Why are We Disagreeing with ID?

[lee_merrill]

@CrisprCAS9

@lee_merrill

This gets back to irreducible complexity, are there selectable paths to a cilium, a flagellum, etc.?

It is not my job to demonstrate your claim. If you are claiming that ID/IC are useful, then you need to demonstrate the applicability of the argument to some actual example. That’s the way this works.

“With the criterion of two protein-protein binding sites, we can quickly see why stupendously complex structures such as the cilium, the flagellum, and the machinery that builds them are beyond Darwinian evolution. The flagellum has dozens of protein parts that specifically bind to each other; the cilium has hundreds. The IFT particle itself has sixteen proteins; even complex A, the smaller subset of IFT, has half a dozen protein parts, enormously beyond the reach of Darwinian processes. In fact, drawing the edge of evolution at complexes of three different kinds of cellular proteins means that the great majority of functional cellular features are across that line, not just the most intricate ones that command our attention such as the cilium and flagellum. Most proteins in the cell work as teams of a half dozen or more.” (The Edge of Evolution, p. 146)

@Faizal_Ali

This assumes that what Behe considers a “selectable path” is how such things arise.

It isn’t.

Then a selectable path is unlikely, do we agree?

@T_aquaticus

The hypothesis is that an irreducibly complex system can not evolve through pathways that involve neutral mutations. How do we falsify that hypothesis?

@Faizal_Ali

Is that Behe’s hypothesis? This is a genuine question, I don’t know that he has ever worded it in quite that manner.
To my understanding (and according to how @lee_merrill keeps presenting it) Behe argues that a system of a given level of complexity cannot arise without a number of selectable steps, and sometimes (e.g. for a “CCC”) a “selectable step” would require that two or more mutations occur at the same time. He then argues that the number of “selectable steps” required exceeds the number that could be expected to arise thru unguided natural processes.

I must not have been speaking clearly, Behe’s edge is at a “double-CCC” (CCC: chloroquine-complexity cluster, 10^20 organisms needed for chloroquine resistance to arise). Since a CCC evidently requires 2 deleterious mutations, and a new protein-protein binding site (at 4-6 deleterious mutations) is on the order of a CCC of difficulty, Behe places his edge at a “double-CCC”, or two new protein-protein binding sites.

[T_aquaticus]

@lee_merrill

Since a CCC evidently requires 2 deleterious mutations, and a new protein-protein binding site (at 4-6 deleterious mutations) is on the order of a CCC of difficulty, Behe places his edge at a “double-CCC”, or two new protein-protein binding sites.

Where did Behe demonstrate that every protein-protein binding site requires 4 to 6 deleterious mutations?

How is it that among a few billion B cell clones there are hundreds of thousands of randomly evolved protein-protein binding sites that aid in immunity?

[CrisprCAS9]

@lee_merrill

[Quote] (The Edge of Evolution, p. 146)

Repeating the claim you need to support does nothing to support it. Try again.

[Faizal_Ali]

Furthermore:

@lee_merrill

@Faizal_Ali

Is that Behe’s hypothesis? This is a genuine question, I don’t know that he has ever worded it in quite that manner.
To my understanding (and according to how @lee_merrill keeps presenting it) Behe argues that a system of a given level of complexity cannot arise without a number of selectable steps, and sometimes (e.g. for a “CCC”) a “selectable step” would require that two or more mutations occur at the same time. He then argues that the number of “selectable steps” required exceeds the number that could be expected to arise thru unguided natural processes.

I must not have been speaking clearly, Behe’s edge is at a “double-CCC” (CCC: chloroquine-complexity cluster, 10^20 organisms needed for chloroquine resistance to arise). Since a CCC evidently requires 2 deleterious mutations, and a new protein-protein binding site (at 4-6 deleterious mutations) is on the order of a CCC of difficulty, Behe places his edge at a “double-CCC”, or two new protein-protein binding sites.

First of all, your attempted clarification does not indicate that I have in any way misunderstood your position.

Secondly, exactly what do you mean by this: “Since a CCC evidently requires 2 deleterious mutations, and a new protein-protein binding site (at 4-6 deleterious mutations) is on the order of a CCC of difficulty.”

If a CCC requires 2 deleterious mutations (according to Behe’s fantasy-based model) then wouldn’t a protein-protein binding site requiring 4-6 deleterious mutations be a double or triple CCC level of difficulty? You seem confused on this.

[Faizal_Ali]

@lee_merrill

But a random walk to a new protein-protein binding site is not going to get very far, very fast.

Why not? Behe admitted this happened in HIV, and that is just one example. One in which he had specifically denied this had ever happened and even wrote about. So imagine how many must
exist in all the organisms that Behe has not even looked at.

@lee_merrill

Then a selectable path is unlikely, do we agree?

I agree that Nigel Tufnel’s amps go up to 11. That doesn’t mean they are any louder than all the amps whose volume knobs only go up to ten.

@lee_merrill

Since a CCC evidently requires 2 deleterious mutations

But it doesn’t, as you should know by now. Here, a gentle reminder:

https://www.pnas.org/doi/full/10.1073/pnas.1322965111

[Dan_Eastwood]

@colewd

I think either statement is fine.

OK then.

1. Design which we already know (COMMA) are produced by a mind, or
2. Design (comma) which we know are produced by a mind,

… can be inferred from observing a purposeful arrangement of parts.

Note we could drop “mind” altogether, leaving: Design can be inferred from observing a purposeful arrangement of parts. Is this an adequate definition for Intelligent Design? I’m guessing you will say “no”, but why?

If you see what I’m getting at, “mind” in the definition of ID makes it perfectly valid, even necessary, to make some prediction about the mind behind the design in order to have a testable hypothesis.

Also, since all matter is comprised of fundamental “parts”, fit together by the laws of physics, it would appear that by your definition, all matter is designed. I do not think this definition of ID is falsifiable by any means.

If I have changed your meaning at any point, please note the error and follow through to how this could be falsified.

@colewd

ID is not required to create a testable model of gravity.

It appears to be a complete non-sequitur. That’s why I keep asking you for an example that might actually be relevant … like a pocket-watch.

@colewd

evidence for nature is not evidence AGAINST design

It is evidence against design as a direct cause.

Perhaps you do not understand what it means “to falsify” a hypothesis. So what if it can happen in nature, it could also be designed. This removes the necessity of ID, but does not remove the possibility.

Also, the definition of ID we have agreed on makes no mention of necessity or direct cause.

Again the design inference is falsified when you can put a successfully tested natural hypothesis against it as you have tentatively identified the direct cause.

And here you say outright that you are testing a natural hypothesis, not a design hypothesis. This is what prevaricating looks like.

[Dan_Eastwood]

@colewd

You are continuing to beg to invoke a straw man argument. Have you thought about your need to do this?

You continue to abuse definitions, prevaricate when asked to provide definitions, torture logic, and make unsupportable claims. Have you thought about your need to do this?

[Dan_Eastwood]

@colewd

@Dan_Eastwood

You are the one supporting claims of Intelligent Design. You support that a purposeful arrangement of parts implies design. Therefore a designer is capable of purposefully arranging parts. This should be … you know … obvious.

I agree your statement is logically true however the argument is not about the designer. That becomes a philosophical discussion. Again, evidence for design…hard stop.

Back to this one, and tying up the loose ends. Since all matter is evidence of design (see above), then evidence for “nature” is by definition also evidence for Design. Go figure.

Evolution can be falsified in a number of ways that are clearly defined. That says something important, because if ID science, then it should make predictions that are clearly falsifiable. If there were any real science in ID, then people would be applying it instead of arguing about it on Internet forums.

[RonSewell (RonS)]

@colewd

Design which is a known product of a mind can be inferred from observing a purposeful arrangement of parts. (Behe). The more closely matched parts the stronger the design inference.

How would you infer design for this desert obelisk, which had no matched parts, or evident purpose for that matter.

[colewd (Bill Cole)]

@Dan_Eastwood

Evolution can be falsified in a number of ways that are clearly defined. That says something important, because if ID science, then it should make predictions that are clearly falsifiable. If there were any real science in ID, then people would be applying it instead of arguing about it on Internet forums.

Hi Dan
I think a lot of the confusion comes from evolution and design being an either or discussion. IMO both have merits and strengths and weaknesses. Design is a limited argument but is a useful tool to explain some things in nature that the natural mechanisms that are properties of matter cannot like purposely arranged parts.

Design is limited but can be a useful alternative method to shake out new ideas. It is beyond me why people are fighting the use of this new tool and method for detecting design in nature.

[colewd (Bill Cole)]

@RonSewell

How would you infer design for this desert obelisk, which had no matched parts, or evident purpose for that matter.

Hi Ron

With this type of object design detection is difficult.

[nwrickert (Neil Rickert)]

@colewd

It is beyond me why people are fighting the use of this new tool and method for detecting design in nature.

As far as I can tell, your “new tool” has failed to detect anything.

@colewd

With this type of object design detection is difficult.

And apparently it cannot even detect a case where design is obvious.

[lee_merrill]

@T_aquaticus

Where did Behe demonstrate that every protein-protein binding site requires 4 to 6 deleterious mutations?

In his book, The Edge of Evolution, pp. 133-134, here is an excerpt: “So one way to get a new binding site would be to change just five or six amino acids in a coherent patch in the right way. [12] This very rough estimation fits nicely with studies that have been done on protein structure. [13]” (p. 134)

@T_aquaticus

How is it that among a few billion B cell clones there are hundreds of thousands of randomly evolved protein-protein binding sites that aid in immunity?

Because the immune system is set up to generate binding sites, but evolution inside the cell isn’t set up that way.

@CrisprCAS9

@lee_merrill

[Quote] (The Edge of Evolution, p. 146)

Repeating the claim you need to support does nothing to support it.

But it was mentioned that "Most proteins in the cell work as teams of a half dozen or more.” Thus these would be beyond Behe’s edge of two new protein-protein binding sites.

[Mercer (John Mercer)]

@colewd

I think a lot of the confusion comes from evolution and design being an either or discussion.

I think you’re avoiding the concept of a scientific hypothesis again.

@colewd

IMO both have merits and strengths and weaknesses.

You don’t have a hypothesis for design; that makes it nonexistent as science.

@colewd

Design is a limited argument but is a useful tool to explain some things in nature that the natural mechanism that are properties of matter cannot like purposely arranged parts.

Hypotheses are far better tools than arguments. You should consider formulating and testing one sometime.

When I visit elementary schools to talk about science, I ask the students to consider two hypotheses:

1. My dog sits when I say “Sit!” because s/he understands the literal meaning of the word.
2. My dog sits when I say “Sit!” because s/he understands only the way I say the word, not its meaning.

Do you see that these hypotheses generate empirical predictions that even an 8-year-old can understand? This is how real science works.

Do you see the terms “argument,” “tool,” “discussion,” or any of your other favorites in there? Why do you go on about those things instead of hypotheses?

[lee_merrill]

@Faizal_Ali

If a CCC requires 2 deleterious mutations (according to Behe’s fantasy-based model) then wouldn’t a protein-protein binding site requiring 4-6 deleterious mutations be a double or triple CCC level of difficulty?

Different mutation rates might be the reason.

@Faizal_Ali

@lee_merrill

But a random walk to a new protein-protein binding site is not going to get very far, very fast.

Why not? Behe admitted this happened in HIV, and that is just one example. One in which he had specifically denied this had ever happened and even wrote about. So imagine how many must
exist in all the organisms that Behe has not even looked at.

Well, HIV is special, since it has a high mutation rate, and a huge number of viruses.

@Faizal_Ali

@lee_merrill

Since a CCC evidently requires 2 deleterious mutations

But it doesn’t, as you should know by now. Here, a gentle reminder:

https://www.pnas.org/doi/full/10.1073/pnas.1322965111

Are you arguing that the two minimum mutations needed are not deleterious? If so, a reminder that they decrease significantly on the withdrawal of chloroquine.

[Faizal_Ali]

@colewd

Hi Ron

With this type of object design detection is difficult.

Really? So you have a hard time determining whether that was designed and not a naturally occurring structure?

I should know by now never to underestimate your ability to astound. You’re still the champion, I should never had doubted you.

[RonSewell (RonS)]

@colewd

With this type of object design detection is difficult.

I would suggest that design detection is obvious and immediate. The reason being that people are familiar with what is natural and what is manufactured through a lifetime of experience. It is due to this familiarity that there is recognition that sheet metal is designed and its placement in a desert is not natural. The same applies to all designed objects from knives to watches to trucks to laptops on mars or otherwise. We recognize design because we are familiar with manufacture and human made objects. The designs put forward by ID we recognize under the category of natural, and thus emerging naturally.

[Roy (30-year veteran)]

@lee_merrill

@Faizal_Ali

So he might begrudgingly admit that neutral processes can produce some changes…

But a random walk to a new protein-protein binding site is not going to get very far, very fast.

Since you can’t calculate poker probabilities, I doubt you know the mathematics of random walks either.

Feel free to demonstrate some expertise by, say, showing us how to calculate the expected distance from the starting point after a random walk of N steps on a flat plane.

If/when you realise you can’t, perhaps you could stop making baseless assertions.

[Faizal_Ali]

@lee_merrill

Different mutation rates might be the reason.

Huh.

@lee_merrill

Well, HIV is special, since it has a high mutation rate, and a huge number of viruses.

But Behe said there were no new protein complexes. Wrote it in a book. Then an undergrad spent a few minutes on the internet and found a new protein complex.

So when Behe says there are no other new protein complexes anywhere because he says so, should we believe him?

@lee_merrill

Are you arguing that the two minimum mutations needed are not deleterious?

No, I am informing you that it is known for a fact that they are not deleterious. For the umpteenth time. And each time I inform you of this, you respond with pablum like this:

@lee_merrill

If so, a reminder that they decrease significantly on the withdrawal of chloroquine.

Snork.

[CrisprCAS9]

@lee_merrill

But it was mentioned that "Most proteins in the cell work as teams of a half dozen or more.” Thus these would be beyond Behe’s edge of two new protein-protein binding sites.

Only if there are no possible intermediate steps, which is the thing you’ve been repeatedly asked to demonstrate. Because whether you realize it or not, you’ve made the claim that there are no possible pathways. It’s your responsibility to support that claim.