BooBoo wrote:You can read Behe's response to Ken Miller's criticism here:

http://www.evolutionnews.org/2015/01/ke ... 92691.html

So Behe originally claims that K76T is strongly deleterious, and Miller responds that it's neutral. And in this response, Behe attacks the claim that it's neutral by pointing out that it's beneficial. That seemed a bit fishy in itself.

Simple soul that I am, I wondered if that mutation could be neutral in one situation, and beneficial in another.

So I took a quick look at Miller's fig 4, the diagram from the PNAS paper, and sure enough, it's been established to be neutral if you start from the unmodified HB3 strain, and beneficial if you go via the D39 strain first.

That's not even surprising - a mutation that does nothing much on its own, but does something else if it's preceded by another one, even less surprising since the previous mutation is in the very next amino acid.

Given that the whole thrust of the work on chloroquine resistance is that in all these pathways to the the resistant strain, the mutations are sequential, it seems to me that Behe is just continuing to miss the same point - and missing it in the same way as I'm seeing quite a bit in my travels on this sort of topic - find some minor point, misconstrue it with a lot of huffing and puffing, and then use the misconstrual to discredit the opponent.

Straining out a gnat, and swallowing a camel, in fact.

Would appreciate if one of the biologists could confirm whether if I've read this right..

*Edited for typos

BooBoo wrote:

Rumraket wrote:
This is Behe's original and wrong claim. Simultaneity is not required, and probably not how CCC evolves.

You can read Behe's response to Ken Miller's criticism here:

http://www.evolutionnews.org/2015/01/ke ... 92691.html

Unfortunately, Miller dodges my challenge to provide a quantitative account of the rarity of the origin of chloroquine resistance. I had asked him to "Please keep the rhetoric to a minimum." Alas, to no avail. He cites no relevant numbers, makes no calculations -- just words.

What a fucking imbecile. How gullible does someone have to be to buy this guff?

BooBoo wrote:

Rumraket wrote:
This is Behe's original and wrong claim. Simultaneity is not required, and probably not how CCC evolves.

You can read Behe's response to Ken Miller's criticism here:

http://www.evolutionnews.org/2015/01/ke ... 92691.html

And we see that Behe totally skips the whole thing about simultaneity in his original claim, as if he never claimed it. Now he's just blathering that contextually deleterious mutations are "ominous for Darwinism". Weird how CCC then even evolves.

BooBoo wrote:He also responded to other critics before:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2644969/

http://www.genetics.org/content/181/2/821.full
He keeps making the same elementary mistake of specifying the outcome beforehand, then complaining this particular outcome is unlikely and so would only happen on average once every [insert long waiting time]:

Finally, Behe notes that for one prespecified pair of mutations in one gene in humans with the first one neutral, we obtain a “prohibitively long waiting time” of 216 million years. However, there are at least 20,000 genes in the human genome and for each gene tens if not hundreds of pairs of mutations that can occur in each one. Our results show that the waiting time for one pair of mutations is well approximated by an exponential distribution. If there are k nonoverlapping possibilities for double mutations, then by an elementary result in probability, the waiting time for the first occurrence is the minimum of k independent exponentials and hence has an exponential distribution with a mean that is divided by k. From this we see that, in the case in which the first mutant is neutral or mildy deleterious, double mutations can easily have caused a large number of changes in the human genome since our divergence from chimpanzees. Of course, if the first mutant already confers an advantage, then such changes are easier.

Booboo, did you even read Behe's response? From where I'm sitting it looks to me like you simply discovered "Behe has responded" and then that's good enough for you to start passing on the link.

Jesus fucking Christ these ID types are infinitely gullible. The IDiots at the discovery institute have merely to fart in their general direction and their acolytes are fainting at them as if it was Jesus himself that spoke.

Rumraket wrote:He keeps making the same elementary mistake of specifying the outcome beforehand, then complaining this particular outcome is unlikely and so would only happen on average once every [insert long waiting time]:

It's worse than that. What Behe is doing is treating a probability calculation as a waiting time. If I say that something has a probability of happening once in 200 million years, that doesn't mean I have to wait 200 million years for it to happen, it means that it's unlikely to occur more frequently. It doesn't prohibit it happening in a nanosecond, it only states that, if it does, it probably won't happen again for that long. Indeed, it happening twice in two nanoseconds is not prohibited, it just makes it unlikely that it will occur for another 400 million years. He's treating a statistical calculation as time-dependent.

And that's setting aside the fact that ALL such arguments that rely on low probability are spurious arguments from personal incredulity anyway.

hackenslash wrote:

Rumraket wrote:He keeps making the same elementary mistake of specifying the outcome beforehand, then complaining this particular outcome is unlikely and so would only happen on average once every [insert long waiting time]:

It's worse than that. What Behe is doing is treating a probability calculation as a waiting time. If I say that something has a probability of happening once in 200 million years, that doesn't mean I have to wait 200 million years for it to happen, it means that it's unlikely to occur more frequently. It doesn't prohibit it happening in a nanosecond, it only states that, if it does, it probably won't happen again for that long. Indeed, it happening twice in two nanoseconds is not prohibited, it just makes it unlikely that it will occur for another 400 million years. He's treating a statistical calculation as time-dependent.

It gets worse still. As Miller points out:

Let’s accept Behe’s number of 1 in 1020 for the evolution of a complex mutation like his CCC. As he admits, CCC’s have arisen multiple times in the malaria parasite population since the drug was first introduced in 1947. In fact, resistance to the drug appeared in the late 1950s and early 1960s, within just 15 years of its widespread use. So it only took a decade and a half for one of Behe’s CCC’s to emerge in the parasite population. Now, suppose that another drug, equal in effectiveness to chloroquine, were to come into wide use. According to Behe, resistance to both drugs would require two CCCs, and the probability of double resistance arising would be a CCC squared. That’s 1 in 1020 x 1020 or one chance in 1 in 1040. According to Behe’s math, that’s such a large number that we can call it impossible:

“…throughout the course of history there would have been slightly fewer than 1040 cells, a bit less than we’d expect to need to get a double CCC. The conclusion, then, is that the odds are slightly against even one double CCC showing up by Darwinian processes in the entire course of life on earth.” (Behe, 2007, p. 63).

Wow! Not even once in the history of life on earth? Pretty impressive. But the math is wrong, and it’s easy to see why. Chloroquine resistance arose in just a decade and a half, and is now common in the gene pool of this widespread parasite. Introduce a new drug for which the odds of evolving resistance are also 1 in 1020, and we can expect that it will take just about as long, 15 years, to evolve resistance to the second drug. Once you get that first CCC established in a population, the odds of developing a second one are not CCC squared. Rather, they are still 1 in 1020. Behe gets his super-long odds by pretending that both CCCs have to arise at once, in the same cell, purely by chance. They don’t, and I pointed this out in my Nature review when Behe attempted to apply his reasoning to human genetics:

I would take slight issue with that. I don't think Behe "pretend(s) that both CCCs have to arise at once, in the same cell." I think he is using the calculation that would be used to determine those odds and using it to determine the odds of the mutations occurring sequentially. His error, that is to say, is one involving high school level mathematics, rather than biology.

Indeed, but I'd also add that even were it the case that arch-fuckwit Behe's original strawman were accurate, namely that these mutations had to arise simultaneously in a single individual, this event still has a non-zero probability, and my former critique applies.

He's a moron and, at the risk of committing the genetic fallacy, if he told me that Darwin sailed on The Beagle, I'd be asking for citations.

I'm not sure that I am not missing the underlying point here (entirely possible). Behe is claiming, and BooBoo is trying to support, that chloroquine resistance must be such a rare thing to have evolved 'naturally' that for it to have actually happened (which no-one disputes) there must have been an intervention by some intelligent designer within the last few decades.

Is that correct?

Onyx8 wrote:I'm not sure that I am not missing the underlying point here (entirely possible). Behe is claiming, and BooBoo is trying to support, that chloroquine resistance must be such a rare thing to have evolved 'naturally' that for it to have actually happened (which no-one disputes) there must have been an intervention by some intelligent designer within the last few decades.

Is that correct?

No. Behe is fine with CCC evolving. His argument is that this is the "limit of Darwinian evolution" (or Edge of evolution, as his book was called). Because the malaria parasite populations are very large (much larger than the populations of large multicellular eukaryotes), there is no way something that requires two mutations or more could possibly evolve in the relatively short timescales that animals evolved in. That's basically the crux of his argument. So while chloroquine resistance evolved, there's no way something large and complex like plants and animals could in the amount of time available to life on Earth.

For example, we diverged from the common ancestor we share with the chimp about 5-6 million years ago. Even though our genomes are very similar (like 96% or thereabout), that still makes the genomes between chimps and humans different by hundreds of millions of nucleotides*.

This is where Behe is doing two things wrong.

1) He doesn't, apparently, understand that it's meaningless to specify two(or more) particular mutations and then derive the average waiting time for their arrival, when hundreds of mutations happen in parallel every generation.
He could have picked any two of these hundreds of mutations and calculated the same average waiting time for their emergence. Yet hundreds of them still happen, so what the hell is the point of the calculation?

It is pure propaganda meant to baffle the ID acolytes with numbers.

2) He's extrapolating the case of evolving effective chloroquine resistance to evolving large complex body plans and so on. Here he's basically saying that because this small set of mutational pathways are the only ones available to the malaria parasite which yield effective chloroquine resistance, there's no way some other particular outcome requiring even more mutations and with smaller population sizes (like Homo Sapiens evolving from our common ancestor) could have been found by a blind evolutionary process because a result requiring so many mutations is extremely improbable to be found in such a large search space. So, you know, god mustadunnit.

In part the same basic flaw is underlying both prongs of the argument. Point to all the things that could have been different (mutational events), but happened the way they did to get this particular result, derive the odds and then say "see how improbable that was? Therefore Jesus!"

The other issue is that you can't just extrapolate this particular case of chloroquine resistance to the entire history of life and large multicellular bodyplan evolution in particular. Most of the things that evolve aren't "the only functional solutions available" to evolution, just because it seems to be the case for malaria gaining chloroquine resistance. While chloroquine resistance requires specific mutations for effective transport, in the evolution of large multicellular eukaryotes almost all of the responsible mutations are mutations in gene expression networks that alter developmental timings. There are no "only this will work".

* 4% of 3.2 billion basepairs is 128 million. But of course, since close to 90% of our genome is junk, only a minority of these have any phenotypic effect. And then even more of the remaining are only nearly neutral and so on and so forth.

hackenslash wrote:Indeed, but I'd also add that even were it the case that arch-fuckwit Behe's original strawman were accurate, namely that these mutations had to arise simultaneously in a single individual, this event still has a non-zero probability, and my former critique applies.

True of course, but it's wrong to dismiss Behe's argument exclusively on there being a non-zero probability. If the probability of an event happening in a given time period is quantifiable, and the outcome relies on a lot of those events happening, then it's not intrinsically wrong to talk about waiting times.

If the probability is low enough, and the number of events required for the outcome is high enough, then the likelihood of a short waiting time will be too small to be credible - which is what Behe wrongly claims.

If it was reported that someone kept winning the lottery, at odds of 1 in 15 million, you'd pretty soon question either the odds or the reporting.

Behe questions the reporting, but it's on the basis of odds that he's made up. And not only does he make them up, he addresses the criticism with obfuscation.

BTW, @RR, I'd appreciate if you could cast an eye over the point I made earlier, tell me if I'm talking out of my arse or not.

TopCat wrote:

BooBoo wrote:You can read Behe's response to Ken Miller's criticism here:

http://www.evolutionnews.org/2015/01/ke ... 92691.html

So Behe originally claims that K76T is strongly deleterious, and Miller responds that it's neutral. And in this response, Behe attacks the claim that it's neutral by pointing out that it's beneficial. That seemed a bit fishy in itself.

Simple soul that I am, I wondered if that mutation could be neutral in one situation, and beneficial in another.

So I took a quick look at Miller's fig 4, the diagram from the PNAS paper, and sure enough, it's been established to be neutral if you start from the unmodified HB3 strain, and beneficial if you go via the D39 strain first.

That's not even surprising - a mutation that does nothing much on its own, but does something else if it's preceded by another one, even less surprising since the previous mutation is in the very next amino acid.

Given that the whole thrust of the work on chloroquine resistance is that in all these pathways to the the resistant strain, the mutations are sequential, it seems to me that Behe is just continuing to miss the same point - and missing it in the same way as I'm seeing quite a bit in my travels on this sort of topic - find some minor point, misconstrue it with a lot of huffing and puffing, and then use the misconstrual to discredit the opponent.

Straining out a gnat, and swallowing a camel, in fact.

Would appreciate if one of the biologists could confirm whether if I've read this right..

*Edited for typos

You're correct.

Ta. Still getting my eye in, with this biology malarkey.

hackenslash wrote:Indeed, but I'd also add that even were it the case that arch-fuckwit Behe's original strawman were accurate, namely that these mutations had to arise simultaneously in a single individual, this event still has a non-zero probability, and my former critique applies.

Yes. The lottery ticket fallacy also applies. I don't know if it's possible to get to the number of fallacies his argument is based on, they are so many. Peer review, of course, would have picked those up. But the "peer review" he receives is probably from the likes of Casey Luskin and Stephen Meyer. Like they'll be any help. So he's now getting proper peer review from Ken Miller, PZ Myers, Larry Moran, etc. And he doesn't like it one bit. Much easier to just publish whatever bullshit you want, knowing the rubes will eat it up. The contempt these people have for their audience is almost palpable.

TopCat wrote:If it was reported that someone kept winning the lottery, at odds of 1 in 15 million, you'd pretty soon question either the odds or the reporting.

That illustrates one of Behe's errors. Someone does keep winning the lottery. It's just almost always a different person each time.

Shrunk wrote:

TopCat wrote:If it was reported that someone kept winning the lottery, at odds of 1 in 15 million, you'd pretty soon question either the odds or the reporting.

That illustrates one of Behe's errors. Someone does keep winning the lottery. It's just almost always a different person each time.

Yes indeed. You do know that that's not what I meant though?

TopCat wrote:

Shrunk wrote:

TopCat wrote:If it was reported that someone kept winning the lottery, at odds of 1 in 15 million, you'd pretty soon question either the odds or the reporting.

That illustrates one of Behe's errors. Someone does keep winning the lottery. It's just almost always a different person each time.

Yes indeed. You do know that that's not what I meant though?

Yes. Behe, however, does not understand the difference.

Shrunk wrote:

TopCat wrote:

Shrunk wrote:

TopCat wrote:If it was reported that someone kept winning the lottery, at odds of 1 in 15 million, you'd pretty soon question either the odds or the reporting.

That illustrates one of Behe's errors. Someone does keep winning the lottery. It's just almost always a different person each time.

Yes indeed. You do know that that's not what I meant though?

Yes. Behe, however, does not understand the difference.

I've noticed. Quite extraordinary.

TopCat wrote:I've noticed. Quite extraordinary.

Yes, quite. But, really, what motivation is there for him to correctly understand these concepts or, if he does understand them, to publicly admit that his claims have been disproven? Look at Boo Boo's posts here. Does he betray the slightest interest in actually following this discussion? Like Rumraket says, he'll just take anything Behe says at face value without questioning. So why would Behe want to disrupt that?\

Here's a thread started by another member of Behe's fan club:

http://www.rationalskepticism.org/evolu ... 48025.html

That one's quite hilarious. Dude just keeps cutting and pasting stuff that vaguely seems to confirm Behe's claims, if you don't pay any sort of close attention, but which actually do the opposite. One article he cited actually directly refuted Behe's claims in the "Edge of Evolution", even naming Behe specifically. That's the audience that Behe and his fellow IDiots are playing to. Not exactly the most discerning.

Oh we have seen much, much worse around here. Anyone remember Jireh/Coroama? That guy didn't even read what he posted, he simply searched for key words and then copy-pasted something he thought was befitting the subject matter off of some creationist apologetics site.

At one point I mentioned RNA in a response to him, and he started mindlessly linking creationist websites full of quotemines and propaganda against the RNA-world hypothesis. But that was not at all what I was talking about, my post merely contained the word RNA. At another point I linked a paper from a group of researchers at the Evolutionary Bioinformatics laboratory at the university of illinois, at which point Jireh/Coroama pasted a "response" to another paper on the Discovery Institute website. Why did he link that? Because the paper I linked had the same authors as the paper the DI post was responding to. Totally different paper and subject.

At one point he functionally admitted that when a description of the cell or some biochemical reaction included the word "complex", or that the information content in DNA could be measured in bits, he thought that in itself was evidence of intelligent design.