his 1983 book God and the New Physics, right now, thanks.
If you think that an alternative must be mechanistic, or that only if it is then can it be considered reasonable (or science) then you are welcome to your opinion.
Comment by Pez — June 30, 2007 @ 6:29 pm
June 30th, 2007 at 6:34 pm
Pez:
If you are convinced by Behe's arguments, then surely you understand Behe's calculations and you can explain how he arrived at his 10^-20 number and why it implies that humans could never have evolved a similar adaptation in the time they have been around. I'm looking forward to your explanation. Don't be shy now.
Comment by Raevmo — June 30, 2007 @ 6:34 pm
June 30th, 2007 at 6:37 pm
JAM,
I imagine Behe chose drug resistance in malaria and HIV because we have huge populations to work with and have investigated them for some time. I also guess there is a little bit of an answer to "you don't believe in evolution? What about drug resistance then?"
I'll have another look at it the numbers and see if, as a reader of this popular work, I can shed any light on it.
Very likely, however, I will stick to the things that I can discuss and Raevmo's concern will have to be left to professional biologists or even mathematicians to do much with it.
That's you, right?
Comment by Pez — June 30, 2007 @ 6:37 pm
June 30th, 2007 at 6:38 pm
Thanks for your concern over my social skills Raevmo.
I'll see what I can do for you.
Comment by Pez — June 30, 2007 @ 6:38 pm
June 30th, 2007 at 6:46 pm
Raevmo,
First question:
Where does Behe get his number of 10^20?
This is on page 57 and he actually is citing Nicholas White of Mahidol University in Thailand.
(Hayton, K. and Su, X.Z. 2004. Genetic and biochemical aspects of drug resistance in malarial parasites. Curr. Drug Targets Infect. Disord. 4:1-10)
Of course, I've not looked into this publication, but I'm sure you and JAM will.
Comment by Pez — June 30, 2007 @ 6:46 pm
June 30th, 2007 at 6:50 pm
Pez:
Thank you Pez, I appreciate it. I wasn't really worried about your social skills though, I'm sure you're doing just fine in that respect (it's us scientists that often lack in the social skills). But if you have to rely on the say-so of biologists and/or mathematicians, why do you believe Behe's argument in the first place? Judging by the reviews I've seen so far, Behe's scientific peers reject his arguments as unsound. Why don't you believe his educated critics? Could it be that you simply wish to believe Behe because he shares your philosophical outlook on life?
Comment by Raevmo — June 30, 2007 @ 6:50 pm
June 30th, 2007 at 6:57 pm
Pez:
Thanks for the reference. I will try to have a look (but I may not have access to that journal).
Comment by Raevmo — June 30, 2007 @ 6:57 pm
June 30th, 2007 at 7:07 pm
Raevmo,
The second part of your question is answered on page 60:"why it implies that humans could never have evolved a similar adaptation in the time they have been around. "
The population in the human lineage over the last 10 million years has averaged roughly a million individuals (citation omitted).
Giving the generation time of a conservative ten years we have a trillion creatures in the line of descent.
"The ratio of humanoid creatures in the last ten million years to the number of parasites needed for chloroquine resistance is one to one hundred million."
It takes this line ten million years to produce one trillion reproductive events.
If the odds were one in a trillion we would have achieved the adaptation in ten million years. If they were one in ten trillion we would achieve it in ten million times ten years. One in one hundred trillion would take ten million times one hundred years – and so on, until you reach 100,000,000 years times ten million
Comment by Pez — June 30, 2007 @ 7:07 pm
June 30th, 2007 at 7:14 pm
Raevmo,
1) Yes, it's true, I am biased.
2) Yes, it's true that, like everybody else (your scientific selves included), my information is primarily secondhand and authoritative.
3) Behe does not share my philosophical outlook on life, however his work does support my prejudices in many ways.
4) Scientists and mathematicians have long been assembled against the probability of RM + NS doing what evolutionary biologists say it can do.
5) Is it possible that since over 80% of evolutionary biologists have a philosophical outlook on life which is opposed to Behe's they might be predisposed to dismissing his work?
6) Why is it necessary that I be able to analyze the biological features myself to argue against such positions as The Truman Show represents Behe's model?
7) Why didn't JAM, a professional biologist who has read Behe's book give you the information I just did?
Comment by Pez — June 30, 2007 @ 7:14 pm
June 30th, 2007 at 7:17 pm
Thank you Pez. I see now how Behe gets from 10^-20 to 10^15 years for humans to evolve a similar adaptation. 10^15, that's a lot longer than the universe supposedly has existed. So now the question is whether the 10^-20 estimate is really justified. Behe referred to a paper that you kindly supplied upthread. I have found the paper and will read it. I'll get back to you.
Comment by Raevmo — June 30, 2007 @ 7:17 pm
June 30th, 2007 at 7:31 pm
TP:
Um… you don't seem to have grasped the gist of EAM either, TP. From ISCID:
Moreover, as Turner explains (it's his model, after all), adaptation and evolution are intentional processes, neither accidental or coincidental to organisms as hapless blobs of matter shaped by outside forces.
As I have always understood it – from Turner – EAM does not consider matter itself to be vital or conscious. It considers life forms to be vital and conscious (along a quantitative as well as qualitative continuum), thus allowing organisms to be the agents of their own intelligent design and their species' adaptive evolution over time.
I don't mind if you want to add your own bling and flourishes to other people's models in order to claim the result as your own, but you haven't made this distinction with EAM. You've simply inserted your own concept of 'conscious matter' to the EAM model as if it were there all along. It was not.
Matter is not alive – life forms are alive. There is a strong aspect of vitalism to the EAM model. You should not be changing it to suit your own purposes while still claiming it's EAM.
Just clarifying for the record. Now… carry on!
Comment by Joy — June 30, 2007 @ 7:31 pm
June 30th, 2007 at 7:31 pm
But we can't culture them worth a hoot, so you can't get experimental data close to the step Behe claims to be measuring. Any examination of clinical isolates only occurs after loads of selection on a roller coaster, constantly-changing fitness landscape.
That doesn't make sense, since there are so many other cases of drug resistance for which there are good experimental models. Behe is citing ecological data.
Why would professionals be required to determine how Behe derived a number in a book aimed at the lay reader?
Done. Would you like a PDF? It contains no derivation of the 10E-20 number, so it doesn't help. It's just a review, so it doesn't contain the actual evidence, either. Scientists rarely cite reviews in matters of disagreement.
Would it be accurate to say that Behe doesn't bother to lay out the calculation of his 10E-20 probability for his readers, Pez?
If the 10E-20 probability has no basis in reality, then the other stuff isn't really relevant, is it?
Comment by JAM — June 30, 2007 @ 7:31 pm
June 30th, 2007 at 7:34 pm
Hi Pez,
You wrote…
Um… I think you missed something.
I think it strengthens Behe's argument for him to offer a mechanistic model. I was giving him credit for at least trying. An attempt at a model is better than no model at all.
I was giving Behe the benefit of the doubt.
However, I will be reevaluating that based on your suggested interpretation of the last chapter.
Comment by Thought Provoker — June 30, 2007 @ 7:34 pm
June 30th, 2007 at 7:34 pm
Pez:
And so am I.
Aha. He's a catholic and he believes in common descent. So I'm guessing you're protestant and/or you don't believe in common descent. Correctemundo?
Absolutely. But Behe still has to get his facts and logic straight, and the question is if he really did. I don't think so, but I'll have to look more carefully.
I don't know about the Truman Show argument. But I'm still left wondering why you support Behe's argument if you don't grasp the biological details. You're basically saying you take Behe's position on faith.
Dunno. Maybe she wants to let the proponents of Behe speak for themselves?
Comment by Raevmo — June 30, 2007 @ 7:34 pm
June 30th, 2007 at 7:35 pm
Pez, I'm a scientist, but not even close to being an evolutionary biologist. With whom in your dichotomy have I assembled?
Comment by JAM — June 30, 2007 @ 7:35 pm
June 30th, 2007 at 7:35 pm
Raevmo,
Here are some passages from the book that convey both the essence and the details of Behe's argument:
From p. 57:
And on p. 59 (note the math error):
On p. 60:
And wrapping it up, on p. 61:
The argument depends on an equivocation on the word "complexity".
More on this in a future comment.
Comment by keiths — June 30, 2007 @ 7:35 pm
June 30th, 2007 at 7:43 pm
Hi Keiths,
You had a typo on one "is"
I hope people appreciate the fact that you are willing to retype this.
Unfortunately, you are making me feel guilty for holding back on my criticism of Behe.
Like I said, I give Behe some credit for at least trying.
I will tell you what. I will see how you do and then I will present the "Hey, Behe, there are more than two dimensions in the fitness landscape" argument.
Ok?
Comment by Thought Provoker — June 30, 2007 @ 7:43 pm
June 30th, 2007 at 7:50 pm
TP wrote:
Thanks. I've fixed it.
Comment by keiths — June 30, 2007 @ 7:50 pm
June 30th, 2007 at 8:39 pm
Hi, keiths,
It seems that Behe is
sayingimplying that the number of players and the time required are directly proportional. So if the one is decreased by a certain factor, the other must be increased by the same factor to keep all things equal. Why is this an error? What exactly is the error?Edit: then again, was this the math error you were referring to?
Comment by AnaxagorasRules — June 30, 2007 @ 8:39 pm
June 30th, 2007 at 9:18 pm
JAM,
Re: A link to the paper? – sure, thanks.
Re:
This is correct, he did not plug the numbers into the equation for us. He tells us that White points out how the calculation is done, and he gives us the result.
Is there a disagreement over how many people are treated with chloroquine, how many cases of malaria there are, or how long chloroquine has been in use?
Re:
It's not a dichotomy, is it?
===
TP,
Um.
No I didn't miss anything.
You missed that this was not Behe's model.
===
Raevmo,
Close enough.
5) Is it possible that since over 80% of evolutionary biologists have a philosophical outlook on life which is opposed to Behe's they might be predisposed to dismissing his work?
Sounds good. Thanks.
===
Keith,
I didn't notice the math error.
Could you point it out?
Comment by Pez — June 30, 2007 @ 9:18 pm
July 1st, 2007 at 3:27 am
Anaxagoras Rules, Pez,
Behe calculates the time required for CQ resistance to develop, given a hypothetical reduction in the average parasite load from a trillion cells to a million. The correct answer is that it would take a million times as long as it currently does, but Behe claims it would take only a million years.
Given that CQ resistance has arisen less than 10 times in the last 50 years, the average latency is more than five years. Multiplying this by a million gives an expected time of more than five million years in our hypothetical case. Even taking the increasing population into account, the number is considerably more than a million years.
Fortunately, this particular error is isolated. Behe doesn't carry it forward into his later calculations (which are problematic enough as it is).
Comment by keiths — July 1, 2007 @ 3:27 am
July 1st, 2007 at 3:35 am
The most obvious error in Behe's argument is that he equivocates on the meaning of "complexity."
Here he essentially defines complexity as improbability (EoE, p. 60):
The conclusion of his argument reads as follows (EoE, p. 61):
Keeping in mind that complexity equals improbability by his definition, his conclusion amounts to saying that rare mutations occur rarely, and even more rarely when the number of trials is reduced. True, but hardly informative.
Here's how he'd like for you to interpret his conclusion (in my own words):
Chloroquine resistance is a simple trait, requiring only a couple of point mutations. Yet there hasn't been enough time for even a single mutation of equivalent complexity to arise in the humanoid line. Humans are full of traits that are more complex than chloroquine resistance. Darwinian processes could not have produced these traits; therefore they must have been designed.
Behe confirms that my interpretation of his argument is correct, and even extends it to all mammals (EoE, p. 61):
The problem is that this argument uses the concept of complexity in two different ways: the usual way, in which a complex phenomenon is something intricate and involved, and Behe's idiosyncratic way, in which complex simply means improbable.
Behe either does not notice the equivocation, or fails to acknowledge it. Either way, he doesn't even attempt to establish that events that meet the first definition of 'complex' also meet the second. His argument therefore fails.
Comment by keiths — July 1, 2007 @ 3:35 am
July 1st, 2007 at 3:41 am
Sorry, I'd have to send you the PDF. The link wouldn't work for you.
He didn't give us the equation, either. It's pretty sad that he can spare a whole page to introduce us to scientific notation, but nothing at all for the calculation of this important probability.
No, you're not even close. He tells us that White offers a number. The issue is whether that number represents the mutation rate or it really represents the results of mutation filtered (i.e., attenuated) through thousands of generations of rapidly-changing, even reversing, selection.
None of those. The disagreement is over whether Behe's calculation has anything to do with measuring the raw variation generated by mutation.
If it's not, what is it? And where do I fit in it, dichotomy or not?
Here it is again:
As a scientist who is not an evolutionary biologist, if your claim is true, I must be assembled with other scientists and mathematicians against RM+NS. However, that's not remotely close to being true.
Is my interpretation incorrect?
Comment by JAM — July 1, 2007 @ 3:41 am
July 1st, 2007 at 4:10 am
I read Behe's argument (if accurately presented in this thread, my not having read his book) like this:
The variety of intricate genetic structures in humans is unlikely to have evolved by Darwinian mutational processes in the amount of time available to hominid life, given what we know from observation of mutations involved in chloroquine complexity clusters. The idea that it did so is thus improbable.
I don't see any equivocation there.
The argument has this form:
1) Observed rate of simple mutational change for species A is R
2) Species B has a far more complex mutational history than does species A
3) But species B's mutatational history almost certainly could not have generated its observed genetic features if the historical rate of its mutational change was anywhere close to R
4) Therefore, its historical rate of mutational change must have been much greater than R
5) But there is no plausible Darwinian mechanism that would have resulted in species B's historical rate of prior mutational change being greater than R to the requisite degree.
Therefore, species B's observed genetic features almost certainly could not have resulted solely from the operation of known Darwinian mechanisms in its evolutionary history.
Comment by stunney — July 1, 2007 @ 4:10 am
July 1st, 2007 at 5:05 am
JAM,
Too bad about the paper.
Whether or not this is a raw mutation rate does seem somewhat ambiguous. However, since it is an "estimate" of "roughly" 10^20, and it is an expression derived from observed populations (and not based upon theory), then likely the ambiguities of strong negative selection in the wild versus strong positive selection in the observed and treated populations have been accounted for. Also, the fact that instances of resistance can be traced to perhaps as few as four different events (and less than ten) suggests a rarity of mutations and a strong advantage to those protozoans which acquired it.
So what's the problem with his citing a review article if none of the variables presented in it would be in disagreement? Before ID-critics took umbrage, was there disagreement over the value of 10^20? Was this number highly contested?
No, you're not even close.
The term 'assembled' has a very clear meaning among real people.
Since when does the assembly of scientists and mathematicians imply an exhaustive collection? Just because scientists and mathematicians assemble does not mean that all scientists and mathematicians assemble. Scientists can assemble without including you.
For example, have you never heard of an assembly of citizens in which not all of the citizens were present?
Comment by Pez — July 1, 2007 @ 5:05 am
July 1st, 2007 at 11:41 am
By the way, keiths, I don't agree with you on the supposed math error.
You and Behe agree that the difference is one hundredfold but you want to apply the realistic, observed rate of less than ten events observed in fifty years, while Behe used the derived rate of one mutation per year. This value comes from the paragraph preceding the one you quoted on page 59.
On the other hand, Behe is using one mutation per trillion billion cells for the example rather than the cited mutation per hundred billion billion cells.
Why did he do this? What am I missing on that – anybody?
Comment by Pez — July 1, 2007 @ 11:41 am
July 1st, 2007 at 12:25 pm
Well, the numbers are contradictory, so there's clearly an error there.
It doesn't matter for the purposes of this thread. Behe's argument fails, for the same reasons, even if the math error is corrected.
Comment by keiths — July 1, 2007 @ 12:25 pm
July 1st, 2007 at 12:46 pm
On page 75, Behe quotes from the Hayton and Su paper twice. The first quote can be found on page 5. Here is the second quote:
Note 17 refers to the Hayton et al paper. Yet, this quote cannot be found anywhere in that paper.
Comment by KC — July 1, 2007 @ 12:46 pm
July 1st, 2007 at 1:17 pm
There's no such thing as "Darwinian mutational processes," stunney. Darwin didn't know a thing about mutations. Darwin merely noticed the existence of variation.
Are the mutations involved in CQR detected before or after hundreds, if not thousands, of rounds of selection with the alternating presence and absence of CQ?
If one is only making observations after selection, how can one credibly claim to be looking at the mutation rate?
You're ignoring the fact that the data are obtained after selection. In the mosquito, which Plasmodium grow better: CQR mutants or wild-type?
No, sorry, Behe hasn't come close to observing a rate of simple mutational change. We can only see it after it is filtered by selection.
Why do you think Behe chose this, anyway?
Behe is doing his best to make it ambiguous for his lay audience. In reality, it's not ambiguous at all.
But it's not based on observation of mutation rates, which are observable in many other organisms, but not this one. Therefore, any attempt to portray it as a measurement of mutation rate is sophistry.
How do you figure that?
Why does it not suggest a rarity of selection conditions to deplete the wild-type Plasmodium sufficiently so that they do not overwhelm the CQR mutants in the mosquito stages of the life cycle?
Because he's been exposed under oath as being intellectually lazy in not reading the primary literature, for starters (see the Dover transcripts). Scientists point to review articles as a way to help a reader get up to speed, not as a way to cite data critical to the matter at hand.
This is the first time anyone's come up with such a low probability. Guess what people who measure mutation rates BEFORE selection come up with, Pez!
Yes, it does.
It is explicitly inclusive without any qualifiers. Are you claiming that I am an outlier among scientists?
Why use the inclusive, unqualified "scientists" when we know that in reality, it's a ridiculously tiny minority?
Comment by JAM — July 1, 2007 @ 1:17 pm
July 1st, 2007 at 2:12 pm
JAM wrote:
This is about as pedantic as saying that there is no Marxist theory of the Bolshevik Revolution because it happened in 1917 and Marx died in 1883.
Perhaps because one thinks of mutation rate and selection as being sufficiently causally independent processes in this case for the purpose of one's argument.
No, matey, I'm not ignoring it. I'm interpreting what Behe is arguing. That's why I said: "I read Behe's argument (if accurately presented in this thread, my not having read his book) like this" and "The argument has this form". But sure, maybe Behe's ignoring it.
I'm not sure what you mean by 'grow better'. But if it's what I think you mean, I'd guess wild-type.
You're misinterpreting the word 'simple' as I use it in the reconstruction. It does not mean 'unfiltered by selection'. It means 'not very complex'.
Probably because he thought it was significant. But you'd have to ask him. I merely tried to reconstruct his argument because it did not seem to involve equivocation on the term 'complex', as had been alleged.
Comment by stunney — July 1, 2007 @ 2:12 pm
July 1st, 2007 at 4:04 pm
JAM,
This is a good point.
What is the evidence from the uptake and transfer from mosquitoes?
Is it?
Then I am misled by Behe's reference to Nicholas White.
Explicitly exclusive it certainly is not.
Try Googling "scientists assembled"
http://www.google.com/search?c...
and see if the presence of every scientist on earth is required (explicit or implicit), or if every field is represented.
When baseball fans assemble to honour a team do ALL baseball fans assemble?
When Darwin carefully assembled data did he assemble ALL the data?
When citizens assemble to protest to ALL the citizens protest?
When scientists assemble to discuss global warming do ALL scientists assemble?
When world leaders assemble to discuss an issue do ALL the leaders in the world show up in one place?
We're going to need some awfully big conference rooms.
1) The term is not inclusive. To be inclusive would require the qualifier "all".
2) My use wasn't wasn't unqualified – it was qualified by the activity of "being against the probability of RM and NS doing what evolutionary biologists claim ".
Just as "citizens assembled to complain about spending cuts" is qualified by the type of people being assembled.
3) If "we know that in reality, it's a ridiculously tiny minority" then why pretend that I mean it to be all inclusive?
Your behaviour on this ridiculous point speaks poorly of you – as it does in your "nobody says "Darwinism … " Darwin didn't know about mutations, etc … " complaints.
Comment by Pez — July 1, 2007 @ 4:04 pm
July 1st, 2007 at 11:22 pm
Not at all. Your complaint isn't even remotely analogous. It has nothing to do with the date; it has to do with content.
Whether they are causally independent doesn't matter. What does matter is that one is filtered through the other, and Behe tries to pretend that no filtering has happened.
Fair enough.
He's definitely ignoring it.
You'd be right, and Behe ignores it, despite mentioning the phenomenon in human hosts.
The word 'simple' isn't the relevant one. The word 'mutational' is the issue. It's simply not an accurate measure of mutational change, and unless Behe is completely deluded, he knows this.
——-
Why, thanks!
I'd suggest looking at the papers cited in the review Behe cited in his literature bluff:
Host defense mechanisms contribute a major antiparasitic effect, with which any spontaneously generated drug-resistant mutant malaria parasite must contend. This reduces significantly the survival probability of individual malaria parasites. Even if the resistant mutant does survive the initial drug treatment and multiplies, the chance that this will result in sufficient gametocytes for transmission is reduced as a result of both asexual-stage immunity (which reduces the multiplication rate and lowers the density at which the infection is controlled) and specific antigametocyte (transmission-blocking) immunity. Furthermore, other parasite genotypes are likely to be present, since infections are acquired continuously. These compete with the resistant parasites for red cells and increase the possibility of outbreeding of multigenic-resistance mechanisms or competition in the feeding anopheline mosquito.
But you don't need me to tell you that. White does so himself.
The use of the definite article implies it.
I agree. I said that it was explicitly inclusive without qualification.
I looked at the first ten, and none fit your usage. All that were parallel were qualified.
I would hope so! We both know that Behe doesn't!
So how many PRACTICING scientists and mathematicians have done so?
Comment by JAM — July 1, 2007 @ 11:22 pm
July 1st, 2007 at 11:57 pm
JAM wrote:
Bullshit. As in, bollocking bullshit. Don't even try, sunshine, 'cos you'd be full of crap if you did. And I do mean full of it. Your point was pedantic, period.
As I said, I haven't read his book (nor intend to). On the other hand, you haven't shown—-or even attempted to show—why no filtering happening would have made a significant and relevant enough difference in this case.
Pay better attention next time.
Write a refereed article if you feel so strongly about it. Frankly my dear, I don't give a damn.
Write that article then. Perhaps you'd be a hero if you did. Then again, perhaps you wouldn't.
It obviously was the relevant one for the purpose of my post, however.
I think the relevant question is, how significant and relevant enough is it relative to his argument. Perhaps he'd tell you that it's not inaccurate enough, and so your missing the point in a can't-see-the-wood-for-the-trees kinda way.
Maybe you should ask him about it.
Comment by stunney — July 1, 2007 @ 11:57 pm
July 2nd, 2007 at 12:14 am
JAM,
Since when does the assembly of scientists and mathematicians imply an exhaustive collection?
The use of the definite article where? Not in front of "the assembly", as this does nothing to imply that this is the only assembly, or an all inclusive one.
And,as it does not appear there, certainly not in the statement that has you declaring this false dichotomy:
In fact, quite the opposite – "The" assembly of scientists or ""the" scientists assembled…" would be in the exact need of qualification to make complete inclusiveness explicit.
Explicitly exclusive it certainly is not.
Yep, a little slip there. Of course I meant "explicitly inclusive it is not". And it is not.
It is only explicitly inclusive if it's, you know, explicit. It would be made explicit by saying ALL scientists and mathematicians, or EVERY scientist and mathematician, etc.
Referring generally to people who are scientists and mathematicians as being assembled is not all-inclusive.
Try Googling "scientists assembled"
http://www.google.com/search?c…
and see if the presence of every scientist on earth is required (explicit or implicit), or if every field is represented.
None fit my usage? You mean specifically that none claims that scientists and mathematicians have long been assembled against the probability of RM and NS doing what evolutionary biologists claim they can? Yes, that is true.
But they support my contention that "assembled" does not make implicit nor explicit exhaustive inclusion unless such is specified.
A few samples:
In no case do the "scientists assembled" represent ALL the scientists.
My "scientists assembled against the probability…" is parallel to "scientists assembled at mission control…", "scientists assembled in the International Conference…" or "scientists assembled at the mecca of molecular biology…"
In some cases the assembly is qualified by number, in some by function, in some by location, etc.
Just as in my case, they were qualified by their opinions. Which qualification you admit below …
2) My use wasn't wasn't unqualified – it was qualified by the activity of "being against the probability of RM and NS doing what evolutionary biologists claim ".
I don't have a number.
My statement is factual, however.
This was a reply to Raevmo, who said:
Now Raevmo was not implying that EVERY peer rejects Behe's arguments when he failed to qualify "scientific peers".
And in answer to "relying upon the say-so of (educated) biologists and mathematicians" it is completely legitimate to refer to the fact that there are educated scientists and mathematicians also who do not reject Behe's arguments.
===
As for believing Behe's argument, I will have to suspend support of his use of the probability 1 : 10^20 and his reliance upon it in his argument.
As it stands now I have no counter to your point about the selectivity of the resistant parasite in the mosquito host.
Behe, or someone else, will have to defend as I can't.
Comment by Pez — July 2, 2007 @ 12:14 am
July 2nd, 2007 at 1:26 am
Raevmo and JAM,
I have just over an hour before I leave for the week.
If there is anything outstanding (for some reason) that you think I ought to respond to bear that in mind.
Comment by Pez — July 2, 2007 @ 1:26 am
July 2nd, 2007 at 1:42 am
Pez:
I'm still reading up a bit on drug resistance in malaria parasites, in between thinking up nasty exam questions (I might even include one about malaria), so no, no urgent outstanding stuff as far as I'm concerned. Enjoy your holiday.
Comment by Raevmo — July 2, 2007 @ 1:42 am
July 2nd, 2007 at 1:46 am
Thanks Raevmo,
I'll catch up with you guys next weekend.
Comment by Pez — July 2, 2007 @ 1:46 am
July 2nd, 2007 at 3:09 am
Correct. Not all-inclusive, but simply inclusive. That's what "generally" means.
Correct, because the scientists are specified in each case.
If that's the case, which scientists are you specifying?
Correct. He is saying that going by what he has read to date, MOST will.
Why would you place education above experience? Science and mathematics are subjects one learns at advanced levels by apprenticeship and experience.
Excellent!
I don't think Behe can.
I'm out for a couple of days.
Comment by JAM — July 2, 2007 @ 3:09 am
July 2nd, 2007 at 11:31 am
Comment by keiths — July 2, 2007 @ 11:31 am
July 2nd, 2007 at 5:33 pm
Hey JAM:
Do you have information that the mutation in question is catastrophic to malaria when in it's mosquito host or is it just neutral to slightly damaging?
When looking at organisms in changing environments I can think of lots of adaptations that might be helpful at one time and harmful in another.
The sickle cell mutation for one. If I'm not mistaken it is helpful in the presence of malaria and harmful in it's absence. Are you saying that such adaptations are as unlikely as Behe suggests and therefore beyond the edge of evolution?
Comment by fifth monarchy man — July 2, 2007 @ 5:33 pm
July 2nd, 2007 at 6:11 pm
I just finished Behe's book a couple of days ago. I need to re-read the relevant sections in order to understand the main arguments here.
Comment by Bilbo — July 2, 2007 @ 6:11 pm
July 2nd, 2007 at 6:19 pm
JAM's argument about selection in a mosiquito host is pretty weak.
To begin with, the fitness ratio of CQR malaria in the absence of chloroquine is .76 or .85. So one generation in a mosquito isn't going to make any difference.
Second, White's calculation of the 10^20 is for the per-parasite probability of developing resistance. It doesn't appear to be for selection of de novo resistance as JAM claims.
Third, White's calculation only includes the population of parasites in sick people. As White states, "Taken together, the balance of evidence strongly favors acute symptomatic infection as the source of de novo antimalarial resistance." Gametocytes carrying the resistance genes reach transmissible densities when the resistant biomass has expanded to a population size close to that necessary to produce illness (>10^7 parasites). So it is not like the mutation is going to be lost from sexual recombination in the mosquito.
Fourth, Behe says the probability is "roughly" 10^20 and throwing rocks at that number has a de minimus effect on the thesis of the book. Remember, Behe considers CQR something Darwinism CAN do.
Fifth, failure of an adaption to be selected for collateral reasons unrelated to the adapation itself is a real world problem for evolution, not ID. There are few conditions with better selective pressure than drug resistance. So JAM if wants to argue that the mutation happens more often but only rarely gets selected, he is making a good point about why Darwinism is even less probable.
Comment by Jehu — July 2, 2007 @ 6:19 pm
July 3rd, 2007 at 10:23 am
JAM fails to mention, that the case of reversing selection actually weakens the argument of large scale Darwinian transmutation. JAM fails to recognize that if anything, Behe was being too generous!
Just as in the case of Galopogos finches reverting to previous beak sizes in the absence of selection, so malaria, in the absence of CQ tends to revert to it's non-CQR configuration. Ooops!
Comment by Salvador T. Cordova — July 3, 2007 @ 10:23 am
July 3rd, 2007 at 10:25 am
Which one Keiths, haven't you been reading UD? How about you cut and paste it here to TT to prove to the reader I did. Or shall I spoon feed it to you since you're badgering me.
Comment by Salvador T. Cordova — July 3, 2007 @ 10:25 am
July 3rd, 2007 at 11:38 am
The Galápagos are geologically young islands. The island finches resemble mainland finches, but have evolved into a variety of species, taking over the ecological niches of everything from warblers to sparrows to woodpeckers. What is really amazing is that we can actually observe this process in wild populations.
In the case of wild populations, there's always selection.
Changes in beak traits is the prediction based on how Natural Selection works. What is observed is that drought causes specialization in Galápagos Finches as populations diverge to acquire increasingly limited and hard to acquire resources. In periods of plenty, the Finches become more generalized in order to best take advantage of as many food resources as possible. These changes happen very rapidly and are more than sufficient to account for the observed rate of historical evolutionary change.
Peter and Rosemary Grant spent more than 20 years observing a population of finches on just one island of the Galápagos. A fascinating and heroic scientific study.
Comment by Zachriel — July 3, 2007 @ 11:38 am
July 3rd, 2007 at 2:46 pm
Sal, I would check Spetner's Not By Chance, pp. 202-205 for his discussion on the Galápagos finches and similar studies done with Laysan finches. There are strong hints of non-random/non-Darwinian development in the finch populations. Spetner marks it as a possible area of NREH research.
If I am not mistaken, wasn't there an article blogged about here at TT that demonstrated how baby chickens already have all the genes necessary to get the full beak variation range of the Galápagos finches? I read it somewhere, I thought it was on here, but the scientists in the study were able to generate all the different finch beak patterns in normal chickens.
If the genes are already latent, there may be an even stronger case for front-loaded, environmentally triggered population change, where the trait appears spontaneously in many different members of the population when necessary. This would spread the trait in the population without having to rely on NS or even descent.
Comment by Atom — July 3, 2007 @ 2:46 pm
July 3rd, 2007 at 5:07 pm
Darn, forgot to bring EoE with me to the library. Could have answered at least one of the questions here. Library closed for the 4th. I'll try to be more prepared Thursday.
Comment by Bilbo — July 3, 2007 @ 5:07 pm
July 3rd, 2007 at 7:27 pm
Went home and got EoE. So why does Behe focus on malaria? From the book:
Comment by Bilbo — July 3, 2007 @ 7:27 pm
July 3rd, 2007 at 7:38 pm
Opposite the title page of EoE, there is a diagram of a vertical line, divided into three parts. The top 3/4 of the line is shaded dark black, and is labeled on the left of the line, "The Surprising Depth of Fine-Tuning of Nature for Life on Earth." On the right, there is a list of the ways Nature has been fine-tuned, starting from "Laws of Nature," and ending with, "Phyla, Cell Types, Classes." These are the categories where Behe thinks the evidence is good that intelligent design played a major role.
The next, much smaller segment of the line is shaded gray, and comprises "The Tentative Edge of Random Evolution," and consists of three categories: "Orders, Families, and Genera." This is the gray area, where the evidence isn't clear enough for us to determine if design was necessary, or if these categories could have come about by random mutation and natural selection alone.
The bottom segment is shaded white, and comprises "Contigency in Biology," and consists of five categories: "Species, Varieties, Individuals, Random mutations, and Environmental accidents." These are the categories where Behe thinks the evidence is good that random mutation and natural selection can account for everything.
So Behe would have no problem with finches' beaks being explained by natural selection acting upon random mutation.
Comment by Bilbo — July 3, 2007 @ 7:38 pm
July 3rd, 2007 at 8:06 pm
Atom:
That's in the OP of the More Evidence of a Changing Paradigm thread, Atom. It's expression, not mutation. Adaptive changes in beak size/shape could then be considered "epigenetic" – sensitive to selection pressures, but not a result of random mutations in the beak gene. Thus selection pressure can reverse changes over generations also without mutation of the responsible "Toolbox" gene, BMP4.
Comment by Joy — July 3, 2007 @ 8:06 pm
July 3rd, 2007 at 8:25 pm
Atom,
Gag. I know I've been promising some spetner stuff. KC is actually a good critic of Spetner's work. I would welcome hearing him first, before I give my endorsement.
Salvador
Comment by Salvador T. Cordova — July 3, 2007 @ 8:25 pm
July 3rd, 2007 at 10:45 pm
Quoting the very same Peter Grant from Beak of the Finch.
It pays to be observant. (Note the tentative prediction from evolutionary theory.)
Comment by Zachriel — July 3, 2007 @ 10:45 pm
July 4th, 2007 at 4:51 am
What is a tentative prediction?
Comment by Vladimir Krondan — July 4, 2007 @ 4:51 am
July 4th, 2007 at 8:04 am
hypothesis, a tentative assumption made in order to draw out and test its logical or empirical consequences.
The hypothesis is an important component of the scientific method: hypothesis, prediction, observation, validation, repeat. The hypothesis should be specific and it should lead to distinguishing empirical predictions.
If the prediction is confirmed, it adds confidence to that aspect of the theory. If not confirmed, then the theory must bend or break to accomodate the new facts. In either case, new hypotheses are proposed to further test and extend the results. All scientific theories are considered tentative and subject to revision in the light of new facts"”including the Theory of Evolution and the Theory of Gravity, both of which have been subject to substantial modification over time.
Comment by Zachriel — July 4, 2007 @ 8:04 am
July 4th, 2007 at 10:38 am
Zach:
Um… Evolution by means of expression of pre-existing "Toolbox" genes is as 'exciting' to me as to Grant. It confirms a prediction of EAM, that actual evolution proceeds via expression of endogenous capabilities in response to selective pressures, not by means of random accidents damaging genes while the non-viable damage is 'selected out' by means of being non-viable. That process occasionally provides a useful accident, but mostly it causes disease.
We should find that these ancient "Toolbox" genes and their differential expression not only give life forms endogenous means of direct adaptation, but that they also impose constraints on what is possible. Resulting in fairly neat nested hierarchies. This is not RM-NS, it's front-loaded Devo-in-action. Developmental expression was devalued when NDS 'orthodoxy' took over. I am delighted it's making a strong comeback, since RM-NS is as weak as its ever been.
Comment by Joy — July 4, 2007 @ 10:38 am
July 4th, 2007 at 2:18 pm
Joy, the idea of toolbox genes and evolutionary development is standard in evolutionary theory. Do you understand how this works in orthodox theory? Consider how many different ways the limbs in tetrapods have been adapted, walking, running, climbing, swimming, flying, grasping, etc.
Is there some sort of empirical difference that you can point to?
Comment by Zachriel — July 4, 2007 @ 2:18 pm
July 4th, 2007 at 2:41 pm
Zach:
Yeah, I know. It incorporates what it can no longer ignore, but only when forced to by massive citizen unrest. Though, as the NYT story went, some still urge caution before accepting such heresies. Jerry Coyne, in particular. Or, according to Yoon the author…
Let it never be said 'orthodoxy' isn't open-minded. So I say, RM-NS it's not. Glad y'all have finally come aboard.
Meanwhile, it's the 4th of July, and here on the homestead there's a mess of tricorns and pirates running around celebrating total anarchy. Capture the Flag starts at 4, third wave of disc golf on the top nine is ongoing. We plan to launch some rockets just for fun, eat a lot of blackberries and watermelon, roast some weenies and 'mallows over the fire, maybe play dangerous with some sparklers when it gets dark. It's Independence Day. We're being Independent. §;o)
Comment by Joy — July 4, 2007 @ 2:41 pm
July 4th, 2007 at 3:34 pm
I take that as a "No."
Comment by Zachriel — July 4, 2007 @ 3:34 pm
July 5th, 2007 at 1:37 pm
man, it has a lower level of fitness. It doesn't have to be catastrophic to be selected against in a major way, because fertilization occurs in the mosquito.
The math is very complex, so you'd think that Behe would have presented something other than multiplication.
Absolutely. That's why Behe's misrepresentation of the emergence of CQR as the mutation rate is so ludicrous.
Not at all. I'm saying that Behe chose this case so that he could set the mutation rate at >1000-fold less than it really is.
——————
I'd say that your understanding of population genetics is what's weak here.
But there isn't just one generation in the mosquito. How many sporozoites are produced by each oocyst, Jehu?
Is this measurement from a mammalian host? If so, how many generations occur? Remember, the number of generations is the exponent for the fitness ratio, so the fitness ratio for CQR bugs after 100 haploid generations is (0.85)E10=0.0000000875.
That's precisely what he means by "developing."
But in the laboratory, much higher mutation rates than 1 in every 10E12 are recorded (12).
Mutations may be associated with fitness disadvantages (i.e., in the absence of the drug they are less fit and multiply less well than their drug-sensitive counterparts). Another factor that may explain the discrepancy between in vitro and much lower apparent in vivo rates of spontaneous mutation is host immunity. Even a previously nonimmune individual develops a specific immune response to a malaria infection. This response is systematically evaded by the parasite population through programmed antigenic variation of the main red cell surface"“expressed epitopes. In falciparum malaria, P. falciparum erythrocyte membrane protein 1 (PfEMP1), which is encoded by the var multigene family, changes in 2"“3% of parasites each asexual cycle (15). The untreated infection is characterized by successive waves of parasites, each comprising largely one antigenically distinct surface phenotype. It is likely that this specific immune response directed against the immunodominant surface antigens will reduce the probability of the usually single mutant parasite ever multiplying sufficiently to transmit as for P. falciparum; there is only a 2"“3% chance that the genetic event causing resistance would arise in the antigenically variant subpopulation that will expand to reach transmissible densities.
———-
This is precisely why it emerges from populations so infrequently. You just shot Behe in the foot, Sal.
Comment by JAM — July 5, 2007 @ 1:37 pm
July 5th, 2007 at 2:05 pm
Hardly, it actually shows why Behe was understating the ineptitude of Darwinian evolution.
By the way, I posed a question which you did not answer at UD, and I'll pose it here.
I asked a simple question, and you obfuscated and didn't answer. The particular form of restance in question was the 76 and 220 resistance. You started obfuscating about dosage levels of CQ. That was just obfuscation. If a malarial strain has a 76 and 220 form of resitance in place, then it has a 76 and 220 form of resitance.
So let me try to rephrase the question. Did Behe argue that a malarial strain will have CQ resistance if and only if it has the 76 and 220 mutations that confer resistance?
You have 3 options:
1. yes
2. no
3. JAM doesn't know how to answer
If you answer #3, then explain why you don't know how to answer.
Comment by Salvador T. Cordova — July 5, 2007 @ 2:05 pm
July 5th, 2007 at 2:15 pm
Actually JAM, here is somethingh to consider:
1. Malaria without CQR and a 76 muatation.
2. Malaria without CQR and a 220 muatation
3. Malaria with a 76 and 220 muatation
If we find all 3, which we do, this will show 76 and 220 are required to form a 76-220 CQR malarial strain. It says nothing of any other possible routes to CQR (unlike the strawman argument you spammed UD with).
Comment by Salvador T. Cordova — July 5, 2007 @ 2:15 pm
July 5th, 2007 at 3:55 pm
Behe's thesis is that mutations don't occur frequently enough to drive evolution.
By the way, you're wrong. I did answer it. I look forward to your retraction and apology for the false accusation.
———
Malaria doesn't have mutations. It is a disease, not an organism. That being said, the words that follow "malaria" are hopelessly ambiguous. Does "without" also point to "a 76 mutation"
Here's what we do know: Plasmodium without CQR and no change in K76 have not been isolated from patients AFAIK. Reversion back to K76 abolishes CQR. It's likely necessary, although K76T and K76I are very different changes.
What you'll never learn from Behe is that the SINGLE change in K76 does confer CQR experimentally:
Fidock et al.
Mutations in the P. falciparum Digestive
Vacuole Transmembrane Protein PfCRT and Evidence
for Their Role in Chloroquine Resistance
Molecular Cell, Vol. 6, 861"“871
So tell me, in light of those data, on what evidentiary basis does Behe assume that:
1) two substitutions must be present to get things started, and
2) they must occur simultaneously?
Isn't that circular, Sal?
Comment by JAM — July 5, 2007 @ 3:55 pm
July 5th, 2007 at 4:09 pm
Since you and Sal are referring to an exchange on another blog would you spell out the specifics for TT readers?
Comment by Bradford — July 5, 2007 @ 4:09 pm
July 5th, 2007 at 4:47 pm
Bradford,
To spool the TT readers on the debate, the argument is (as it usually is), over what Behe actually asserted.
JAM asks me a question in the form of a Fallacy of interrogation . Examples of which are:
The question presupposes a definite answer to another question which has not even been asked. This trick is often used by lawyers in cross-examination, when they ask questions like:
The way JAM applies Fallacy of interrogation to this discussion is by asking:
Behe assumes no such thing.
Behe says:
If there is an assumption, it is only as a supposition, not a presumed absolute truth. JAM would do well to distinguish whether he is saying Behe:
1. assumes abosolutely there is no possibility except:
2. or the "assumption" is only a hypothetical used to compare with physical evidence
I assert JAM is making a highly uncharitable reading of Behe's wrtings. He's using debate tactics right out of the infidels manual of unwholesome debate tactics "Logic & Fallacies" from the infidels website.
My line of questioning to JAM was to make it evident he was using an unwholsome debate tactic, and that I was quite onto what he was doing.
Comment by Salvador T. Cordova — July 5, 2007 @ 4:47 pm
July 5th, 2007 at 4:47 pm
Unless one believes that there is a giant conspiracy, the fact that scientists that have reviewed Behe's book have almost unanimously rejected Behe's scientific claims should give one pause. I haven't read Behe's book yet, but it's already quite clear to me that it's mostly religious zealots who don't give a damn about the truth that are still defending Behe's claims. Salvador's attempts to defend Behe are a case in point. Does anyone really believe these scientists are all lying? It makes me sad to see how far people are willing to go to defend the indefensible.
Comment by Raevmo — July 5, 2007 @ 4:47 pm
July 5th, 2007 at 4:57 pm
I think you are being a bit premature, especially since you haven't read the book.
Miller used outright misrepresentations of Behe's work. He accused Behe of not following or waving off papers Behe has publicly commented on or even had specific references to in his book. Miller couldn't even get the citations right in his review of Behe's paper. See: Ken Miller, the honest Darwinist. In addition, Miller misrepresented Behe's and made factually incorrect statements in a court of law, and then keeps repeating those misrepresentations in a scientific journal.
Whether I'm zealot or scoundrel is beside the point. The question is what are the evident limits of evolution, in Behe's words, The Edge of Evolution.
No, one of the scientists is telling the truth. His name is Michael Behe.
Comment by Salvador T. Cordova — July 5, 2007 @ 4:57 pm
July 5th, 2007 at 4:59 pm
That's a knee jerk reaction to any IDist who cites anything favorable to ID. We've seen it on this site too. What really matters is whether the critics are citing errors in citations, explanations and more or whether they are simply doing what they always do i.e. assert no design across the board even when there is manifestly no scientific case for their opposing assertion.
Comment by Bradford — July 5, 2007 @ 4:59 pm
July 5th, 2007 at 5:00 pm
Yawn, there comes Raevmo with his appeal to authority.
Of course Raevmo uses the qualifier "scientists" to describe the reviewers. Indeed, it would be too much a strain on his objectivity to admit that those reviewing "scientists" are well-known atheists with an anti-ID agenda.
Comment by Jean — July 5, 2007 @ 5:00 pm
July 5th, 2007 at 5:02 pm
Raevmo:
Salvador's exchanges have been with a small handful of scientists. Before going to the lying mantra make sure your own assertions are in order. Particularly so as you acknowledge not having read the book the debate centers around.
Comment by Bradford — July 5, 2007 @ 5:02 pm
July 5th, 2007 at 5:05 pm
Most scientists have not read Behe's book. It is not a priority item for most of them. Neither is the book's success or failure linked to the ultimate fate of ID.
Comment by Bradford — July 5, 2007 @ 5:05 pm
July 5th, 2007 at 5:13 pm
He assumes precisely that:
"The likelihood that Homo sapiens achieved any single mutation of the kind required for malaria to become resistant to chloroquine"“not the easiest mutation, to be sure, but still only a shift of two amino acids"“the likelihood that such a mutation could arise just once in the entire course of the human lineage in the past ten million years, is minuscule"“of the same order as, say, the likelihood of you personally winning the Powerball lottery by buying a single ticket."
His assumptions are wrong.
Behe derives what he offers to be absolute truth from those false assumptions.
Read what Behe wrote above.
Either way, the "centerpiece example" of the book is not consistent with the evidence.
That's pretty funny coming from someone who falsely accused me of avoiding his question, and can't be bothered to retract his false claim.
Since the experimental data clearly show that a single mutation is sufficient to confer resistance, was Behe's failure to cite those data a result of an intent to deceive his audience or was it a result of pathetically sloppy scholarship?
I don't know. Which do you think is true? Are there any other viable explanations for not citing these data?
Fidock et al.
Mutations in the P. falciparum Digestive
Vacuole Transmembrane Protein PfCRT and Evidence
for Their Role in Chloroquine Resistance
Molecular Cell, Vol. 6, 861"“871
In what way is it unwholesome to point out that the assumptions Behe made in what he describes as his book's "centerpiece example" are false?
Comment by JAM — July 5, 2007 @ 5:13 pm
July 5th, 2007 at 5:16 pm
Sal:
I might well be, that's why I mentioned I have not read the book.
I wonder why anyone would choose to believe Behe over so many of his peers. An honest person would be at least indifferent with respect to Behe's claims. I can only conclude that Sal simply does not want to believe Behe's critics because their critique conflicts with Sal's religious beliefs. Moreover, since Sal is not convinced yet of an old earth, we have good reasons to doubt his ability to judge scientific arguments.
Comment by Raevmo — July 5, 2007 @ 5:16 pm
July 5th, 2007 at 5:18 pm
Jean wrote:
Jean, you're funny. Ever heard of Ken Miller?
Comment by keiths — July 5, 2007 @ 5:18 pm
July 5th, 2007 at 5:26 pm
Keith, no you're funny. Miller is just about the only non-atheist reviewer you can shove forward, which proves my point exactly.
Comment by Jean — July 5, 2007 @ 5:26 pm
July 5th, 2007 at 5:36 pm
Bradford:
But the scientific reviewers have read his book. And so will I in due time. It's not a priority for me because I have other stuff to do, like grading biology and chemistry students for their statistics exam. And writing scientific papers. And getting grants. I want to have tenure too. Oh, and I want to have a live with my girlfriend.
Comment by Raevmo — July 5, 2007 @ 5:36 pm
July 5th, 2007 at 5:37 pm
If he's telling the truth, why does he talk about a "single mutation of the kind required for malaria to become resistant to chloroquine"“not the easiest mutation, to be sure, but still only a shift of two amino acids…," while not citing the data in this paper, that show experimentally (not ecologically) that a change of a single amino acid residue (K76) is sufficient to confer resistance to chloroquine?
Fidock et al.
Mutations in the P. falciparum Digestive
Vacuole Transmembrane Protein PfCRT and Evidence
for Their Role in Chloroquine Resistance
Molecular Cell, Vol. 6, 861"“871
For that matter, how can YOU claim to know that he is telling the truth without addressing the data in this paper, Sal?
Here are the probabilities calculated from known mutation rates:
K76T: 10E-9
K76I: 10E-9
K76T or K76I: 2 x 10E-9
K76T and A220S: 10E-18
(K76T or K76I) and A220S: 2 x 10E-18
(K76T or K76I) and (A220S or (A144T and L160Y)): 3 x 10E-18
The math is pretty easy. So when Behe throws around 10E-20, the closest probability above is K76T and A220S. Including any other possibilities only increases the probability and moves you further away from Behe's number.
Comment by JAM — July 5, 2007 @ 5:37 pm
July 5th, 2007 at 5:40 pm
That was not an assumption, the likelihood was a deduction from observed evidence, that the likelihoods were remote. You apparently can't distinguished between assumptions and deductions.
The deduction was that CQR arose slowly because the space of possible CQRs is small relative to the resources to find them. That was not an assumption in the manner you're trying to pin on Behe.
And so JAM, you curiously omit discussion of these facts of Behe's work which would refute your starawman insinuation that Behe a priori ASSUMES the only possible route to CQ resistance (CQR) are:
In fact, you seem to avoid making citations that refute your strawman. Behe puts certain qualifiers:
There are possibly several forms of CQR (Chloroquine Resistant)malarial strains. One of the most prominent is PfCRT [P. falciparum chloroquine resistance trait].
But even with respect to PfCRT resitance alone, not to mention other forms of CQR, Behe writes:
Later Behe uses the phrase, "almost always", he doesn't insist, NEVER. Suce exceptions are, as I pointed out, Origin and Dissemination of Chloroquine-Resistant Plasmodium falciparum with Mutant pfcrt Alleles in the Philippines
Comment by Salvador T. Cordova — July 5, 2007 @ 5:40 pm
July 5th, 2007 at 5:40 pm
Jean, I'm a Christian and I've read the book.
I've also apparently surveyed far more of the relevant CQR literature than Behe has, unless he is dishonest or incompetent.
How can anyone argue that two substitutions are required when it has been experimentally demonstrated that only one is sufficient to confer resistance?
Comment by JAM — July 5, 2007 @ 5:40 pm
July 5th, 2007 at 5:47 pm
Jean:
They are not all atheists. Most of them are I suppose , but a considerable minority is theist, so your argument doesn't cut it. There are quite a few theists in my own biology department. Please use some real arguments next time. You have made a fool of yourself already so many times, please think before you respond again.
Comment by Raevmo — July 5, 2007 @ 5:47 pm
July 5th, 2007 at 5:47 pm
You're accusing Behe of not citing the data in the paper. Let those who have Behe's book refer to page 281 of Edge of Evolution. Contrary to JAMs claims of evasions, Behe specifically cites:
Comment by Salvador T. Cordova — July 5, 2007 @ 5:47 pm
July 5th, 2007 at 5:52 pm
Oh yeah???? But are you a Catholic!?
Whoops, I'm sorry…. I meant a 'romanist'.
Comment by Doug — July 5, 2007 @ 5:52 pm
July 5th, 2007 at 6:05 pm
Sal, you seem to have trouble reading. I pointed out that Behe didn't cite the data in that paper that show that a single aa change is sufficient. The fact that Behe cited the paper does absolutely nothing to rebut my claim. In fact, it makes Behe look even worse.
Do you not understand the clear difference between citing the data in a paper and citing the paper?
Wrong. That was a deduction based on the assumption that the frequencies of haplotypes observed in populations represented mutation frequencies.
I have. You apparently haven't found a way to address the observation that a single change at 76 is sufficient to confer resistance, which demolishes both of Behe's assumptions.
The deduction was based on the false assumption that haplotypes observed after generations of selection represent multiple simultaneous mutations.
I don't think so.
But he explicitly denies that is the case in CQR.
Behe hasn't done any scientific work in a decade.
Behe states it explicitly, Sal: "…single mutation of the kind required for malaria to become resistant to chloroquine"“not the easiest mutation, to be sure, but still only a shift of two amino acids"¦,"
A single mutation changing two amino acid residues is not required for resistance. Only one change to K76 is required. This has been shown experimentally. Behe only cites ecological data.
That's true, but it does nothing at all to qualify his false claim that two are required.
That's what is found in populations after selection. But a change in only one amino acid residue is required. Why do you have so much trouble with this, Sal? Behe claims that two are required simultaneously (he calls them a "single mutation"), the data say that only one is required. That's a billion-fold error in his "centerpiece example."
Comment by JAM — July 5, 2007 @ 6:05 pm
July 5th, 2007 at 6:08 pm
What is Behe saying?
1. Is Behe assuming abosolutely there is no possibility except:
2. or the "assumption" is only a hypothetical used to compare with physical evidence
3. or this is approximate deduction, based on comparing the hypothetical with the physical evidence
I invite JAM to clarify.
Comment by Salvador T. Cordova — July 5, 2007 @ 6:08 pm
July 5th, 2007 at 6:20 pm
Raevmo, answer this simple question. Of the people who reviewed Behe's book, how many of them are atheists with an anti-ID agenda?
Go ahead and make my point for me.
These reviews are not written by scientists who held no previous views on the topic or who happen to just get the review assignment. These reviewers of yours – whom you pretend are the embodiment of unbiased scientific integrity – tend to be hardcore atheists who have a track record of publishing anti-ID literature. Yet you appeal to their authority, as if they could write no wrongs.
Why are you committed to such obvious fallacies?
Comment by Jean — July 5, 2007 @ 6:20 pm
July 5th, 2007 at 6:27 pm
I see some semantic games are being played. In theory K76 might in and of itself do the trick, but because of other factors, it is unlikely. Behe cited the 2000 study by Fidock. Did he cite the study, only then to close his eyes to the data, as JAM insinuates?
Consider this 2005 study on the question of the sufficiency of K76T alone:
A critical role for PfCRT K76T in Plasmodium falciparum verapamil-reversible chloroquine resistance
Comment by Salvador T. Cordova — July 5, 2007 @ 6:27 pm
July 5th, 2007 at 6:27 pm
Sal, I already clarified.
It's your turn: please explain why Behe didn't tell you about the experimental evidence demonstrating that only a single change–to K76–is required to get CQR.
Comment by JAM — July 5, 2007 @ 6:27 pm
July 5th, 2007 at 6:28 pm
JAM,
I a response is help up in the spam queue. In order to speed things up, I responded at UD.
Sal
Comment by Salvador T. Cordova — July 5, 2007 @ 6:28 pm
July 5th, 2007 at 6:38 pm
JAM,
In sum, there is a 2005 paper that refutes your assertion. That post is held up in the spam buffer for whatever reason.
But here is an excerpt:
Sal
Comment by Salvador T. Cordova — July 5, 2007 @ 6:38 pm
July 5th, 2007 at 6:50 pm
Sal, you are behaving predictably. I didn't specify K76*T*, so you didn't refute my assertion at all.
Have you considered reading the Molecular Cell paper I cited, and that Behe cited while omitting the mention of data that fried his assumptions?
If you did so before lashing out so confidently, it might save you considerable embarassment.
Comment by JAM — July 5, 2007 @ 6:50 pm
July 5th, 2007 at 6:52 pm
Sal,
Again, it's your turn: please explain why Behe didn't bother to tell you about the experimental evidence demonstrating that only a single change"“to K76"“is required to get CQR.
The fact that he cited the paper that includes this evidence makes him look very, very bad.
Comment by JAM — July 5, 2007 @ 6:52 pm
July 5th, 2007 at 7:10 pm
I happen to have the paper in question. It is Mutations in the P. falciparum Digestive Vacuole Transmembrane Protein PfCRT and Evidence for Their Role in Chloroquine Resistance.
I'm sorry I'm having a bit of trouble finding the table of numbers in that paper you just gave. Can you help out?
I should point out something.
The K76I mutation appears to be an in-vitro (in the laboratory only) derivative of something that came from the Suday 106/1 clones, which by the way had all of the requisite mutation for CQR in place before K76I appaeared spontaneously.
Can you help cite the specific paragraph in that paper that justifies your numbers?
Also, in Table 2, K76I just doesn't appear in any in vivo strains.
Comment by Salvador T. Cordova — July 5, 2007 @ 7:10 pm
July 5th, 2007 at 7:35 pm
For the readers benefit, I'm pointing out JAM made a literature bluff.
Comment by Salvador T. Cordova — July 5, 2007 @ 7:35 pm
July 5th, 2007 at 7:41 pm
Jean:
So you really believe it's an atheist conspiracy. You are even more stupid than I gave you credit for, and that's telling a lot given your previous embarassingly dimwitted posts.
Comment by Raevmo — July 5, 2007 @ 7:41 pm
July 5th, 2007 at 8:10 pm
It's about time! Why did you feel the need to retype the title?
So when will you answer my question: why didn't Behe tell his readers that it shows conclusively that only one amino-acid substitution is necessary for CQR?
The probabilities don't come from that paper. As I clearly wrote, they come from known mutation rates. Are you disputing that mutation rates in eukaryotes are > or = 10E-9?
I can see how my juxtaposition might have confused you before reading the paper, but now that you have the paper, can't you see that it isn't about mutation rates? Do you realize that scientists take the data (not quotes) from multiple papers and integrate them?
No, they don't. You already know that. There are multiple CQR haplotypes that don't include A220S.
"In vitro" means "in the laboratory only" Are you claiming that I can't do in vivo experiments in the laboratory only?
"Appears" is the operative word here. How does that appearance affect the fact that it clearly is sufficient for conferring resistance, which refutes Behe's claim that two simultaneous changes are required?
And how can you credibly claim that the Sudan isolates had "of the requisite mutation for CQR in place," when in fact, they weren't CQR, and when K76I alone is sufficient for CQR?
Doesn't the fact that K76I is sufficient explicitly mean that none of the others are "requisite"
And what does that say about your silly semantic game of pretending that a change to K76 could only have been K76T and not K76I?
That paper isn't about mutation rates, Sal. There are reams of data supporting a minimum rate of 10E-9 per nucleotide per replication event.
So what? They showed experimentally that it was sufficient. What's to preclude a sequential pathway of K76I > other changes > I76T, each one contributing to fitness either in humans with CQ or in mosquitos without CQ? Have you checked out the genetic code lately?
No, you're just showing the readers that you can't read papers.
Comment by JAM — July 5, 2007 @ 8:10 pm
July 5th, 2007 at 8:13 pm
Jean,
Since you believe that you are able to discern motive in those who criticize Behe's claims offered (in the absence of any new data from the lab or field), what motive explains Miller's alliance with your alleged vast atheist conspiracy?
Comment by JAM — July 5, 2007 @ 8:13 pm
July 5th, 2007 at 8:26 pm
Thank you for clarifying that.
But why insist on that being the rate, were talking mutations pertaining to amino acids, and it ain't quite so easy when we consider transistions vs. transversion and then the specific codons involved. For example Serine occupies only 2 elements in the 64 codes, whereas Leucine occupies 6 elements. So, you're numbers are just as crude as Behe's, why represent your figures as more accurate?
Besides, I think I'm going to have fun with your insistence that a mutation in 76 is all that's need. You said:
From the 2000 Fidock paper JAM touts:
Gee JAM, the Sudan strain has six of the seven muation consistently found in Old World CQR, including (surprise surprise) A220S
Notes:
I believe A220S = Alanine to Serine in position 220
Comment by Salvador T. Cordova — July 5, 2007 @ 8:26 pm
July 5th, 2007 at 9:54 pm
Hi Salvador,
Are you having fun?
I really didn't want to weigh in on this discussion too much further than I akready have, but it looks like you are just having too much fun wallowing in the details. I couldn't resist.
Here is what Behe had to say concerning the general nature of Edge of Evolution…
Behe sets up two choices based on common assumptions. But what if it turns out there is no such thing as natural randomness?
Does that automatically imply an intelligent designer?
Behe is trying to frame this debate by constraining "Darwinism" to a very restrictive model of methodology (RM + NS) while providing loose handwaving as his explanatory model (and Pez argued with me that he didn't even do that). Behe can claim automatic victory if he can convince his readers that his simplistic presentation of his opponent's model just isn't good enough for even a single example. It's a nice position to be in if you can get away with it.
Sal, you have a mechanistic model. "GodDidIt" is sufficient explanation since an omnipotent being is quite capable of doing whatever is needed.
If you have noticed, we have been discussing a Third Choice for a mechanistic model.
Your model my be closer to what you call "mainstream ID" than this Third Choice, however, by Behe's own decision on where to draw his boundaries, Behe appears to be confirming this Third Choice is an ID hypothesis and that he has provided "confirmed" support for it.
Comment by Thought Provoker — July 5, 2007 @ 9:54 pm
July 5th, 2007 at 10:01 pm
How is Behe the one constraining? Is not RM+NS the prominent paradigm?
Comment by Bradford — July 5, 2007 @ 10:01 pm
July 5th, 2007 at 10:54 pm
Hi Bradford,
You asked…
Excuse me from answering a question with a question, but I am out of my element here.
Would you consider the Serial Endosymbiotic Theory just a form of RM+NS?
Comment by Thought Provoker — July 5, 2007 @ 10:54 pm
July 6th, 2007 at 12:37 am
Yes, and JAM and others who are "in the know" realize I just decapitated him.
His K76-only argument is indefensible, and his repeated claims actually demonstrate he mis-read the very study he claims refutes me and Behe. He was counting on the fact I was unwilling and unable to call his bluff. He counted wrong. 
Gag! The word randomness has so many conotations. An intelligently designed modem signal has all the characteristics of randomness statistically speaking. That's why it sound's like white noise. Randomness may be:
1. a result of our collective lack of knowledge
2. nature is capricious at it's root
I do not know which is true. I do know that it's a weak argument to say something with the appearance of randomness (like a modem signal) is therefore the product of a mindless mechanism.
No, at least not formally. I would only say it does reasonably for me personally. If you accept there is a third choice, I have no reason to discourage your exploration. I simply lean otherwise, but I don't view it as inherently flawed (like Darwinian evolution). If you wonder why I haven't entertained it more, visit the YoungCosmos weblog and you'll see the serious theoretical issues I'm grappling with for the theories I have interest in. You'll see I entertain legitmate and civil objections to my ideas there. You can tell however, I have a totally different attitude toward Darwinian evolution than I do toward Old-Universe theories.
I did mention in your thread that Behe made passing reference to Quantum Evolution and the work of McFadden in Endogenous Adaptive Mutations (EAM). I believe retro-causality may be in evidence in biology, but from what I know of physics, it can't be the cure-all in and of itself.
What we little we know of retrocausal systems and their capabilities shows them to be limited. For example, a delayed-choice retrocausal system which scientists built could only affect the past as far back as a few nano-seconds (the time it takes for light to travel a few meters). And even then, it was hard to say that it was useful for anything (i.e. big deal if it made a photon a particle or wave in the past, that sort of retrocausality has limited appication, unless framed as a quantum computation).
These retrocausal systems were a delicately constructed system and was brittle. I don't see biology exploiting retrocausal phenomena willy-nilly. For retrocausal systems (quantum computers are sort of this way) to work, they need design.
You can presume an impersonal mandelbrot set is the source of the universe. I think the question is formally undecidable (ala Godel), but one idea is surely loser to the truth than another.
But, since you may be curious, if we have physical evidence for:
1. Recent creation, c-decay
2. Noah's flood
3. Tower of Babel and origin of language
I would be inclined to thing the Intelligent Designer has tried to communicate to us. But that is a personal view, not a scientific one.
Further these ideas have nothing to do with theocracy or gaining politcal power. It has everything to do with a highly personal interest in finding meaning in my personal life.
Comment by Salvador T. Cordova — July 6, 2007 @ 12:37 am
July 6th, 2007 at 6:48 am
TP asks:
No. However there is more to this. Quoting the source:
Look at the whole picture. There is a before and after with reference to merging scenarios. As the author notes the merging is of already "complex genome make-ups." How did the merged subsets acquire their complexity? We have speculations at an origins timeframe and RM + NS after origins but prior to the mergings. How do we account for changes post-mergings if not also by reference to RM + NS?
Comment by Bradford — July 6, 2007 @ 6:48 am
July 6th, 2007 at 10:07 am
That's an odd attitude considering you have never responded to JAM's points. Consider this exchange.
You didn't answer JAM's point that Behe is conflating the result of a process of evolutionary change in an organism, one with a complex life cycle under varying selection, with mutation rate. They are not the same"”regardless of any handwaving on your part. You simply pretend it isn't important, even though it is at the heart of Behe's argument.
And as to your own point, you are putting forth a strawman. Theories of Natural Selection do not posit change will always occur in a single direction, but rather that variations within populations are selected according to their fit with the local environment. And that is what is observed!
In the case of Plasmodium parasites, they have a complex life cycle that is not always under selection for drug resistance, and drug resistant strains may be otherwise less fit. Hence, we see a complex series of mutations that include drug resistance and multiple adjustments to the genome to improve overall fitness. However, the exact life cycle of Plasmodium is still not fully understood, especially with regards to ooctyes.
Because there are reams of data. Typical mutation rates per nucleotide in Eukaryotes vary from 10^-8 to 10^-9. This study by Paget-McNicol and Saul measured a specific nucleotide mutation rate in P. falciparum as 2.5*10^-9, concluding that "anti-malarial resistance will inevitably arise when mutant alleles are selected under drug pressure".
Comment by Zachriel — July 6, 2007 @ 10:07 am
July 6th, 2007 at 10:25 am
Hi Bradford,
I realize that Serial Endosymbiotic Theory (SET) references RM+NS but then again so does Behe's version of ID. The basic question is whether or not Behe considered things like SET when defining his "sharp limits" to Darwinism. I think it is obvious he did not.
Behe is drawing a specific RM+NS circle around what he calls "Darwinism" and then claims that if anything is found in nature that falls outside this tight circle the results are…
"1) Darwinism's prediction is falsified; 2) Design's prediction is confirmed."
Comment by Thought Provoker — July 6, 2007 @ 10:25 am
July 6th, 2007 at 11:53 am
I don't respond to all of his bait. Zach, I'm disappointed. Why are you not defending me? Are you going to defend his misinterpretation of A76? Are you going to let him get away with it?
I ignored the rest of that post. If you let stuff like that go, I see little point in continuing dialogue with you until you acknowledge this glaring error. If JAM will strain to find gnats and yet swallow camels, what's the point. He bluffed with A76 to try to suggest I and Behe were wrong, when in fact he totally could read and represent the very papers he accused me of ignoring.
So Zach, are you going to defend his mis-interpretation of A76. How about any other Drarwinist here? Or will you all just go mum because JAM is on your side?
So Zach, was JAM right about A76 or was I? Will you follow the party line or will you admit JAM totally botched it with respect to the interpretation of Fidock 2000. And don't pretend this was a small point either. He tried to use this ridiculous A76 interpretation agains me and Behe.
What say you about JAMs interpretation of A76 being sufficient for CQR?
Comment by Salvador T. Cordova — July 6, 2007 @ 11:53 am
July 6th, 2007 at 12:06 pm
Sal,
Unlike you, I have the integrity to admit a mistake. I missed that they had put K76I it into the Dd2 context. Therefore, your claim that I was bluffing is unsupported.
However, your victory dance and claim that you decapitated me are only bluster. Unfortunately for you, I must have been confusing it with this one, in which either K76T or K76I confer resistance alone:
Arch Biochem Biophys. 2006 Aug 15;452(2):119-28
Functional reconstitution of purified chloroquine resistance membrane transporter expressed in yeast.
Tan W, Gou DM, Tai E, Zhao YZ, Chow LM.
Would you like a PDF?
Also, I'm confused by your embrace of a negative result in cultured Plasmodium in culture at #96 of the UD thread, while expressing complete disdain for results from culture in #100. The only difference seems to be whether you like the result or not. Is that accurate?
So, which one of us is right about K76 (not A76)?
And regardless of which one of us is right, how does that affect your refusal to address the fact that Behe is conflating the result of a process of evolutionary change in an organism, one with a complex life cycle under varying selection, with mutation rate?
There's still no evidence that two mutations must occur simultaneously.
And what does your use of the violent ad hominem metaphor of decapitation say about your motivation here? Is it a desire to win at any cost, or a desire to learn the truth?
Comment by JAM — July 6, 2007 @ 12:06 pm
July 6th, 2007 at 12:07 pm
TP writes:
TP, I just got the book and read only the first chapter but it seems to me Behe is using malaria to build a case. In the previous comment I made on this I argued that RM = NS was relevant pre and post merger. Would that not be relevant to malaria? IOW, even accepting all the author's points re: SET, a critique of RM + NS is relevant to the accuracy of current paradigms is it not?
Comment by Bradford — July 6, 2007 @ 12:07 pm
July 6th, 2007 at 12:15 pm
Yes, but why choose a system in which culture methods have been nearly impossible until recently, and in which mutation rates are much more difficult to measure, if Behe's goal is to extrapolate to the mutation rate of humans?
Why not just start with human cells in culture, for example?
Don't negative conclusions (Behe's is that mutation fails to supply sufficient variation to allow natural selection to act) require loads of evidence?
Comment by JAM — July 6, 2007 @ 12:15 pm
July 6th, 2007 at 12:21 pm
I'm not going to answer the questions until finishing the book other than to note that sufficient evidence is a given at all times.
Comment by Bradford — July 6, 2007 @ 12:21 pm
July 6th, 2007 at 12:31 pm
Let's get this straght then, you said:
You mean, you said something that was untrue and tried to use this untruth against me and Behe.
Don't try to sugar coat your mistake. That wasn't just a mistake, that was outright incompetence. Hehehe!:mrgreen:
And you're a scientist?
Comment by Salvador T. Cordova — July 6, 2007 @ 12:31 pm
July 6th, 2007 at 12:36 pm
Now that JAM has partially fessed up to his error, I invite him to publicly retract this little screed:
Now JAM, for all the readers, repeat after me: "I JAM totally blew my calculations because my presumption of A76 was totally wrong. I withdraw my mistaken claim. I said the math was easy. But in fact, I couldn't even get my facts straight. I was wrong. I was wrong".:twisted:
Comment by Salvador T. Cordova — July 6, 2007 @ 12:36 pm
July 6th, 2007 at 12:42 pm
I believe JAM has already corrected his previous misstatement.
Well, are you going to answer my concerns?
Comment by Zachriel — July 6, 2007 @ 12:42 pm
July 6th, 2007 at 12:52 pm
Zachriel:
When I read these estimates my reaction is a question. What is the rate necessary to generate outcome x and what is the basis for the claim?
Comment by Bradford — July 6, 2007 @ 12:52 pm
July 6th, 2007 at 1:04 pm
The only thing that was untrue was my identification of which paper contained the evidence. I corrected that and offered to send you a PDF of the more relevant paper.
There's still no evidence supporting Behe's assumption that two mutations must occur simultaneously. Even if it turned out that two mutations were necessary, neither you nor Behe have offered a bit of evidence to support his requirement of simultaneous mutations.
I didn't sugar coat anything. I admitted my error and offered you a PDF of the correct paper.
Can you point me to a single public forum in which you have admitted an error, Sal?
Yep. And unlike you, I have the integrity to admit my errors.
And you're a Christian?
When are you going to admit that your claim that I was avoiding your questions on UD was nothing but wishful thinking on your part?
That was a citation for what was written above it.
Sal, you are confused. As Zachriel patiently explained to you, this is based on mounds of data on mutation rates.
My facts about mutation rates are still straight. They didn't depend on the Molecular Cell paper. Heck, you can't even admit that "A76" has nothing to do with anything. The wild-type residue is called K76.
I'm still waiting for you to support Behe's assumption that two mutations must occur simultaneously with any evidence.
Have you found any evidence that the mutations must occur simultaneously, Sal?
And if that assumption is incorrect, doesn't that make Behe's calculation of probability a billion-fold more likely?
Comment by JAM — July 6, 2007 @ 1:04 pm
July 6th, 2007 at 1:13 pm
Interesting stuff in that Tan et al. paper JAM mentioned above. It appears that a mutation in K76 (T or I) is crucial, but presumably not quite sufficient to confer full-blown resistance (sorry about format; copying from PDF often yields bad results)
Comment by Raevmo — July 6, 2007 @ 1:13 pm
July 6th, 2007 at 1:21 pm
Behe is assuming:
1) that two substitutions must occur simultaneously, and
2) is using the rate observed after complex selection and misrepresenting it as the mutation rate.
Behe clearly has no evidentiary basis for either assumption, and Sal clearly can't find any evidence either.
If we used the measured mutation rate in Plasmodium of 2.5E-9 (no different from that in humans), the probability of two simultaneous mutations is 6.3E-18, almost 1000-fold more likely than Behe's 10E-20.
The most likely hypothesis is that the mutations were acquired sequentially. If we treat Plasmodium as a haploid organism that only reproduces asexually, a new, specific mutation per infectious cycle is statistically nearly certain, as each life cycle involves 10E8-10E13 mitotic cell divisions.
If we look at reality and note that Plasmodium reproduces sexually in the mosquito, the probability becomes several orders of magnitude higher, as synergistic substitutions can be assembled by intragenic recombination.
All that being said, it is clear from the data that the infrequent emergence of populations of resistant Plasmodium is a result of reversing fitness landscapes, because the fitness of CQR mutant haplotypes is uniformly lower than wild-type haplotypes in the absence of CQ. Behe even notes this, but ignores it in his conclusions.
Comment by JAM — July 6, 2007 @ 1:21 pm
July 7th, 2007 at 8:07 pm
Nick does the numbers. See,
I. M. Hastings, P. G. Bray, S. A. Ward (2002). "PARASITOLOGY: A Requiem for Chloroquine." Science 4 October 2002: Vol. 298. no. 5591, pp. 74-75. DOI: 10.1126/science.1077573
Comment by Zachriel — July 7, 2007 @ 8:07 pm
July 7th, 2007 at 10:56 pm
From the parallel thread over at Uncommon Descent:
White's table is described as "Approximate per-parasite frequencies for genetic events (mutations or gene amplifications) which lead to the emergence of clinically significant drug resistance of Plasmodium falciparum in vivo."
JAM: Yes, but it is clear that selection for CQR is intermittent and very complex when it is present. You can't look through the funhouse lens of that kind of selection and claim to be looking directly at mutation rates.
White concurs, "Immunity also considerably reduces the emergence of resistance (White 1999b). Host defence contributes a major anti-parasitic effect, and any spontaneously generated drug-resistant mutant malaria parasite must contend not only with the antimalarial drug concentrations that are present, but also with host immunity," and then considers many other factors that affect the rate of emergence.
Comment by Zachriel — July 7, 2007 @ 10:56 pm
July 7th, 2007 at 11:52 pm
Z, let me predict the reply of Sal et al.:
Yeah, but because White used the term "mutation frequency" once [even though the context makes it clear that he wasn't using it accurately], Behe must be right that two simultaneous substitutions are required.
Comment by JAM — July 7, 2007 @ 11:52 pm
July 11th, 2007 at 9:16 pm
OFF-Topic to JAM
You're being watched!
Comment by Zachriel — July 11, 2007 @ 9:16 pm
July 11th, 2007 at 10:29 pm
JAM: Expecting an answer from Salvatore that isn't an outright distortion of the actual data or one that completely ignores what you've said (as he is desperately trying to avoid the point you've actually raised, while still claiming victory) is vastly optimistic of you. I've been impressed with your patience throughout this.
Comment by Aegeri — July 11, 2007 @ 10:29 pm
July 11th, 2007 at 10:37 pm
It's JAM appreciation night. JAM, ID critics come loaded for bear when they sense an event like Dover and Behe's new book. It's as if ID will go away when high profilers are debunked. Behe's book is more than a blip on the screen but not all that much more.
Comment by Bradford — July 11, 2007 @ 10:37 pm
July 12th, 2007 at 4:16 am
Salvador,
You're claiming to want to know what the "Edge of Evolution" is. This is a problem people have been working on for 70 odd years; it's why Haldane, Fisher, Kimura and these guys are so famous. They were all working hard calculating and building models which tell us what the "Edge of Evolution" is.
I didn't know anything about malaria prior to reading these posts and a couple of these papers, but it's apparent to me now that Plasmodium is a terrible "model organism" for Behe to try to derive mutation rates from. It's life cycle is just to darned complex. It has both sexual and asexual reproduction, asexual reproduction in the liver, a different mode of asexual reproduction in the blood, then sexual reproduction in the mosquito gut followed by (yet another mode of) asexual reproduction in the mosquito. Each of these different places will have different CQ concentrations, and different fitness landscapes for our little parasite, and in the case of sexual reproduction there's a lot of work to do to account for the different possibilities of crossover. So just building a model of the CQR population genetics is very hard work, and it appears that Behe just hasn't done this.
Seriously, pull your head back into your shell, swallow your pride for 2 seconds, and go out and purchase a good text on population genetics which has a lot of example problems to work through. Work through the problems. Then you'll at least understand what you're criticising.
Comment by Patrick Caldon — July 12, 2007 @ 4:16 am
July 12th, 2007 at 8:17 am
True, but others disagree.
As Intelligent Design is at least in part a political movement, it requires a response.
Comment by Zachriel — July 12, 2007 @ 8:17 am
July 12th, 2007 at 11:11 am
Refer me to the part of Behe's book that is political.
Comment by Bradford — July 12, 2007 @ 11:11 am
July 12th, 2007 at 12:25 pm
Thanks. Just so you know, this has continued at UD with me being banned, apparently for using the same words as Behe did. Here is Sal's most recent post [bolding by me]:
Here's what Behe wrote:
"The likelihood that Homo sapiens achieved any single mutation of the kind required for malaria to become resistant to chloroquine"“not the easiest mutation, to be sure, but still only a shift of two amino acids"“…
So the only conclusion a rational person can reach is that my use of Behe's actual words is a "strawman" and "baloney."
I'd like to thank the proprietors here for not showing Sal's intellectual cowardice and being open to discussion.
Comment by JAM — July 12, 2007 @ 12:25 pm
July 12th, 2007 at 12:53 pm
Response to Ken Miller
JAM is invited to keep repeating his strawman arguments which are refuted by Behe in his response to Miller.
PS
By the way Zach, you had to wait for JAM to admit his egregious error (the Fidock paper) before conceding it. Would you have let him get away with it had I not called him on it and had he not fessed up?
The same goes for Aegeri. hehehe.
Comment by Salvador T. Cordova — July 12, 2007 @ 12:53 pm
July 12th, 2007 at 1:19 pm
Or so. That's correct. Evolution does not always work in a specific direction, and not every conceivable adaptation is guaranteed to appear. Evolution is stochastic and opportunistic. In other words, Behe was incorrect on the facts, and would have no point anyway.
That's an odd attitude for someone who blogs on a forum that consistently censors opposing views.
JAM's error above was hardly egregious as all he did was cite the wrong paper. He then offered the correct paper. That's what he is supposed to do.
Comment by Zachriel — July 12, 2007 @ 1:19 pm
July 12th, 2007 at 1:46 pm
The second quoted section in my previous comment should be attributed to Salvador T. Cordova.
Comment by Zachriel — July 12, 2007 @ 1:46 pm
July 12th, 2007 at 1:46 pm
Sal, you thanked DaveScot for disinviting me at UD, so I doubt the sincerity of any invitation.
Second, my argument isn't a straw man, and your pointing to another forum in which Behe is frantically backpedalling from his claims in the book doesn't make it a straw man. Behe clearly contradicts himself, which does nothing to show that my direct quoting of him is a straw man. I suppose that goes with your Orwellian view in which I'm wrong for noting that "single mutation" means "single mutation," instead of "two mutations."
Is your need to submit to authority so strong that you can't see/admit the contradictions?
And Sal refused my offer on UD, apparently because he is afraid to contrast Behe's rhetoric with the evidence.
Comment by JAM — July 12, 2007 @ 1:46 pm
July 12th, 2007 at 4:45 pm
Maybe he missed it too.
As for egregious errors, I don't remember you either noting or conceding this one from DaveScot:
"The answer is simple and I'm surprised you (or anyone else I read here) didn't know the answer. The answer is that each single point copy error can be to any one of four nucleotides (ACTG)."
Did you tell Dave that since the wild-type base has to be one of those four, that only three of them would be mutations, since a T->T "copy error" is anything but an error for DNA, but a howler for Dave?
Or are you only concerned about errors that your opponents make?
Comment by JAM — July 12, 2007 @ 4:45 pm
July 17th, 2007 at 7:18 pm
Wrong thread. Please ignore.
Comment by Zachriel — July 17, 2007 @ 7:18 pm