Experimental evidence for very long term processes

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IIRC that is based on the number of times this has been observed and recorded. There will also be unobserved events, which in the absence of chloroquine would give no advantage, and so were lost. 10^20 gives a rough upper bound on the probability of developing chloroquine resistance.
Also IIRC there is more than one mutation that allows resistance.

Genetic recombination is combinatorial.

\mathcal{O}(N!) > \mathcal{O}(c^N)

Which generally means that factorial growth eats geometric growth for lunch. A specific sequence may still be a difficult target, but in general finding some sequence to get the job done is not so hard as some people claim.

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[quote=“RonSewell, post:17, topic:16724”]
Frankly, I place little stock in Behe’s malarial calculations
[/quote]r

10^20, the number that Behe uses, is the number of parasite multiplications that is required for developing HCQ resistance. It is not the result of his calculation, it is not his number, but that of the eminent malariologist Nicolas White.

Reassure me, you’re kidding, right?

Ok, let’s extrapolate.
So we know that 10^20 organisms are required for p. falciparum to develop a modestly complex adaptation requiring a minimum of two mutations. Extrapolating this result, how many organisms would be required for a pig like creature to develop the much more complex adaptations able to morph it into a whale like creature?
To help you ponder the challenge, here is a non exhaustive list of the required adaptations:

  • forelimbs transformed into flippers, reduction of hind limbs and pelvis, tail transformed into fluke (incl. ball vertebra for vertical movement)
  • re-orientation of the foetus for subaquatic birth (tail-first)
  • modification of mammary glands for nursing under water
  • re-organization of kidney tissue for intake of salt water
  • special lung surfactant (lung has to re-expand rapidly upon coming up to the surface)
  • intra-abdominal counter-current heat exchange system (testes are inside the body next to the muscles that generate heat during swimming)
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You can’t extrapolate the probability of independent, individually beneficial mutations accumulating from the probability of a specific combination of mutations occurring.

Can you point to a single adaptation of modern cetaceans that is not explicable as a continuous series of morphological variations?

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Nope. Straightforwardly false.

What is the measure of complexity you are using here to compare chloroquine resistance to … what exactly, on whales?

The number of mutations required for chloroquine resistance is being compared to what …?

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This sounds to me like you think the name attached makes a difference. Noone cares. What matters (if anything) is how it was arrived at, not who arrived at it and who quoted whom. Point is, nobody was breeding a colony of some 10²⁰ malaria parasites before they observed the adaptation in question. The number (whose relevancy you have yet to articulate) was at best arrived at as an estimate.

No, we don’t. But do go on.

Four.

What, that sounds ridiculous to you? Alright, show me where my extrapolation failed. What did I not take into account? What calculation did I misperform?

Oh, fair enough, I do not actually believe it was anywhere near four. Mammal populations this small, from what I understand, would not survive at all. But see, that’s an argument. That’s not just pointing fingers at the number and gasping incredulously, like what you are doing. There is a reason I’d be incredulous about the number being as small as four, and it is rooted in an understanding, if only a superficial one, of the effects of genetic bottlenecks. Can I render a better estimate? Not unprepared I wouldn’t. I don’t know what’s wrong with 10¹¹. I asked you what your point was, you never got around to answering that[1].

If you want to say that 10¹¹ is less than enough, by all means, say it. If you want to say that 10²⁰ is a minimum, say that, too. But don’t just stop at ‘come on, bro’, try and give some explanation for why you’d guess something else, if you would, or at least for what is specifically wrong with these numbers.

And if you do want to give an actual estimate of your own, be prepared to answer how you arrive at it. What data are you taking into account? Not just estimates of [insert ‘eminent researcher’ here], but actual measured data. What is the statistical spread on the data, and how does it propagate into your own estimate? What factors were accounted for, and how well, and how did considering their impact, as well as the impact of unaccounted for contributors, propagate into a more accurate error calculation with your estimate?

Don’t be a Bill Cole. Show us the math.

  1. This, for the record, I do not blame you for. You are dealing with enough attention as it is, and I get it. For that matter, most of it is from users more qualified in the subject matter than yours truly, too. So, frankly, I’d appreciate your responses to their criticisms more, as I’d get to learn more from than than I would if you took the time to answer mine instead. ↩︎

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I was rifting on the common ID mantra that new information cannot arise naturally, and that adaptation is due to loss of information. I agree; that is a silly idea.

It would not be the first time. Plesiosaurs, ichthyosaurs, and mosasaurs underwent similar adaptations to take advantage of an aquatic environment.

You can name the bones in a flipper from having taken first aid. This is more explicable as due to descent than necessity of function.

How is this a barrier? The earlier whales still had hind limbs.

Humans have breach births, but they are selected against. I expect that changing selection pressure would alter whale birth presentation in fairly short order. There is some discussion that increased incidence of c-sections might be impacting selection for hip size in humans.

Ever wade into a frigid lake?

Anyways, there may have been little adaptation required to begin with. The closest relative, hippos, are internal. One learns such useful stuff chasing PS threads!

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But, in fact, none of that sounds particularly daunting. Remember, too, that what we know from fossils is that the transition from land to water wasn’t abrupt. Many, many land mammals in fact spend some time in water, and there’s a lot of opportunity for semi-aquatic existence along the way which means that none of these traits just have to pop up one day. Just look at pinnipeds, for example, or otters. Some of these things, e.g., the skeletal changes, are probably mostly just a matter of changes in gene expression. Some are barely even that – reorienting birth to “breech” is something which happens by accident in individual mammals all the time, for example. And in the vast lineage of mammals, who have the distinction of being endothermic, who can be shocked when creatures have the ability to manage temperatures in their bodies?

I’m all for the freedom to engage in absurd levels of personal incredulity; everyone is free to deny that the sun is a star or that humans usually have five fingers on each hand. But the thing to be remembered is that these sorts of absurdities are best kept close, and secret. Voicing them does no good for anyone.

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No, we don’t know that.

We not only do not know that, but you know that we do not know that, since there was a long discussion on the many ways in which that number is flawed, including but not limited to it being a very rough estimate not backed up by any calculations at all that is based solely on an extremely small sample size of observed spreads of resistant malaria in humans that includes many other relevant factors that you (and Behe) ignored despite them being quoted from the original paper by Nicholas White where that number appeared.

All this can be found in this thread, which you took part in. You are repeating the claim you made then as if the objections in that thread, most of which you failed to address, were never made.

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This is what he wants you to believe. But it is simply not true. White’s figure was a very rough guesstimate of how often chloroquine resistance has arisen in parasites infecting a human host who were treated with the drug. It does not take into account how often it may have arisen in other organisms, in people who were not treated, or who successfully recovered despite the presence of resistant organisms, etc.

The number is also affected by a several other factors that are peculiar to this organism other than simply the odds of particular mutations occurring.

A more general concern: Even if it is true that a particular trait can only evolve every 1020 generations, there is no reason to presume this applies to every other trait that requires the same number of mutations. That is just appallingly poor reasoning.

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Exactly. First of all Gilbert gets the number of mutations wrong, saying it’s at least 2 implies it could be as low as 2 mutations requiring 1020 organisms. But chloroquine resistance (let’s just call it CR), at least high-level resistance requires more than two. In some cases 5 or more.

But more importantly here the issue is there are only a very small handful of pathways through which those CR mutations can evolve, and several of the intermediates on the way to high-level resistance are either neutral, or even deleterious.

The difficulty with CR is not the number of mutations it takes to result in high-level resistance, it’s that there are only a very small number of possible pathways through which it can evolve, that mutation rates for the plasmodium parasites are very low, and that for most of these pathways there are neutral and/or deleterious steps involved. It is the conjunction of all these factors that combine to produce the rarity with with CR arises.

NONE of these factors are known to apply to ANY attribute of whale evolution, and we have examples of other adaptations than CR requiring just as many mutations, but where there are many more alternative pathways available (for each fitness-increasing mutation there are more alternatives that can take it’s place, and for each coordinated mutation there are more background mutations enabling them), where beneficial steps are possible all the way from the first mutation, the organisms have higher mutation rates, do not require extreme bottlenecking through a disease-carrying vector like mosquitoes etc. etc.

We just have zero reason to think CR can be generalized in the way @Giltil accepts Behe and others to be doing.

In one of Lynch’s replies to Behe & Snoke 2004, Lynch produced this figure:

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Skærmbillede 2024-04-25 110950564×530 56.9 KB

It shows the number of generations to reach a trait requiring two coordinated mutations (with the intermediate—either mutation alone—being neutral and the conjunction of both mutations being beneficial) as a function of population size, number of alternative mutations that can result in the trait, and selection coefficient. n=2 is if only two specific mutations can result in the trait, n=10 and =50 is if there are 10 or 50 different alternative sets of 2 mutations are possible. It really makes a colossal difference if the number of alternative pathways increases even by a little, with exponential gains in how fast the trait can establish as the number of pathways go up.

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You should be ashamed of using such a grotesque and dishonest comparison! Are you not aware that many serious thinkers, past and present, were and are sceptical of the idea that the process of random variation plus natural selection has the power to morph a pig like creature into a whale?

Too bad for you, but I can assure you that the skepticism I refer to above isn’t about to go away, let alone be kept quiet and secret.

Voicing them is good for science.
I invite you to ponder the following quote:
« A fair result can be obtained only by fully stating and balancing the facts and arguments on both sides of each question ». Charles Darwin

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Of all things you could choose to reply to, often in the very same post, why do you so consistently pick the low-hanging fruit? Forget the credulity crap, your own response is of no more worth than the portion of the comment you are replying to. Please offer something of substance to what I and others have said instead.

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Ok, let’s ponder Lynch’s figure.
It shows that for a population of 100 000 individuals, for s=0,01 and n=2, 10 and 50, it takes respectively more than 10^9, 3x10^8 and 2x10^7 generations to reach a trait requiring two coordinated mutations.
On the other hand, it took no more than 5 million years to morph a population of pig like creatures into truly aquatic whale like ones. Given a very generous estimates for effective population size of 100,000 individuals per generation and a generation turnover time of 5 years, it means this transformation took no more than 10^6 generation. Not sure Lynch is very helpful here.

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You’re missing the point. It’s the large change in arrival time that occurs by relatively small increases in n (or Ne), not whether the specific scenario itself has a short arrival time.

In the end the scenario still models one where duplication of a specific gene has to occur, and then 2 mutations has to occur in one of the duplicates for it to gain a new function, with no possibility of bringing the two mutations together through recombination. This isn’t waiting for any adaptive trait to arrive (how evolution actually works), it’s still waiting for a specific one using a range of values.

With a sufficiently restrictive set of assumptions (like, there’s only this one adaptation possible, and only through duplication and double-mutation of this particular gene that doesn’t undergo recombination) you can always just increase the waiting time to whatever arbitrary level you desire. The problem comes when you want to connect your scenario to the real world. What set of conditions apply to the fossil record, such as whale evolution? How many alternative ways of adapting were possible, and how restrictive were the pathways through which each of them could have evolved?

What reason do we have for thinking Behe’s scenario, or the specifics of CR apply to any of them?

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Right, Lynch is irrelevant here… because he’s talking about coordinated mutations. And the mutations in whale evolution were not coordinated. All of the numbers you have presented in this thread are completely pointless to the topic of whale evolution.

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We don’t know whether any of them were (presumably there are going to be mutations which epistatically interact with others), we just don’t have to assume there was a specific target we’re waiting for, nor that there was only a very narrow pathway through which whatever evolved could have.

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There is another reason this number would not offer guidance on the limit of complex adaptation.

What if chloroquine resistance is a miracle? Designed? The work of biotech angels?

After all, it is arbitrary to assume that natural processes were sufficient to result in drug resistance, but not the evolution of whales. Both appeared in nature, so why the one and not the other?

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False.

It’s not anyone’s “calculation.” IIRC, White has pointed out Behe’s misrepresentation very clearly. Moreover, what sort of scientist would base a grand thesis on a single sentence from the secondary literature?

BTW, Here’s what White wrote:

Chloroquine resistance in P. falciparum may be multigenic and is initially conferred by mutations in a gene encoding a transporter (PfCRT) (13). In the presence of PfCRT mutations, mutations in a second transporter (PfMDR1) modulate the level of resistance in vitro, but the role of PfMDR1 mutations in determining the therapeutic response following chloroquine treatment remains unclear (13). At least one other as-yet unidentified gene is thought to be involved. Resistance to chloroquine in P. falciparum has arisen spontaneously less than ten times in the past fifty years (14). This suggests that the per-parasite probability of developing resistance de novo is on the order of 1 in 10^20 parasite multiplications.

So, where did Behe include any of the other information in that paragraph in his book? Having read all that, how could any competent scientist write that resistance is simply about two single-residue substitutions in a single protein? Why didn’t Behe explain to his readers why he rejects everything else White wrote in that paragraph?

Why did you remove White’s qualification (“suggests”), Gil?

Also from the paper:

900×329 142 KB

Why do Behe and you pretend that only #1 contributes and that factors 2-8 simply don’t exist?

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Yes, there’s an endless supply of blithering gullible dishonest ignorami.

Pondering it leads rapidly to the conclusion that you are the one that needs to ponder it, because you are the one lying by omission.

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The design inference is construed in such a way as to avoid false positive but it doesn’t protect against false negative.