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Author Topic:   Irreducible Complexity and TalkOrigins
Suroof
Junior Member (Idle past 5948 days)
Posts: 22
From: Birmingham
Joined: 12-12-2007


Message 91 of 128 (440691)
12-14-2007 7:43 AM
Reply to: Message 89 by Wounded King
12-14-2007 5:35 AM


Re: Again with the non sequitur.
What sort of logic is that? How does the existence of a simple program to illustrate a point, and which does illustrate that point as a counter to the strawman 'tornado in a junkyard' type calculations so beloved of creationists, which is not intended to be an evolutionary algorithm to produce complexity show that no real evolutionary algorithm exists to explain complexity. It is, once again, a complete non sequitur. Its like saying that the fact that my rabbit isn't a dog shows that no dogs exist.
Sorry, what I meant to say was: Dawkins program isn't an example of an actual EA and actual EAs explaining SC doesn't exist.

This message is a reply to:
 Message 89 by Wounded King, posted 12-14-2007 5:35 AM Wounded King has replied

Replies to this message:
 Message 94 by Wounded King, posted 12-14-2007 8:26 AM Suroof has replied

  
Chiroptera
Inactive Member


Message 92 of 128 (440693)
12-14-2007 7:47 AM
Reply to: Message 90 by Suroof
12-14-2007 7:40 AM


Re: Let's consider this!
Hi, Suroof.
...for example SETI....
We're not talking about SETI -- we're discussing Mt. Rushmore. Let's keep to this one example for now, just to keep things from getting unnecessarily complicated. As I said, this is an important point; once we determine why we can conclude that Mt. Rushmore is designed, then we'll see that it doesn't apply to biological systems like the flagellum or blood clotting.
-
If aliens did observe Mt. Rushmore they would conclude intelligence because the complex arrangement corresponds to an independent known pattern (the human face).
Okay, this is a bunch of words strung together with no real meaning.
The question is pretty simple.
I'm examining Mt. Rushmore. How can I determine whether it was designed or not? Specify the things that I can look at right now that will be a sign that it was designed.

If it's truly good and powerful, it deserves to engender a thousand misunderstandings. -- Ben Ratcliffe

This message is a reply to:
 Message 90 by Suroof, posted 12-14-2007 7:40 AM Suroof has replied

Replies to this message:
 Message 98 by Suroof, posted 12-14-2007 10:11 AM Chiroptera has replied

  
Percy
Member
Posts: 22391
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 93 of 128 (440694)
12-14-2007 7:50 AM
Reply to: Message 84 by Suroof
12-13-2007 9:47 PM


Re: The Edge
Suroof writes:
Of course, the few they have picked on have been shown to be evolvable too.
No they haven't - the blood clotting cascade, the cilium, phototransduction (http://www.arn.org/docs/behe/mb_idfrombiochemistry.htm) and many others
Actually, yes they have been shown to be evolvable and therefore not irreducibly complex. Behe has never submitted his ideas on ID and IC to any scientific peer-reviewed technical journal, but his ideas received so much popular attention through his book Darwin's Black Box that a number of biologists have invested the effort to debunk his ideas anyway. Plus he was completely undressed on the stand at Dover. If blood clotting evolution and so forth are sufficiently interesting to you that you'd like to discuss them in detail then we could do that.
Irreducible complexity does not at present have any status as a valid scientific concept. What the concept of specified complexity (SC) lacks at present, aside from the complete absence of any representation in the technical literature, is an objective definition and an objective quantitative measure. For example, IDists should be able to answer questions like these about SC:
  1. How much SC is there in an extremely simple genome, say the three nucleotide sequence TAG?
  2. How much SC is there in a slightly more complex genome, say CATGATTGGAACTGGACC?
  3. Since the human genome has been decoded, how much SC is there in the human genome?
  4. What is the threshold of SC beyond which something could not have come about naturally, i.e., is IC?
More fatally, ID suffers from an infinite regression that begins with the question, "Who was the creator of life on earth?" If the answer is, "Life from elsewhere in the universe," then the next question is, "Who was the creator of this other life?" Ultimately the answer ends up at God, revealing the inherently religious nature of ID. Behe admitted he believed the intelligent designer was God right on the stand at Dover.
--Percy

This message is a reply to:
 Message 84 by Suroof, posted 12-13-2007 9:47 PM Suroof has replied

Replies to this message:
 Message 96 by Suroof, posted 12-14-2007 9:28 AM Percy has replied

  
Wounded King
Member
Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


Message 94 of 128 (440698)
12-14-2007 8:26 AM
Reply to: Message 91 by Suroof
12-14-2007 7:43 AM


Re: Again with the non sequitur.
So it isn't a non sequitur but rather an unsupported assertion. Obviously it is hard to do when SC is such a numinous term but in what way do the examples of the evolution of complex functions in artificial life evolutionary experiments such as those of Lenski et al.(2003) fail to meet the neccessary criteria?
TTFN,
WK

This message is a reply to:
 Message 91 by Suroof, posted 12-14-2007 7:43 AM Suroof has replied

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Suroof
Junior Member (Idle past 5948 days)
Posts: 22
From: Birmingham
Joined: 12-12-2007


Message 95 of 128 (440707)
12-14-2007 9:20 AM
Reply to: Message 94 by Wounded King
12-14-2007 8:26 AM


Re: Again with the non sequitur.
Obviously it is hard to do when SC is such a numinous term but in what way do the examples of the evolution of complex functions in artificial life evolutionary experiments such as those of Lenski et al.(2003) fail to meet the neccessary criteria?
This is an example of a computer programmed EA model that has some built in assumptions that do not correlate to real life evolution. Dembski discusses the paper in his book Uncommon Dissent. As Dembski observes "the computer programmers built into the simulation what they thought evolution needed to make it work". An extract from the book, and some further discussion can be found here: Evolution by Intelligent Design: A Response to Lenski et al.

This message is a reply to:
 Message 94 by Wounded King, posted 12-14-2007 8:26 AM Wounded King has not replied

  
Suroof
Junior Member (Idle past 5948 days)
Posts: 22
From: Birmingham
Joined: 12-12-2007


Message 96 of 128 (440713)
12-14-2007 9:28 AM
Reply to: Message 93 by Percy
12-14-2007 7:50 AM


Re: The Edge
If blood clotting evolution and so forth are sufficiently interesting to you that you'd like to discuss them in detail then we could do that.
Yes, if you have any idea as to how the irreducible core of the blood clotting system (as described in message 65) evolved in a Darwinian step-by-step model please show us.

This message is a reply to:
 Message 93 by Percy, posted 12-14-2007 7:50 AM Percy has replied

Replies to this message:
 Message 97 by RickJB, posted 12-14-2007 10:05 AM Suroof has replied
 Message 109 by Percy, posted 12-14-2007 2:10 PM Suroof has not replied

  
RickJB
Member (Idle past 4990 days)
Posts: 917
From: London, UK
Joined: 04-14-2006


Message 97 of 128 (440724)
12-14-2007 10:05 AM
Reply to: Message 96 by Suroof
12-14-2007 9:28 AM


Re: The Edge
Suroof writes:
Yes, if you have any idea as to how the irreducible core of the blood clotting system (as described in message 65) evolved in a Darwinian step-by-step model please show us.
From TalkOrigins:
Here then is an example of how such "irreducible" mutual dependencies can arise by evolution, illustrating the same process described by Muller in 1918. Miller's article goes into more detail and covers stages that I omit in this shorter account. I am simply focused here on showing the evolution of mutual dependencies, or interlocking complexity.
(A) Start with a system consisting simply of two proteins; the clot-maker and the protease. The protease is "activated" by contact with tissue proteins - as would happen when there is a break in a blood vessel. The activated protease is then able to activate the clot-maker, and the clot is formed.
(B) Now have a gene duplication for the protease. This is a reasonably common process in evolution; an entire section of the genome gets doubled; so that now there are two genes, both producing the same protease protein. There is no difference to the working of blood clotting; as all the proteins involved are the same.
(C) Now have a small modification to one of the duplicated genes. There are now two slightly different forms of the protease. Call them protease-A and protease-B. Either one would manage fine for blood clotting. In that sense, the system of three proteins is no longer irreducible; it has redundancy.
(D) Now suppose that there are mutations to protease-A which give it a capacity to activate protease-B. That is, both proteins get activated at the break in a vessel by contact with tissue proteins; but protease-B gets additional activation from the activated protease-A. This kind of additional activation can have some selective benefits, in speeding up the response of the whole system.
(E) Finally, now that protease-B is activated by protease-A, it no longer depends on activation from the tissue proteins, and further modifications can reduce this activation pathway. This makes the whole system "irreducible" again, because all three proteins are now required for clotting.
The fundamental point here is that an irreducibly complex core of three proteins can arise from a simpler system by evolutionary changes. Behe's argument depends on a strawman of evolution. Behe ignores the role of modifications to proteins, and bases his argument simply on the problem with getting a system by adding parts one by one.
Link here.
Much more interesting than "Godidit"....

This message is a reply to:
 Message 96 by Suroof, posted 12-14-2007 9:28 AM Suroof has replied

Replies to this message:
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Suroof
Junior Member (Idle past 5948 days)
Posts: 22
From: Birmingham
Joined: 12-12-2007


Message 98 of 128 (440725)
12-14-2007 10:11 AM
Reply to: Message 92 by Chiroptera
12-14-2007 7:47 AM


Re: Let's consider this!
How can I determine whether it was designed or not? Specify the things that I can look at right now that will be a sign that it was designed
Well, put more simply, you conclude design because you recognise a pattern (purposeful and arranged) that could not have been produced by chance.

This message is a reply to:
 Message 92 by Chiroptera, posted 12-14-2007 7:47 AM Chiroptera has replied

Replies to this message:
 Message 102 by Chiroptera, posted 12-14-2007 11:36 AM Suroof has replied

  
Suroof
Junior Member (Idle past 5948 days)
Posts: 22
From: Birmingham
Joined: 12-12-2007


Message 99 of 128 (440732)
12-14-2007 10:32 AM
Reply to: Message 97 by RickJB
12-14-2007 10:05 AM


Re: The Edge
Link here.
Much more interesting than "Godidit"....
I'm guessing this is taken from Miller's Finding Darwin's God. It suffers from some major flaws
(A) Start with a system consisting simply of two proteins; the clot-maker and the protease. The protease is "activated" by contact with tissue proteins - as would happen when there is a break in a blood vessel. The activated protease is then able to activate the clot-maker, and the clot is formed.
The problem here is there is nothing to reverse the process once the clot is made. Assuming this simplistic process did exist, the clot-maker would be activated immediately after a wound and never broken down; it would probably even be misdirected because the protease doesn't cease to work.
The Darwinist problem isn't just about forming a clot, it is regulation.
(B) Now have a gene duplication for the protease. This is a reasonably common process in evolution; an entire section of the genome gets doubled; so that now there are two genes, both producing the same protease protein. There is no difference to the working of blood clotting; as all the proteins involved are the same.
(C) Now have a small modification to one of the duplicated genes. There are now two slightly different forms of the protease. Call them protease-A and protease-B. Either one would manage fine for blood clotting. In that sense, the system of three proteins is no longer irreducible; it has redundancy.
(D) Now suppose that there are mutations to protease-A which give it a capacity to activate protease-B. That is, both proteins get activated at the break in a vessel by contact with tissue proteins; but protease-B gets additional activation from the activated protease-A. This kind of additional activation can have some selective benefits, in speeding up the response of the whole system.
(E) Finally, now that protease-B is activated by protease-A, it no longer depends on activation from the tissue proteins, and further modifications can reduce this activation pathway. This makes the whole system "irreducible" again, because all three proteins are now required for clotting.
The above scenario suffers from several problems, described in Behe's response to Miller here: http://www.arn.org/...mb_indefenseofbloodclottingcascade.htm
Edited by Suroof, : No reason given.

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Replies to this message:
 Message 100 by AdminNosy, posted 12-14-2007 10:38 AM Suroof has replied

  
AdminNosy
Administrator
Posts: 4754
From: Vancouver, BC, Canada
Joined: 11-11-2003


Message 100 of 128 (440733)
12-14-2007 10:38 AM
Reply to: Message 99 by Suroof
12-14-2007 10:32 AM


What is your argument?
The above scenario suffers from several problems, described in Behe's response to Miller here:
You explain what the problems are. You can use the link as further support. As you note others are supplying the arguments not just links.

This message is a reply to:
 Message 99 by Suroof, posted 12-14-2007 10:32 AM Suroof has replied

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Suroof
Junior Member (Idle past 5948 days)
Posts: 22
From: Birmingham
Joined: 12-12-2007


Message 101 of 128 (440742)
12-14-2007 10:52 AM
Reply to: Message 100 by AdminNosy
12-14-2007 10:38 AM


Re: What is your argument?
You explain what the problems are. You can use the link as further support. As you note others are supplying the arguments not just links.
I've explained that Miller's scenario does not account for regulation. A second problem which Behe identifies is the over exaggarated use of gene duplication. Firstly if these duplications are initially redundant but later necessary, there is no reason why they should be selected. Secondly gene duplication can only produce copies not complicated new steps with extremely specified features for enzyme-substrate interactions. As Behe wrote "With clotting, however, the task of initiating and adding proteins to the cascade appears to be quite problematic. With one protein acting on the next, which acts on the next, and so forth, duplicating a given protein doesn't yield a new step in the cascade. Both copies of the duplicated protein would have the same target protein which they activate, and would themselves be activated by the same protein as before. In order to explain how the cascade arose, therefore, an investigator would have to propose a detailed route whereby a duplicated protein turns into a step in the cascade, with a new target, and a new activator. Furthermore, because clotting can easily go awry and cause severe problems when it is uncontrolled, a serious model for the evolution of blood clotting would have to include such things as: a quantitative description of the starting state, including tangentially interacting systems; a description of the initial regulatory mechanisms; a quantitatively-justified proposal for a step-by-step route to the new state; a detailed plan for how regulatory mechanisms accommodated the changes; and more."
I would put it into my own words but Behe's explanation of the other problems couldn't be simpler: "Here are several more problems with the brief scenario. First, it should be noted that the problem the scenario is trying to solve--hemostasis--can't initially be severe, because the starting point is a living organism, which must already be quite well adjusted to its environment. Second, the protein that Miller postulates to be mistargeted to the bloodstream would then no longer be doing its initial job; that would be expected to be detrimental to the organism. Third, Miller begins by postulating the mistargeting of a non-specific protease-precursor (a zymogen) to the bloodstream of some unfortunate organism. (Miller writes that if his scenario is correct, then "the clotting enzymes would have to be near-duplicates of a pancreatic enzyme . . . ." (Miller 1999, 157) Pancreatic enzymes, which have to digest a wide variety of protein foodstuffs, are among the most nonspecific of enzymes). Now, that would pose a severe health threat to the mutant organism even greater than just an unregulated clotting cascade. For example, if the digestive enzyme precursor trypsinogen were mistargeted to the bloodstream, the potential for disaster would be very large. In the pancreas, misactivation of trypsinogen is prevented by the presence of trypsin inhibitor. In Miller's scenario one cannot plausibly suppose there to be a trypsin inhibitor fortuitously circulating in the plasma. If the mistargeted enzyme were accidentally activated, it would most likely cause generalized damage in the absence of a regulatory mechanism. It would not be a viable evolutionary intermediate.
Problems of regulation aside, it is difficult to see the advantage of the protease mistargeted to the bloodstream in the first place. While Miller's initial cellular or tissue protease would by necessity be localized to the site of a cut, a circulating zymogen would not. In modern organisms thrombinogen has a vitamin K-dependent gla-domain which allows it to localize to cell surfaces. In order to be effective before membrane-binding features had been acquired, it would seem that the postulated circulating protease would have to be present at rather high concentrations, exacerbating the regulatory difficulties discussed above."
Edited by Suroof, : No reason given.

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Chiroptera
Inactive Member


Message 102 of 128 (440746)
12-14-2007 11:36 AM
Reply to: Message 98 by Suroof
12-14-2007 10:11 AM


Re: Let's consider this!
...because you recognise a pattern (purposeful and arranged)...
You are not being very precise here. Not all patterns are purposeful or arranged. A snowflake, for example, or any other crystal has a definite pattern, yet it forms through the ordinary laws of physics as individual water molecules attach to the growing crystal.
We need some way of determining whether or not the pattern that we see on Mt. Rushmore is "purposeful" or "arranged".
-
... that could not have been produced by chance.
But it's always possible to have been produced by chance. Again, you're not being very clear.
Besides that, you are discounting some natural process working in a way that I don't yet understand or recognize.
So far, you have not yet been able to figure out how to discount a natural process that we have not yet identified. Nor have we discounted the possibility, however unlikely, possibility that it occurred through chance.

If it's truly good and powerful, it deserves to engender a thousand misunderstandings. -- Ben Ratcliffe

This message is a reply to:
 Message 98 by Suroof, posted 12-14-2007 10:11 AM Suroof has replied

Replies to this message:
 Message 105 by Suroof, posted 12-14-2007 12:05 PM Chiroptera has replied

  
RickJB
Member (Idle past 4990 days)
Posts: 917
From: London, UK
Joined: 04-14-2006


Message 103 of 128 (440747)
12-14-2007 11:36 AM
Reply to: Message 101 by Suroof
12-14-2007 10:52 AM


Re: What is your argument?
Suroof writes:
Firstly if these duplications are initially redundant but later necessary, there is no reason why they should be selected.
Gene duplication can be free from selective pressure if mutations have no deleterious effects.
Suroof writes:
Secondly gene duplication can only produce copies not complicated new steps with extremely specified features for enzyme-substrate interactions.
Gene duplication gives rise to mutation. The accumulation of mutations produce new features.

This message is a reply to:
 Message 101 by Suroof, posted 12-14-2007 10:52 AM Suroof has replied

Replies to this message:
 Message 104 by Suroof, posted 12-14-2007 11:57 AM RickJB has replied

  
Suroof
Junior Member (Idle past 5948 days)
Posts: 22
From: Birmingham
Joined: 12-12-2007


Message 104 of 128 (440751)
12-14-2007 11:57 AM
Reply to: Message 103 by RickJB
12-14-2007 11:36 AM


Re: What is your argument?
Gene duplication can be free from selective pressure if mutations have no deleterious effects.Gene duplication gives rise to mutation. The accumulation of mutations produce new features.
As stated before, however, a duplicated protein even with the necessary modifications would have to have a new target and a new activator, and system of regulation. "Because clotting can easily go awry and cause severe problems when it is uncontrolled, a serious model for the evolution of blood clotting would have to include such things as: a quantitative description of the starting state, including tangentially interacting systems; a description of the initial regulatory mechanisms; a quantitatively-justified proposal for a step-by-step route to the new state; a detailed plan for how regulatory mechanisms accommodated the changes; and more"
Anyhow, Miller's scenario breaks down from the very beginning by proposing an unregulated clotting agent.
Edited by Suroof, : No reason given.

This message is a reply to:
 Message 103 by RickJB, posted 12-14-2007 11:36 AM RickJB has replied

Replies to this message:
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Suroof
Junior Member (Idle past 5948 days)
Posts: 22
From: Birmingham
Joined: 12-12-2007


Message 105 of 128 (440753)
12-14-2007 12:05 PM
Reply to: Message 102 by Chiroptera
12-14-2007 11:36 AM


Re: Let's consider this!
A snowflake, for example, or any other crystal has a definite pattern, yet it forms through the ordinary laws of physics as individual water molecules attach to the growing crystal
Yes, a snowflake is produced by necessity - it is not contingent. The faces on Mt. Rushmore however, are contingent. Further, they are complex (because the probability of that exact pattern forming is extremely low) and specified (because it relates to a known independent pattern - a face). In the rationale for the prime numbers analogy for SETI Debski wrote:
"Nothing in the laws of physics requires radio signals to take one form or another. The prime sequence is therefore contingent rather than necessary. Also, the prime sequence is long and hence complex. Note that if the sequence were extremely short and therefore lacked complexity, it could easily have happened by chance. Finally, the sequence was not merely complex but also exhibited an independently given pattern or specification (it was not just any old sequence of numbers but a mathematically significant one”the prime numbers).
Intelligence leaves behind a characteristic trademark or signature”what within the intelligent design community is now called specified complexity. An event exhibits specified complexity if it is contingent and therefore not necessary; if it is complex and therefore not readily repeatable by chance; and if it is specified in the sense of exhibiting an independently given pattern. Note that a merely improbable event is not sufficient to eliminate chance”by flipping a coin long enough, one will witness a highly complex or improbable event. Even so, one will have no reason to attribute it to anything other than chance.
The important thing about specifications is that they be objectively given and not arbitrarily imposed on events after the fact. For instance, if an archer fires arrows at a wall and then paints bull’s-eyes around them, the archer imposes a pattern after the fact. On the other hand, if the targets are set up in advance (“specified”), and then the archer hits them accurately, one legitimately concludes that it was by design."

This message is a reply to:
 Message 102 by Chiroptera, posted 12-14-2007 11:36 AM Chiroptera has replied

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