Questions for Gunter Bechly and Swamidass on Unbelievable?

I don’t think it rises to the level of bad physics. It is not physics at all. It’s just quantum woo.

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It is my impression that historically the ateleological conception of evolution came from the realization that mere differences in reproductive succes (among variants) explains adaptations without the need for a designer.
In so far as different phenotypes do not have equal reproductive success, one will eventually take over. When it comes to natural selection, it simply doesn’t make sense to invoke hidden actions of God to favor different phenotypes. Their effects on survival and reproduction are essentially mechanical/physical (certain shapes have less air resistance, certain patterns constitute camouflage, etc.) so that God’s involvement is completely superfluous to explain why one variant does better and rises to higher frequency in a population than another.

I’d be happy to take correction here but my impression is that questions about the nature of randomness, and the nature and causes of mutation in evolution, came later.

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Yes, “later” in the sense that the questions are cudgels used politically to attack evolutionary biology. I don’t see a lot of actual interest among IDcreationists in addressing them.

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If you get into theology, consider discussing the doctrine of providence. One concern some have with ID is that it privileges (scientifically demonstrable) design or moments of intervention over the “natural”…which downplays God’s active role in the “natural.” So I’d ask an ID advocate if anything is lost theologically if there is no (scientifically) detectable design. And, would he concede that ID advocates are in danger of downplaying divine providence generally. (I hope this makes sense. I recall Kathryn Applegate making a similar point to Fuz Rana and others…and the latter had no good response.)

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Yes, following Steve Schaffner, I think the randomness of Darwinian evolution is generally defined in terms of mutations not being biased towards fitness in the current environment (according to e.g. Elliott Sober).
Whether this empirical claim is true is now somewhat controversial as I understand, at least under some conditions (see e.g. Arlin Stolzfus’s new book on the topic of mutations and evolution), but theologically unproblematic either way as argued by Sober, Plantinga, and this article which is a bit more detailed. (PDF) Both Random and Guided

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In the strict sense, I don’t think that claim can be true.

We know that the distribution of mutations are biased towards beneficial, compared with e.g. a uniform distribution. That shouldn’t be controversial because it is obviously true to anyone who knows the bare level basics. It seems some thought needs to be put into how precisely word the claim, because as stated it isn’t correct.

Perhaps…

The distribution of mutations is largely independent of the selective forces that act upon them.

I qualify it with “largely” because there are feedbacks where selective forces can influence and increase the likelihood of a beneficial mutation. For example,

  1. An antibiotic that kills bacteria by inducing mutations will increase the likelihood of a beneficial mutation that is resistant to the mutation.

  2. selective pressures can increase oxidative stress, which can increase and shift mutations, which can increase likelihood of an adaptive mutation.

These two examples should also be non-controversial, and are not precisely the set of experimental findings that the claim intends to summarize. I’m not sure the best way to be accurate other than including the wiggle word “largely.”

My wiggle words were ‘except perhaps in statistical terms’, since clearly there are biases in which mutations occur.

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Random means not biased towards fitness in the current environment (i.e. mutations are not particularly beneficial in the environment in which they occur, as opposed to others) was how I put it, and that is the standard Darwinian account as far as I am aware and according to Elliott Sober. I don’t think it is obvious at all that “as stated it isn’t correct” - perhaps the force/meaning of “in the current environment” was not clear.

Claims of mutations which are triggered by and specific for (in an adaptive sense) particular environments have often been hypothesized, as a challenge to Darwinism - but so far there is little reason to think it’s true (that I have seen). Even people like Arlin Stolzfus, who are advocating a greater role for mutations in evolutionary dynamics, do not seem to be saying that mutations are environment-specific in a way which is adaptive. I think it needs to be investigated more, but I don’t think it’s an established conclusion that the way I put the standard Darwinian claim is empirically false (though it may be becoming a bit more controversial, with the development of the Extended Evolutionary Synthesis etc).

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The incorporation of bacteriophage sequence as spacers in CRISPR regions represents a kind of mutation that is triggered by and specific for a particular environment.

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Lac+ reversions were a classic false positive for non-random mutations, and I think those studies also helped in the discovery of the SOS response in bacteria. In those experiments (pulling from faulty memory) they saw a higher than expected number of mutations changing lac- bacteria to lac+ in the presence of lactose. What was actually happening was an SOS response to DNA damage caused by the lack of available sugars. This included transcription of error prone polymerases and an increase in recombination. It was an increase in the random mutation rate, essentially.

Another example I have seen is increased mutation rates in actively transcribed genes. This is probably due to DNA being single stranded during transcription.

In both of those examples we are talking about a general mechanism that isn’t directly tied to a specific environmental cue. One of the rare exceptions is the CRISPR system in bacteria, as noted by glipsnort above. I could be convinced that CRISPR is responsible for non-random mutations.

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This is a bit off from the main discussion here, but Josh, is this the right comparison? Why is “a uniform distribution” relevant here? Anyway, a uniform distribution of outcomes? Or of mutations?
I suspect the case you are thinking of is where you have (say) an A and it can mutate to a G, a C, or a T. If we consider all those three cases equally frequent, then the resulting decline in fitness is greater than if we had a higher rate of transitions (mutation to G) than of transversions (mutation to C or T). Yes, mutational mechanisms are biased toward transitions, and that gets you higher fitness than mutation equally frequent to all three. But it’s not going to be beneficial compared to the starting point (A).

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It’s relevant in that uniform is the MaxEnt distribution, and all other distributions favor some mutations that over others (ie they are biased). And often the bias is towards beneficial, or at least less deleterious.

Of course defining MaxEnt usually depends on convention as to the domain, which often can’t be set in a principled way.

As pedantic as this is, some of the EES crowds and their fans, latch on to this as evidence that they evolutionary science does not work by random mutation. In their view, any bias in the distributions from MaxEnt shows that the mutations are not random (yes, an odd definition of random).

Of course ID picks up on this, or rather they were already there. It is common for them to use a uniform distribution to model evolution, and proclaim evidence of deviations from uniformity as evidence of design.

So my exposition up there there is meant to more clearly stated the actual meaning of the claims, so as to head off those wrong turns before they occur. In the end, those wrong turns are wrong turns, but if they prod us to speak more precisely that is a good thing in the end.

I think it’s important to maintain the distinction between those two cases. The biases I’m familiar with are against mutations with any functional effect, and are therefore likely to produce fewer deleterious and fewer beneficial mutations. (It might be the case that a bias toward mutations of smaller effect, rather than no effect, reduces deleterious mutations more than beneficial ones, since large-effect mutations are more likely to be deleterious. Probably.)

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I like that response. The unsatisfactory part for me is that when mathematicians model randomness in terms of probability theory, it doesn’t rule out ontological randomness. I would prefer we do rule that out, and I think it is in fact possible to do that in biology through intelligent design theory. The claim here is that, as you said, what “looks random to us” might not actually be random. Why wouldn’t it be unsatisfactory when our scientific models don’t comport with what we know to be true? That means the model is deficient and unsatisfactory. So while perhaps the random model sufficed for a time, improvements upon it might be made. IOW, now that we know more about biology, things may not actually look random to us anymore.

What is unsatisfactory about that for you?

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No, but it also doesn’t demonstrate or imply ontological randomness. One does not need to rule out what is literally impossible to test anyway. Ontological randomness as a concept is quite literally impossible to test. It can be neither proven nor disproven. In fact no experiment could possibly even weakly indicate one way or another.

Suppose just for the sake of argument that there is some process that is, by definition, random in the sense that even God does not know the outcome of the process.

Suppose god made a coin such that even he couldn’t predict how it lands. He made it for that purpose, to surprise himself. Or alternatively, God could decide to simply not know how the coin lands, yet let the coin be a normal coin.

Now suppose you are given such a coin by God and asked to determine whether God knows the outcome of how the coin lands? How in h&%# could you do that? Wouldn’t you have to actually ask God if he knows the outcome? And what if he doesn’t tell you? Have fun asking God to tell you the outcomes of events before they happen.

Clearly there is no circumstance in which any theory or experiment, other than God himself deciding to reveal it to you, that could in any way settle the question. Simply tossing the coin and seeing how it lands doesn’t tell you whether God knew how it would land. He’d have to tell you before it landed of course, and only then could you determine if in fact he knew the outcome. No measurement done on the coin would tell you what God knows in the privacy of his own mind.

There is no mainstream theory of mathematics, or physics, or any branch of science that has proven that events or phenomena in the real world discovered by science are ontologically random in the way @Swamidass has defined it earlier. That includes quantum phenomena.

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I understand what you are saying, and I think I actually quite agree. Let me put all my cards on the table here.

I’ve been thinking for quite some time about Craig’s recent arguments regarding the “randomness” of mutations. He says that Francisco Ayala defines “randomness” in this context as “irrespective of usefulness to the organism.” He goes on to argue this means that “random” defined this way doesn’t preclude God’s determining it. Whether or not that is true, I don’t believe this is a strict enough definition of “randomness” in the context of mutations. The actual definition of “random” that pertains to evolutionary theory and indeed, the way scientists understand and model mutations, is “irrespective of their precise position in the sequence” be it DNA, RNA or protein sequences. In other words, mutations do not occur at specific positions in their respective sequences. Since it is the precise position of mutations that matters biologically, Ayala’s definition is true so far as it goes. But Craig thinks Ayala’s definition is sufficient to describe “randomness” in this context, and I do not. Craig thinks that means God can choose precisely where the mutations occur to effect a specific result and this still falls within the meaning of the word “random.” I think that is obviously and demonstrably false.

If that were true, some of the evidence for common descent that Craig himself cites would be undermined. Evolutionary biologists must positively assert through statistical tests that certain mutations are not under selection and are in fact random with respect to their position in the sequence in order for those mutations to be evidence of common descent. If they were not random with respect to their position in the sequence, but only random “irrespective of their usefulness to the organism,” then God could be causing those mutations for some unknown reason. If that were so, then they are not the artifact of common descent but rather artifacts of design. Yet Craig himself appears to accept this evidence. I take that to mean he does not fully understand how these arguments are made or what assumptions are required to make them.

This does not make any sense to me.

Ontological randomness is not any part of mathematical probability theory. Why would you expect mathematics to go outside of the mathematical theory?

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Not true. As long as God is causing mutations rather than creating whole genomes de novo, it doesn’t matter for phylogenetic purposes whether they’re random. The only exception would be if God is supposed to be simulating common descent in the pattern of mutations he causes (or, actually, in the pattern of differences he creates de novo). But that requires a deceptive God.

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The randomness of mutations was established before the structure of DNA was even known. The earliest experiments demonstrated that beneficial mutations do not occur in response to the need for those specific mutations. In other words, the processes that produce mutations appear to be blind to what the organism needs in a given environment.

At the molecular level, some mutations are more probable than others, but mutations are still random despite this fact.

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If mutations weren’t random (unpredictable), I am pretty sure things like cancer and congenial diseases wouldn’t exist.

Edit: @John_Harshman, I meant congenital not congenial. That was a strongly deleterious, single nucleotide deletion mutation :wink:

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