Over at Uncommon Descent, Jonathan McLatchie calls attention to an interview that Scottish Christian apologist David Robertson did with him. The 15-minute video is available there.
The issue is scientific evidence for intelligent design. As so often occurs, they very quickly ran off to the origin of life, and from there to the origin of the Universe. I was amused that from there they tried to answer the question of where God came from, by saying that it was unreasonable to push the origin issue quite that far back. There was also a lot of time spent being unhappy with the idea of a multiverse.
But for me the interesting bit was toward the beginning, where McLatchie argues that the evidence for ID is the observation of Specified Complexity, which he defines as complex patterns that conform to a prespecified pattern. He’s made that argument before, in a 2-minute-long video in a series on 1-minute apologetics. And I’ve complained about it before here. Perhaps he was just constrained by the time limit, and would have done a better job if he had more than 2 minutes.
Nope. It’s the same argument.
His Specified Complexity argument is William Dembski’s pre-2005 argument. It turned out that the argument required a conservation law to show that natural selection could not put this Specified Complexity into the genome. Dembski did have such an argument, but it turned out not to work (see my 2007 article for the details).
In 2005-2006 Dembski changed the argument, by redefining Specified Complexity to have an additional condition. Now you could only call a pattern Specified Complexity if it was not only complex and conformed to a prespecified pattern but also could not be brought about by natural evolutionary forces such as natural selection. A number of people here and at Panda’s Thumb pointed out that this fails to show us how this condition is to be evaluated. It makes SC something that comes in after one has somehow decided that an adaptation cannot have been achieved by natural selection. In short, it has been safeguarded against the criticism that evolution could bring about SC by defining the issue away. That makes SC a useless criterion.
But McLatchie has somehow missed all this history. He is back where Dembski was in the book No Free Lunch: Why Specified Complexity Cannot be Purchased Without Intelligence, published in 2002. McLatchie has totally missed both the refutations of Dembski’s original criterion, and the 2005-2006 fix that rendered the SC criterion useless. In spite of having 15 whole minutes to clean up the mess, McLatchie and Robertson preferred to spend the extra time back at the origin of the Universe.
Truly your ignorance is astounding. It is like you are coming to the subject for the first time in your life.
https://en.wikipedia.org/wiki/Genetic_hitchhiking
You have SO MUCH reading to do.
I’m pretty sure that of the two of us, I’m not the one that needs to spend some time thinking about this…
In a particular case you usually wouldn’t know. But the point was that when rare mutants occur and are favored, and increase in frequency, there come times where genotypes arise that had not previously existed in that population.
Methinks creationists and ID advocates are disturbed by this possibility — it contradicts their assertions that natural selection can only eliminate variation.
The alternatives can only be:
1. Natural selection has no effect on variation.
2. Natural selection increases variation.
3. Natural selection reduces variation.
Do you agree?
How about these?:
4. Natural selection can increase or reduce variation, depending.
5. Natural selection can maintain variation.
Yes, but any of those can happen, depending on the circumstances.
It is like physics. Objects can move left, or right, or up, or down, or forward, or back, or not move at all. Each of those can be true, under different circumstances. And that being the case does not make physical laws of motion useless.
Mung,
Depends … if one thinks of variation as a population-level thing, and the population is well-stirred, a population with 99.99% one allele and 0.01% another would not be considered to have as much variation as one where both are at 50%. So if NS increases the representation of the rarer allele, it must be increasing variation. But if it pushes it past 50% and on to extinction of the first, it is reducing it again.
That’s not exhaustive of the possibilities, but illustrative.
Ah, so your theory predicts everything and nothing and all variants in between?
🙂
That it makes no sense to you is neither here nor there. It does not matter that it does not make sense to you.
It makes sense to people whose opinion actually matters to other people!
phoodoo,
Speaking of the M&M game, many of us remember your confident pronouncement:
You were wrong, of course.
keiths,
Yes, I thought about using that pronouncement to illustrate a point. If one considers a single black M&M in a population of whites to be guaranteed extinction, then two black M&M’s in a thousand can be equally represented as two populations of 500, with one black M&M in each. In both of these, the black is apparently guaranteed extinction. Add another black, and each is a member of a 1 in 333(ish) population. And so on. Until they balance numerically, it does not matter how many black M&Ms one adds, black will always be eliminated … ? But for the latest argument to hold, indefinite co-existence, something must happen as proportions approach 50% to keep them there.
So it’s a paradox. While black is the minority colour, it is proposed to be guaranteed elimination (per phoodoo). But during the supposed period of indefinite co-existence, it is almost certain that one colour will become the minority colour by random fluctuation, and hence be eliminated. The only difference from conventional theory is that ‘guarantee’.
Actually, selection has no effect on the production of variation, which is continuous. The typical human carries about a hundred novel mutations, variations from parental genomes. Selection has no effect on this number.
Do you mean allele frequency in a population? Selection definitely has an effect on the fate of any particular allele. If it not neutral.
keiths,
You were, and still are wrong. The amount of generations it takes to fix is beyond what is feasible.
But of course you don’t understand the concept of a generation.
phoodoo:
Your claim, again:
That’s wrong. If you can’t see it, maybe you should learn how to write “little computer programs”.
What is feasible?
Define generation.
There have been at least two different threads here that conclusively demonstrate that you are the participant confused about what constitutes a generation.
Creationists have an unfortunate tendency to make baseless claims, run away when they are soundly refuted, then return weeks or months later making the same claims as if nothing. That is not a sustainable practice in the age of search engines.
Patrick,
Oh its conclusive to you is it Patrick? Well, that really is something. Is it also conclusive to you that the reason bacteria that get a mutation that enables them to metabolize citrate always revert back to an ancestral state once the bacteria is removed is because that is what neutral drift says should happen?
Because the same people who don’t understand the concept of a generation also don’t understand this.
Allan Miller,
So then, because of drift, we should sometimes expect an entire population of bacteria to obtain the ability to metabolize citrate, even when there is no citrate in the environment right Allan?
You know, just like a black, neutral M&M?
Do you think you can find many populations like this in Lenski’s experiments?
Maybe. Let’s say, just for the sake of illustration, that an entire population of bacteria, purely by drift, fixed the ability to metabolize citrate. Now the question is, how would you know that if there were no citrate to metabolize? As I understand it, you can’t just sequence a genome and say “Hey, look, THIS sequence metabolizes citrate!” You have to see it in action.
And this means that it’s entirely possible that many populations in Lenski’s experiment, purely by drift, have acquired the ability to do something, but there is no way except by coincidence to discover what it might be.
Flint,
Well, if the ability to metabolize citrate were truly a neutral mutation, in the absence of citrate, why should we expect it to be a rarity? Why should it be any less rare then the inability to metabolize citrate? Shouldn’t it be just as common.
Why, like Allan says, should we expect, in the absence of any selection pressure, for the bacteria to “return” to the state of inability? What does return mean, when both genomic states should be as equally likely?
I should think any mutation that becomes fixed in a population due to drift alone would be rare. Isn’t drift to fixation simply the very far end of a normal statistical distribution? If this is the case, then the vast majority of neutral mutations would appear somewhere in the population, perhaps spread a short distance, and then peter out.
And also if this is the case, then I would think that ANY neutral characteristic would be temporary since it is not preserved by selection. Seems to me this would apply to characteristics that spread both through stochastic drift, and those that spread because they were once beneficial, but confer no present benefit.
I have this picture in my head of Lenski’s populations attaining and then losing some sequences generation by generation, all unknowable to both Lenski and to the bacteria themselves – unless they were beneficial and selected.
Flint,
But we already know we have populations that ALL can metabolize citrate, because they are in a citrate solution.
So since you are saying that it would be rare in your words for neutral drift to fix in a population, when it starts off as a minority mutation, it should then also be rare for the bacteria to lose the ability to metabolize citrate once the citrate is removed, since they already has that ability right?
This is the whole part where Allan says he just can’t understand for the life of him what I am talking about. So do you agree with Allan that naturally we should expect the bacteria to revert back eventually, in the absence of citrate, or since they already have the ability, even if there is no citrate in the environment, the mutation should stay in most cases, since as you say its rare for a neutral mutation to drift?
Is this actually the case? I’m willing to agree it is, but I don’t know how the experimenters might identify individual bacteria within a culture that did NOT enjoy this happy mutation.
I don’t see why this would follow. As an analogy, I have in the past worked very very hard to to develop skill and fluidity on a musical instrument – to the point where if I set it down for a week, I can tell I have lost something. Set it down for a year, and I have lost most of it. Many things are hard to reach and easy to lose – ask any lottery winner!
Now I’m also confused. I should expect any and every characteristic to be lost if selection does not preserve it. I don’t recall saying it’s rare for a neutral mutation to drift, when I was trying to say that it is inevitable for a neutral mutation to drift.
You don’t remember saying this?
Good heavens, if you didn’t mean it is a rare event for a neutral mutation to become fixed, then why use words at all?
But this is the whole point, why should it be easy to lose, if it is a neutral mutation??
Allan can’t understand this crazily simple concept, and you also can’t?
Yes, and to anyone else who reads those threads.
The ability to metabolize citrate when citrate is present is not a neutral mutation, it is highly selected. That is the beginning, but unfortunately far from the end, of your confusion.
So just you, then.
phoodoo,
Both genomic states aren’t equally likely. There are more ways to be unable to metabolise citrate than to do so. Therefore, if all mutations are equally fit, one would expect one of the numerically superior can’t-metabolise-citrate alleles to fix, rather than indefinite retention of the fewer ‘can-metabolise’ versions.
Much like our broken Vitamin C gene. There are many, many ways to break that gene; we have just one of those many, many possibilities.
I said it was rare for a neutral mutation to drift to fixation. Not that it’s rare for a neutral mutation to drift at all. It’s the difference between drawing ANY card, and drawing a card that fills an inside straight. The first is inevitable, the second is rare. Both involve drawing cards. Sheesh.
Because neutral mutations are not conserved through selection. I should think this is obvious.
The worst thing about learning in such an adversarial way is that phoodoo’s ah-ha moments have to be suppressed given the amount he has staked on his current pre-ah-ha understanding being the correct understanding.
Some mints with your cognitive dissonance phoodoo?
Seems entropy is a tough thing to grasp. If a single easy swipe of the arm can knock a table full of dishes across the floor, then can a single easy swipe of the arm knock dishes spread across the floor back neatly onto the table? Why, just think – they are either on the table or not, 50-50 chance, right?
Simple bit of math: the probability, given its current frequency, that an allele at a neutral site will eventually become fixed is that current frequency.
… and that’s for a very straightforward reason. If the alleles are all equally fit, one of the copies in the initial population takes over. So the probability that an allele whose frequency is p wins out is just the probability that the winning copy, a copy chosen at random is a copy of that allele. Namely, its starting frequency.
… where frequency is an abbreviation of relative frequency. The relative frequency of an allele is the proportion (fraction) of the population in which the allele occurs.
And in the case of bacteria in a citrate solution, all of the bacteria are of the type that can metabolize citrate. So what are the odds, once we take the citrate away, that the whole population loses the ability to metabolize citrate? Since the current frequency of the allele that can’t metabolize it in the solution is zero.
If we use this bit of logic, then how can we ever propose that a new neutral allele becomes fixed in a population Allan? In the case of the bacteria, the NEW allele for citrate metabolism is already fixed, because if it weren’t the bacteria couldn’t survive. But once the citrate is gone, you lose that allele. So how does that help your sides case about a new allele becoming fixed, when they are already so many other versions of alleles.
Why should we expect any evolution then? Aren’t there always more versions of “other” alleles” then any version of one particular allele?
But the ability to NOT metabolize citrate is neutral right? And its conserved?
Thanks. In population genetics “frequency” has come to mean fraction, not number (as in “gene frequency”). I need to be reminded that in the outside world frequency means the number of occurrences.
Joe Felsenstein,
So if the allele appears in EVERY member of the population (like in the bacteria that has been in citrate) why should we expect it to quickly lose that ability once the citrate has been removed?
phoodoo,
I don’t see what you’re not seeing phoodoo. If you ‘lose that allele’ (the one that can metabolise citrate), then this is nothing less a neutral allele becoming fixed (one that can’t).
I would say the probability AT THAT POINT is zero, but as soon as a neutral mutation happens in the population that adds another neutral allele then the probability for that new allele in non zero. What’s so hard about it? Fixation doesn’t mean it must stay fixed forever and ever
This is just about drift, not evolution in general, that doesn’t make any sense whatsoever. If at least your question was Why should we expect any neutral allele fixation then? And the answer is pretty straightforward: every allele has a frequency > 0 and a chance of getting fixed. Why wouldn’t we expect some to become fixed?
I would say that over time the probability is one. The same process that made citrate metabolism can break it.
Yeah, you’re obviously right. I think it’s safe to say that phoodoo’s confussion stems from this:
Since the current frequency of the allele that can’t metabolize it in the solution is zero
This is the bridge hand fallacy again.
dazz,
At the point when you have ONE that can NOT metabolize citrate, and ALL the others CAN metabolize citrate, why would you expect it to be more likely to fix the non-citrate metabolizing allele? Its one million to ONE, why is the one going to usually prevail?
Why can’t you just as easily say, “the same process that made no-citrate metabolizing, can also break it? “
Of course I wouldn’t expect it to be more likely to get fixed… at that particular point
The way you should think of this is: what are the odds that a fixed neutral allele remains forever? I think the answer is obviously zero: it’s eventually going to drift to disappearance and that doesn’t necessarily mean some other allele must have got fixed there
I think part of your misunderstanding is that you think that the process “reverts” the genome back to were it was once selective pressure for citrate is removed, that’s clearly not the case
phoodoo,
Another way to look at it: if there’s a 1 in a million chances an allele will get fixed once it emerges in a population where every other individual can metabolise citrate. What are the odds that some of these alleles will have gotten fixed after a million of these occurrences? Once that happens the original citrate allele is guaranteed to be gone (not necessary, but sufficient condition). 1 million tries of p = 1 in a million. Binomial distribution? 63%
Do you mean like the “non-ability” to metabolize citrate?
Are the odds that that allele will remain fixed forever zero?
How is that one allele? are you being deliberately stupid?
phoodoo,
You seem to be labouring under the misapprehension that an unlikely event on one trial will remain unlikely irrespective of how many trials occur. It’s the ‘black M&M’ error again.
If you buy millions of lottery tickets, you are far more likely to win the lottery than if you buy one.
If there are N members in a population, and N ‘broken-citrate’ mutations occur within it during a particular period of its history, it is almost certain that a ‘broken-citrate’ allele of one kind or another will fix, if they are neutral wrt the unbroken version.