Methinks it is sort-of like two weasels

[Rumraket (Mikkel R.)]

@lee_merrill

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

But that can’t tell you that it didn’t evolve for the same reason that such a calculation can’t tell you that a particular set of cards can’t be drawn. Merely saying that from the perspective of the ancestral/prior state some particular outcome looks unlikely can’t tell you that the outcome you do have wasn’t, in fact, produced. From the perspective of your great grandparents 10 generations back your existence would seem miraculously remote too. And yet here you are.

So I just have to ask, what is the value or significance of doing such a calculation with respect to evolution? They give us no reason to think that any extant structure didn’t evolve.

I must conclude you have no rational basis for thinking any known biological structure or system was not produced by evolution. There is no reason to think intermediates in flagellum evolution would be nonfunctional(they’d just have functions other than cellular motility), and the a priori probabilites you calculate can’t rationally support the conclusion that X didn’t evolve in the same way they can’t support the conclusion that you aren’t the product of 10 generations of ancestors.

[Roy (34-year veteran)]

@lee_merrill

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…

There are two successful paths^[1] that we know about. No-one has evaluated all the other possible paths to determine whether or not they would lead to chloroquine resistance, or to something else equally useful. So you have absolutely no idea how many alternative paths there might be.

The 1 in 10^20 calculation is wrong too, for multiple reasons, including (i) it doesn’t take in to account the mutations occurring in either order, (ii) it doesn’t take into account the possibility of a second form of resistance having arisen in an organism that was already resistant.

---

1. Actually two successful sets of paths. ↩︎

[Dan_Eastwood]

@lee_merrill

No, equally improbable.

Very well then, improbable, the point remains. You are arguing against math (the theory of statistical inference).

A likelihood is a joint probability, which describes your calculation. I echo @swamidass’s suggestion to consider why working scientists and mathematicians, Christian and atheist, do not accept this form of argument.Could it be that it simply doesn’t work for any similar example you may care to choose?

[Paul_King]

Now it’s time to consider what you have left out of Dembski’s ideas. It’s an important one - specification. While it doesn’t go quite far enough it is still a big step in the right direction. And it does explain my examples quite well.

The basic idea is simple enough and contained in the name - it’s a description of the event, and one that covers the important details of the event while omitting everything else - and removing the “everything else” from consideration when calculating the probability. The only probability that matters is the probability of meeting the specification.

A prediction is a perfectly good specification. In fact it’s the best sort of specification, because it’s made without any hindsight.

So predicting the lottery is impressive because the prediction is a specification.

The draw itself - without the prediction - (probably) has no specification, so it is not impressive at all.

Predicting more heads than tails in a sequence of fair coin tosses is a specification but it has a high probability of being right (0.5 for an odd number of tosses, no matter how many - and never less than 0.25). So that is unimpressive, too.

[lee_merrill]

@Paul_King

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.

Right, so two paths were identified, and all paths were open to evolution, so we’re not excluding any paths by definition. And including these paths in the calculation makes no real difference, as I said before.

@Mercer

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

How so? I need details.

@Mercer

You don’t know this.

Yes, I do know this, 10^20 / 2 is still on the order of 10^20.

@Mercer

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

But I meant that there are two individually non-selectable mutations on each path, that are essential to resistance.

@Mercer

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.

“A minimum of two mutations sufficed for (low) CQ transport activity, and as few as four conferred full activity.” (Summers et al. here) That seems quite clear. Now there may be other paths, but they would likely be less probable than 1 in 10^20, since evolution should have found them in the more than 10^20 trials it went through.

@Mercer

What is the evidence, in terms of numbers of trials?

Do you mean how do we know that there were 10^20 trials? “On the other hand, resistance to chloroquine has appeared fewer than ten times in the whole world in the past half century. Nicholas White of Mahidol University in Thailand points out that if you multiply the number of parasites in a person who is very ill with malaria times the number of people who get malaria per year times the number of years since the introduction of chloroquine, then you can estimate that the odds of a parasite developing resistance to chloroquine is roughly one in a hundred billion billion.16 In shorthand scientific notation, that’s one in 10^20.” (The Edge of Evolution, p. 57)

@Mercer

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

@Mercer

And he reached that conclusion by misrepresenting the evidence.

How so? I need more than mere assertions.

@Mercer

No, existing variation comes from OLD mutations.

But I meant that at one point these mutations were new. And this is the pertinence of Behe’s approach: he notes what evolution actually did, with both existing variation, and with new mutations.

[lee_merrill]

@Rumraket

But that can’t tell you that it didn’t evolve for the same reason that such a calculation can’t tell you that a particular set of cards can’t be drawn.

But I’m saying it’s improbable, not that it cannot happen.

@Rumraket

From the perspective of your great grandparents 10 generations back your existence would seem miraculously remote too. And yet here you are.

Again you are confusing the probability of an event after the fact, with the probability of an event viewed before the fact. Roll a die, with one outcome marked as “success”, the probability viewing the event before the fact is 1/6, and after the fact is either 1 or 0.

@Rumraket

There is no reason to think intermediates in flagellum evolution would be nonfunctional(they’d just have functions other than cellular motility)…

Behe’s edge of evolution is helpful here, if two new protein-protein binding sites are the limit of what evolution can do, then producing a flagellum would require many of these. Now if there are selectable stopping-points along the way, we should see flagella being formed today–but we don’t. This leads me to believe that there are no mostly-selectable pathways to a flagellum.

[lee_merrill]

@Roy

No-one has evaluated all the other possible paths to determine whether or not they would lead to chloroquine resistance, or to something else equally useful. So you have absolutely no idea how many alternative paths there might be.

But as I said above, this is the beauty of Behe’s approach, to note what evolution actually did. No possible paths were excluded, mutations can occur in any order, and other forms of resistance could have occurred in an already-resistant organism.

[lee_merrill]

@Dan_Eastwood

Very well then, improbable , the point remains. You are arguing against math (the theory of statistical inference).

A likelihood is a joint probability, which describes your calculation.

But as far as I understand it, the likeliest mean (of say, the binomial, or exponential or normal distributions) is just the sample mean, so we’re back to 1 in 10^20 for chloroquine resistance.

[Roy (34-year veteran)]

@lee_merrill

@Roy

No-one has evaluated all the other possible paths to determine whether or not they would lead to chloroquine resistance, or to something else equally useful. So you have absolutely no idea how many alternative paths there might be.

But as I said above, this is the beauty of Behe’s approach, to note what evolution actually did. No possible paths were excluded, mutations can occur in any order, and other forms of resistance could have occurred in an already-resistant organism.

Behe is ignoring what could have happened but didn’t. His approach isn’t beautiful, it’s blather.

[Rumraket (Mikkel R.)]

@lee_merrill

@Rumraket

But that can’t tell you that it didn’t evolve for the same reason that such a calculation can’t tell you that a particular set of cards can’t be drawn.

But I’m saying it’s improbable, not that it cannot happen.

And I’m asking what the significance of that statement is, since it can’t rationally tell us that something didn’t evolve.

@lee_merrill

@Rumraket

From the perspective of your great grandparents 10 generations back your existence would seem miraculously remote too. And yet here you are.

Again you are confusing the probability of an event after the fact, with the probability of an event viewed before the fact.

No, me explaining why it isn’t rational to argue against something having occurred by the statement that X is a priori unlikely, with an analogy to your own existence, is not me confusing anything. The analogy simply makes it more obvious why the reasoning you are employing does not support the conclusion you are seeking.

@lee_merrill

Behe’s edge of evolution is helpful here, if two new protein-protein binding sites are the limit of what evolution can do

But we have no reason to think it is. The diametrically opposite is the case. You have unfortunately been misinformed about biochemistry by reading creationist literature I’m sorry to have to tell you.

In fact protein-protein binding is so ubiquitous that it is practically unavoidable by chance, so much so that we know there is selection operating to suppress and reduce the chance occurrence of protein-protein interactions in the cell.

For a nice overview of this phenomenon I recommend this excellent review article:
https://pubs.acs.org/doi/abs/10.1021/acs.chemrev.8b00753

Should one of these protein-protein binding sites however be beneficial, simple and realistic modeling work shows it is easy to select for it instead. It is known that a considerable fraction of proteins are something like one mutation away from forming binding spots on their surface that would make them able to form large fibrils and structures. I have a thread about a year ago where I reference a few papers that detail these phenomena:

An interesting couple of articles on evolution of protein complexes and multimers

I came across this interesting article(pdf here) on how proteins have an easy time forming large multi-protein complexes, so much so that there’s often purifying selection against this tendency: Abstract The self-association of proteins into symmetric complexes is ubiquitous in all kingdoms of life. Symmetric complexes possess unique geometric and functional properties, but their internal symmetry can pose a risk. In sickle-cell disease, the symmetry of haemoglobin exacerbates the effect of a mutation, triggering assembly into harmful fibrils. Here we examine the universality of this mechanism and its relation to protein structure geometry. We introduced point mutations solely designed to increase surface hydrophobicity among 12 distinct symmetric complexes from Escherichia coli. Notably, all responded by forming supramolecular assemblies in vitro, as well as in vivo upon heterologous expression in Saccharomyces cerevisiae. Remarkably, in four cases, micrometre-long fibrils formed…

@lee_merrill

Now if there are selectable stopping-points along the way, we should see flagella being formed today–but we don’t.

How do you know we don’t? What assay did you run, how long did you observe and where? How do you know that some prokaryote out there with some membrane-embedded structure isn’t on it’s way to evolving a flagellum-like structure?

[Paul_King]

@lee_merrill

Right, so two paths were identified, and all paths were open to evolution, so we’re not excluding any paths by definition. And including these paths in the calculation makes no real difference, as I said before.

By definition you are excluding any unidentified paths.

[Roy (34-year veteran)]

@Paul_King

Now it’s time to consider what you have left out of Dembski’s ideas. It’s an important one - specification.

Not that surprising, since Dembski invariably left out any actual specification himself.

[Mercer (John Mercer)]

@lee_merrill

@Mercer

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

How so? I need details.

You provided them below!

@lee_merrill

@Mercer

You don’t know this.

Yes, I do know this, 10^20 / 2 is still on the order of 10^20.

No, you don’t know this. All you know is that Behe wrote this. Behe commonly ignores and/or misrepresents the primary literature.

@lee_merrill

@Mercer

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

But I meant that there are two individually non-selectable mutations on each path, that are essential to resistance.

Forget about paths. How much money would you bet that there is single mutation documented in the primary literature that increases resistance and is therefore selectable?

@lee_merrill

@Mercer

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

“A minimum of two mutations sufficed for (low) CQ transport activity, and as few as four conferred full activity.” (Summers et al. here) That seems quite clear.

That was done in Xenopus oocytes. Quoting text is not analyzing evidence.

You apparently didn’t read the preceding sentence:

Multiple mutational pathways led to saturable CQ transport via PfCRT, but these could be separated into two main lineages.

That’s not the same as only two pathways. Did you read the paper? Examine the data?

@lee_merrill

@Mercer

What is the evidence, in terms of numbers of trials?

Do you mean how do we know that there were 10^20 trials? “On the other hand, resistance to chloroquine has appeared fewer than ten times in the whole world in the past half century. Nicholas White of Mahidol University in Thailand points out that if you multiply the number of parasites in a person who is very ill with malaria times the number of people who get malaria per year times the number of years since the introduction of chloroquine, then you can estimate that the odds of a parasite developing resistance to chloroquine is roughly one in a hundred billion billion.16 In shorthand scientific notation, that’s one in 10^20.” (The Edge of Evolution, p. 57)

That’s the quote mine. That’s not what White pointed out at all, and he has stated that.

Behe’s representation of a single sentence from a review, whether represented accurately or inaccurately, is not evidence. So, how confident are you that the actual evidence is consistent with Behe’s claim?

@lee_merrill

@Mercer

And he reached that conclusion by misrepresenting the evidence.

How so? I need more than mere assertions.

Look at the evidence.

@lee_merrill

@Mercer

No, existing variation comes from OLD mutations.

But I meant that at one point these mutations were new.

Irrelevant.

@lee_merrill

And this is the pertinence of Behe’s approach: he notes what evolution actually did, with both existing variation, and with new mutations.

No, Behe’s simplistic math completely ignores existing variation.

[RonSewell (RonS)]

@lee_merrill

Again you are confusing the probability of an event after the fact, with the probability of an event viewed before the fact. Roll a die, with one outcome marked as “success”, the probability viewing the event before the fact is 1/6, and after the fact is either 1 or 0.

Again, you are confusing the probability of an event, viewed before and after the fact, with a goal. There is no “success”, only outcomes.

@lee_merrill

Now if there are selectable stopping-points along the way, we should see flagella being formed today–but we don’t.

Why should we see flagella being formed today? Given our understanding of biology, is there any reason we would expect that?

As far as the edge of evolution is concerned, everything we see in life around us is within that edge. There is a boundless realm within the imagination but outside the history of life on earth or the limits of reality, which does not exist in actuality. Evolution is as much about constraints as it is about life as we find it, and accounts for both. That is why we observe amphibians, marsupials, reptiles, mammals and birds to be chordate tetrapods. The constraints of evolution is why there is a phylogenic tree of life, and why there are no six legged mammals and winged dragons with arms and legs. It is under design that such fantastical creatures are limitlessly possible. The nested hierarchy is inherent in biology, unlike design which must invoke some arbitrary “reuse of design”.

The general but persistent predicament for ID is that no convincing example of a feature of nature beyond the edge of evolution has ever been advanced, and that which has been suggested is perpetually confined to a zone which is, at best, the edge of currently advancing scientific knowledge.

[lee_merrill]

@Paul_King

Now it’s time to consider what you have left out of Dembski’s ideas. It’s an important one - specification . While it doesn’t go quite far enough it is still a big step in the right direction.

But “the probability that nature did it” includes “it” as a specification of a flagellum, or chloroquine resistance, etc.

@Paul_King

A prediction is a perfectly good specification. In fact it’s the best sort of specification, because it’s made without any hindsight.

No, I think what you are predicting has to have specified information.

[Michelle (Michelle Ols)]

@RonSewell

The constraints of evolution is why there is a phylogenic tree of life, and why there are no six legged mammals and winged dragons with arms and legs. It is under design that such fantastical creatures are limitlessly possible. The nested hierarchy is inherent in biology, unlike design which must invoke some arbitrary “reuse of design”.

The idea of a creature with wings, arms and legs is a very helpful visual example. Many creatures like that exist in fantasy literature, but no actual reuse of parts like that in the real world. Thanks for that!

[Roy (34-year veteran)]

@lee_merrill

Right, so two paths were identified, and all paths were open to evolution, so we’re not excluding any paths by definition. And including these paths in the calculation makes no real difference, as I said before.

A vision is forming…

Michael Behe and Lee Merrill are at the poker table. (There are a couple of other players too)

MB: I have a straight flush. 3, 4, 5, 6 and 7 of spades.

LM: I have a straight flush too! 8, 9, 10, Jack and Queen of clubs! Amazing!

MB: A straight flush has only happened twice at this table. We can use that to estimate the odds of a straight flush happening. If you multiply the number of games played at this table over the past century by the number of players and the number of hands per game, then you can estimate the odds of getting a straight flush as roughly 2 in 5000x5x30, or 1 in 325,000.

LM: There are 12,994,800 possible poker hands…

MB: But only two confirmed ways to get a straight flush.

LM: Right, so two straight flushes were identified, and all possible hands were open to being dealt, so we’re not excluding any possible hands by definition. And including these possible hands in the calculation would make no real difference. So the probability of being dealt a straight flush is 2/12,994,800 or 1 in 6,447,400. And the probability that we both got a straight flush is that squared, or about 1 in 10^14.

OP1: But there are other straight flushes you could have got…

LM: But as I said above, this is the beauty of Behe’s approach, to note what the cards actually did. No other possible straight flushes were excluded, we could have got them in either order, and other straight flushes could have occurred before.

OP1: Huh? You just contradicted yourself.

LM: No I didn’t.

MB: This is an extremely improbable occurrence. That is evidence it happened by design.

OP2: But any other hands would have the same improbability as the ones you got. They’re all equally unlikely.

LM: You are confusing the probability of an event after the fact, with the probability of an event viewed before the fact. The probability of getting these hands after the fact is 1. Also, you’re forgetting that these hands were specified in advance . The “probability of getting these hands” includes “these hands” as a specification…

[Roy (34-year veteran)]

@lee_merrill

@Paul_King

Now it’s time to consider what you have left out of Dembski’s ideas. It’s an important one - specification . While it doesn’t go quite far enough it is still a big step in the right direction.

But “the probability that nature did it” includes “it” as a specification of a flagellum, or chloroquine resistance, etc.

This is what happens when you swallow ID.

[Paul_King]

@lee_merrill

But “the probability that nature did it” includes “it” as a specification of a flagellum, or chloroquine resistance, etc.

Despite the “but” that doesn’t change anything I’ve said. The point is that it is the probability of meeting the specification that matters not the probability of the particular path taken to reach it.

@lee_merrill

No, I think what you are predicting has to have specified information

Certainly not. The prediction is a valid specification in itself - because it is made with no knowledge of the outcome. It is not just “separable” - it is completely separate.

[Dan_Eastwood]

@lee_merrill

But as far as I understand it, the likeliest mean (of say, the binomial, or exponential or normal distributions) is just the sample mean, so we’re back to 1 in 10^20 for chloroquine resistance.

It is the joint probability of the data observed. This can be used to estimate parameters (Maximum Likeihood), including the population mean. The value of the likelihood itself has no interpretation other than the joint probability of all the data. It does not imply the final observation in a series is improbable. That would be equivalent to saying that you are improbable because you could only be the result of a single sperm from your father and a single egg from your mother.

Likelihoods are also used in Likelihood Ratio tests, the ratio of likelihood for two models for the same data. Bayes Factors adjust this for a prior assumption.

There are other difficulties with your calculation: it assumes IID events, ignores selection, ignores “indirect” routes, and ignores deletions. Outside of very specific types of data (phylogenetic analysis). It lacks any definition of “design” that would allow the likelihood of design to be calculated for a likelihood ratio test*. We can force a Bayes Factor by making very silly assumptions, which it the closest “valid” interpretation for what your calculation actually means.

* With the possible exception of a Dependency Graph model (Ewert 2016), but this has other problems.