Has Intelligent Design some merit to get to new theories?

My point was they did not :thinking:

Or look at Miller. In many many articles he repeated his principially unsuccessful rebuttal of IC (level 2). Only in a footnote in his second book you find a glimmer of understanding Behe’s concept (maybe I remember incorrectly, if you want discuss that, I’ll check the book, but I just wanted to answer about ‘admitting failure’, there Doolittle is the best example).

That’s no argument for Behe’s concept, but one against an insufficient try to refute it.

I didn’t.

In another post I detailed about that.

I’m new in this forum, I don’t know how to find an old post quickly. If you’re more qualified in searching that, please help me.

Didn’t get it to finish, or didn’t implement IC?

there are other alternatives. Do you know Conklin

Conklin, E.G. (1953) ‘Edwin Grant Conklin’ in: Finkelstein, L. ‘Religion and Civilization Series. Thirteen Americans: Their Spiritual Autobiographies’ New York; London, Harper & Brothers URL: https://ia802701.us.archive.org/21/items/religionandcivil000911mbp/religionandcivil000911mbp.pdf, letzter Zugriff: S. 47-77

Conklin was a christian, but an evolutionist also. Around the Scopes trial he accepted a position only under the condition that he was allowed to teach evolution.

He wrote an interesting passage after describing problems of evolutionary mechanisms:

There must have been some directing cause, either outside of nature or in nature itself - a deus ex machina or a deus in machina" (p. 71)

(‘deus ex machina’ meaning interventionism, ‘deus in machina’ something like orthogenetic factors, given certain properties of matter and so on.) ‘Deus in machina’ in this form was quite common before the Modern Synthesis. Like many other theories they’re forgotten now. But it’s an interesting aside that quite a few re-emerge in the Extended Snythesis, these time with at least some experimental corroboration.

Not in the slightest. First of all Doolittle never claims that the mice were completely without issue as Behe appears to suggest. What he wrote is:

Let me conclude by mentioning that support for the Yin and Yang scenario is now coming from another quarter. Thus, it has become possible during the last decade to “knock out” genes in experimental organisms. “Knockout mice” are now a common (but expensive) tool in the armamentarium of those scientists anxious to cure the world’s ills. Recently the gene for plaminogen was knocked out of mice, and, predictably, those mice had thrombotic complications because fibrin clots could not be cleared away. Not long after that, the same workers knocked out the gene for fibrinogen in another line of mice. Again, predictably, these mice were ailing, although in this case hemorrhage was the problem. And what do you think happened when these two lines of mice were crossed? For all practical purposes, the mice lacking both genes were normal6 Contrary to claims about irreducible complexity, the entire ensemble of proteins is not needed. Music and harmony can arise from a smaller orchestra. No one doubts that mice deprived of these two genes would be compromised in the wild, but the mere fact that they appear normal in the laboratory setting is a striking example of the point and counterpoint, step-by-step scenario in reverse!

And the authors Bugge et al do state in their paper:

“Remarkably, mice with each of these deficits, even in combination, were born normal in appearance, survived to adulthood, and produced offspring. Thus, the major components of the PA-Plg system are not strictly required for development, growth, and reproduction.”

And later:

Fib Deficiency Alleviates Wasting of Plg-Deficient Mice

To examine the role of single and combined deficiencies in overall growth and survival of the mice, we followed the fate of a prospective cohort of mice initially consisting of 44 control mice, 25 Plg−/− mice, 16 Fib−/− mice, and 23 Plg−/−/Fib−/− mice. Plg−/− mice had essentially normal weight gain until 2 months of age (Figure 1b). Thereafter, a progressive weight loss was observed, which became severe after 4 months. The weight of Plg−/− mice 6 months or older was uniformly less than two-thirds that of control mice (Figure 1a and Figure 1b). In contrast, mice lacking only Fib exhibited normal weight gain as adolescents and no wasting phenomenon as adults, even when followed for more than 12 months (Figure 1a and Figure 1b). Remarkably, in the same genetic background, Plg−/−/Fib−/− mice, despite their lifelong lack of Plg, exhibited the same excellent growth properties as those of control and Fib−/− mice (Figure 1a and Figure 1b). Indeed, no signs of weight loss or wasting were observed in any of more than 20 Plg−/−/Fib−/− mice that were followed for more than a year. This dramatic rescue from the severe-wasting syndrome normally associated with Plg deficiency provided a first indication that general ill health in young Plg−/− mice depended on fibrin(ogen).

And of course we do have to consider that these genes didn’t evolve in mice, which ultimately can’t substitute well for the ancestral state even with gene knockouts, in the evolutionary history of the blood clotting cascade. So the fact that the loss of these genes in a modern context still incurs various health or fitness penalties doesn’t tell us that the ancestral state would be an unviable organism, nor that natural selection wouldn’t favor the gains of these two genes in the ancestral background.

It’s not clear how I am supposed to take this as a misreading by Doolittle, much less a problem for the evolutionary scenario for the blood clotting cascade.

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for what function “the entire ensemble of proteins is not needed” :thinking:

You’re talking about fitness of mice, not coagulation.

It finished generating the IC-part of the string, but as ‘effective’ as pure chance.

In the post I mentioned I provided the output of a run of that modified program.

Did you realize that ‘in the long run’ was a quip :thinking:

Fitness is what matters in evolution, not function. So whatever the function of systems that lack the two genes is, if it still provideded some sort of fitness benefit to organisms at the time, selection could favor and preserve it.

Life, particularly wound healing. See the evidence shown in Fig. 4.

No, wound healing too. This is the problem with ignoring evidence. The idea that a system has a single function, defined by Behe, is absurd, but you’ve swallowed and regurgitated it.

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do we agree that you talk about an indirect path :thinking:

[edit:

Just to check if I got your argument right.

An IC-system (e.g. regulated blood clotting) is embedded in another system (here: a mouse). As long as the mouse can thrive, it doesn’t matter if there are only functionless parts of that IC-system. They can mutate until they get together and provide the function of the IC-system.

Do you agree :thinking:

ist the mouse an IC-system :thinking:

It still seems to me you are making a fundamental error in logic.

Let’s take a biological trait that we have good reason to believe arose thru what you call a “direct Darwinian pathway.”

An ID proponent argues that this trait cannot be produced by someone banging their head against their desk. Therefore, the trait was designed.

Numerous scientists point out the evidence demonstrating that the trait, in fact, arose thru a “direct Darwinian pathway.”

The ID’er responds: “That does not disprove my argument. On the contrary, you have just confirmed that the trait cannot be produced by someone banging their head against their desk.”

In your opinion, does the ID’er win that debate? If we are talking strictly in terms of linguistics, arguably he does. The specific words he used to make his argument were not contradicted by the response i.e. they did not show that the trait can be produced by banging one’s head against a desk.

Which is why if you treat this as merely a debate involving linguistics, as you seem to be, you will entirely miss the point. This is first and foremost a scientific debate.

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I hope that you see the problem with that :thinking:

No, I do not. Please explain what you think the problem with evidence is.

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Sure. Like the example with the evolution of the pathway for vitamin c biosynthesis, that eventually was exapted to serve in preventing scurvy and a host of other organismal functions, but which likely evolved by cumulative selection for preventing oxidative stress, would technically qualify for an indirect pathway because the pathway gained a new function eventually.

Not entirely. I would not agree with the statement that “there are only functionless parts of that IC-system”. The individual parts, or assemblies of fewer sub-components, can have other functions. They might lack what you call “the function of the IC-system”, but that doesn’t make them functionless.

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That’s a good example of the absurdity of the definition. What is the function of a mouse?

I’m glad to read that :slightly_smiling_face:

I look at these issues from the viewpoint of history of evolutionary biology ever since Darwin (and a little bit before). You can analyze what mechanism(s) Darwin proposed and call that ‘darwinian’. Correct me if I’m wrong, Darwin proposed a direct pathway, the Modern Synthesis also.

Many modern theories are non-darwinian in this terminology.

Even Behe agrees :wink:

But that’s a necessary condition for a pathway guided by selection, not a sufficient one. Behe asks for an elaboration of that pathway.

Just as an aside: cumulative selection along a gradient is as proven as a naturalistic theory can be. There are observations, experiments, mathematical models, artificial selection and so on. If you read e.g. Dawkins or other popularizers most examples are exactly concerning structures of this kind. They can explain adaptation perfectly.

But you can ask if there are limits to this mechanism. As soon as you need a change of function it’s a little bit messed, e.g. like a constitutional monarchy with a king with only symbolic function.

it’s absurd to say “an organism is IC”. Orr did that in his Boston Review article at least implicitly.

Why ask me? Did I say that mice are IC?

think about interpretation of a poem. Two authors contradict each other. You can analyze their arguments with only a very loose connection to the poem by itself.

But do you agree that your motivation is winning a culture war and not an objective analysis of divergent theories as they are put forward in a specified discussion between proponents of different world views?

Someone can be right about evidence but using abysmal arguments.

I’m pretty sure Darwin didn’t think purely in terms of “direct” pathways in the way you appear to suggest here.

Darwin spoke of each step “providing a small benefit” to the organism. It’s not clear he meant that in terms of slightly improving the same original function throughout. In a way it’s rather obvious he could not have actually meant it only like that, because he even wrote about things like the swim bladder in fish and insect wings changing functions.

On the origin of species: The illustration of the swimbladder in fishes is a good one, because it shows us clearly the highly important fact that an organ originally constructed for one purpose, namely flotation, may be converted into one for a wholly different purpose, namely respiration. The swimbladder has, also, been worked in as an accessory to the auditory organs of certain fish, or, for I do not know which view is now generally held, a part of the auditory apparatus has been worked in as a complement to the swimbladder. All physiologists admit that the swimbladder is homologous, or ‘ideally similar,’ in position and structure with the lungs of the higher vertebrate animals: hence there seems to me to be no great difficulty in believing that natural selection has actually converted a swimbladder into a lung, or organ used exclusively for respiration.

I don’t think indirect pathways are non-Darwinian.

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