Methinks it is sort-of like two weasels

@lee_merrill Quote Mining does not contribute to an honest or rigorous discussion. This is not FaceBook - we expect better here.

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The combined probability is used. But we know of two paths that lead to chloroquine resistance, this is overwhelmed by the number of trials needed (about 10^20).

I’m not sure what you mean here.

Again, we must distinguish between viewing an event before the fact, and viewing an event after the fact.

Again, we must distinguish between viewing an event before the fact, and viewing an event after the fact. I repeat myself because you all are making the same mistake over and over again. And I’m not saying an outcome didn’t happen, I’m only saying that the event, viewed before the fact, is improbable.

But the probability that some event will occur (say in the case of the lottery) is indeed as you say, 1.

Are you saying that all biological structures are likely? That all hands in poker have probability 1?

Certainly there are single mutations that increase resistance, but there are two mutations that are essential, two individually non-selectable mutations.

But this is not a refutation of my point.

They reference a paper by Summers et al. that shows two likely paths to resistance.

No, I’m interested in the probability that it evolved.

Viewing the event after the fact! But you can still view the event before the fact, and compute that probability.

Well, I’m interested in a sequence of unselected steps, that it what Behe defines as irreducible complexity: “An irreducibly complex evolutionary pathway is one that contains one or more unselected steps (that is, one or more necessary-but-unselected mutations). The degree of irreducible complexity is the number of unselected steps in the pathway” (Wikipedia here)

Behe’s edge of evolution is at an event with probability 1 in 10^40, at the evolution of two new protein binding sites. “The immediate, most important implication is that complexes with more than two different binding sites—ones that require three or more different kinds of proteins—are beyond the edge of evolution, past what is biologically reasonable to expect Darwinian evolution to have accomplished in all of life in all of the billion-year history of the world.” (The Edge of Evolution: The Search for the Limits of Darwinism (p. 146))

Thus a new interaction with 8 binding sites would be beyond Dembski’s probability bound.

But I mean the curve.

Yet existing variation came about via new mutations.

But it just so happens that I agree with his statement! You should take it up with him if you disagree.

I’m well aware that Larry Moran has disagreements with Behe, I only posted that quote to show that he agrees with Behe on certain points.

Before it was the Dembski Probability Bound, it was the Borel Limit, and Dembski misinterprets is badly.

The problem with this method of argument is that is makes every event of similar magnitude equally impossible. Take any event, write down the sequence of preceding events, multiply them all together. If it’s not already past Dembski’s Probability Bound just make the sequence longer until you get there. This is nonsensical as a method of inference, except in very limited circumstances where meaningful probabilities can be calculated. If you don’t believe me, try calculating the probability of what you hade for breakfast give 500 preceding events - you will find that what your breakfast is impossible.

BUT, set the impossible breakfast aside for a moment and consider just what these “multiplied probabilities of events” really mean. I calculate this sort of number regularly; in statistical theory this is called a Likelihood. In fact, It is very common to see likelihoods far smaller than 10^{-150}. This does not mean the data I am analyzing is impossible - it only means the sample size is at moderately large. In other words, this sort of calculation doesn’t mean what you seem to think it means.

The proper way to make use of the sort of calculation is using a Likelihood Ratio Test or a Baye’s Factor, for which references are readily available.

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A belated welcome, @Paul_King :slight_smile:

Based on your comments, which I have been following, I’d say your knowledge of statistics is doing just fine. I meant to comment earlier, but I’ve been busy.

I mean that the a priori probability of the draw coming out as it did is the same as the probability of predicting the same result. Clearly it is not just the probability that matters.

Which is one of the things I am explaining to you. It is one reason why your previous assertion (quoted below) is incorrect. But it is not the most important reason and anyone familiar with Dembski’s work should know it.

Events below Dembski’s universal probability bound can occur, without needing any other explanation. Indeed that must be true since it is trivial to generate events of arbitrarily low probability (excepting practical difficulties in really extreme cases). And Dembski would agree.

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I am discussing general principles, and not limiting myself to specific cases.

And the general principle explains why your assertion that longer paths have lower probabilities has little significance. The longer the path the more alternative paths are likely to be available.

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For reference, here is a nice essay about Dembski’s Probability Bound the Borel Limit.

And this quip from RationalWiki :wink:

In order for you to exist, your parents had to have sex exactly at a given time. One particular sperm cell had to fertilize one particular egg. Taking this back only a few generations we quickly reach the limit of Borel’s “law”. You, Sir, are therefore impossible.

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That may include sequence deletions, which of course cannot be seeing in the current sequence. That allows yet more alternative paths, and is known to lead to the evolution of Irreducibly Complex structures.

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Thank you. Just don’t ask me to do a chi-squared test!

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Nowadays we have computers to do the grunt work. :slight_smile:

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No, equally improbable.

And in the case of mutations, meaningful probabilities can be calculated.

No, improbable, viewed before the fact of the 500 events.

Now you are confusing probabilities and likelihoods. Dembski’s probability bound is just that, a probability bound, not a likelihood bound.

Let me try again, consider rolling a die, the probability of any given number coming up is 1/6. It does not matter if I pick the number before or after the roll, if I am viewing the probability of the event before the fact, the probability of the number picked coming up is still 1/6.

The probability of an event, considered before the fact, is “number of successful events” / “total number of events”, regardless of when or how the successful events are picked.

But can you quantify this? We have specific numbers for Behe’s example, there are 2 successful paths, and 1 success in about 10^20 trials. So not many alternative paths to chloroquine resistance here…

13 posts were split to a new topic: Why are We Disagreeing with ID?

There is no general quantification. It must be done separately for each individual case.
As I said above simply using the probability of the path that was followed is not sufficient - more analysis is required. Identifying the alternative paths and including them in the probability calculation is a part of that analysis.

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We have no such thing. Behe quote-mined a single sentence from a review.

Again, I invite you to bet to demonstrate your faith in Behe.

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You don’t know this.

How would a mutation that increases resistance NOT be selectable? Walk me through the molecular mechanisms.

No, it’s a description of your position.

Did you read it? Did you understand it? How do you know there are no others?

What about the papers that weren’t cited?

Lee, I’m asking whether you are willing to bet on Behe being correct.

What is the evidence, in terms of numbers of trials? Hint: what people say about the evidence is not the evidence.

Structures that meet that definition are easy to evolve by purely Darwinian mechanisms.

Moreover, neither you nor Behe has the slightest idea which mutations were necessary.

And he reached that conclusion by misrepresenting the evidence.

No, existing variation comes from OLD mutations. Thus, Behe’s assumption that organisms are “waiting” for new mutations is untenable.

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