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.
Allan Miller,
You still don’t get your black M&M error. You always only allow it to go one direction. You never allow the black m&M to get the mutation which does allow it to metabolize citrate. So if you always say the M&M’s can only go the direction of “non-metabolizing” and never go the direction of “metabolizing” of course you will claim it will always go to metabolizing.
But there is no good reason to only go in one direction, if both are neutral. Its just complete nonsense.
Furthermore, if we use what Joe claimed, that the frequency of that allele in the population, gives you the odds of it becoming fixed, in a sample of bacteria with ALL alleles being able to metabolize citrate, and only ONE not being able to, the odds are a million to one against. Or a billion to one against.
You must think a billion to one odds against are a certain winner. No wonder you can’t understand the black M&M’s.
phoodoo,
We started on this with your contention that citrate metabolism has no reason to be lost. I have shown you why it IS likely to be lost. Your talk of ‘directions’ is confused. If citrate-metabolising stops being advantageous, it is likely to be lost, and I have shown how and why. It is due to the likelihood that a non-metabolising allele will replace the metabolising allele.
Honestly, you and Sal need to get your stories straight. You are saying that genetic entropy is not possible.
phoodoo,
This is the root of your confusion. It is true that one black M&M in a billion has a 1-in-a-billion chance of becoming fixed. But mutation does not just happen once. After a billion black M&M’s have been produced over the course of history, what are the chances now that the population will still be non-black? Roughly, it’s 37%. Ask me how.
So rather than 1 in a billion against fixation of a non-citrate allele, a billion attempts by repeat mutation means
I tried that already. He either ignored it or didn’t understand it
My comment got truncated by edit, hence the trailing off. I went on to say that the chance goes from 1 in a billion to 2-1 on to 7-1 on to 20-1 on each time you add a billion mutations.
And in fact the maths is about the same if you have 100 trials in a population of 100, or 1000 trials in 1000 etc.
Yes, I know I’m wasting my time. Still, phoodoo is effectively saying that no-one ever wins the lottery, because the chance of doing so is tiny.
Allan Miller,
Allan,
Your talk of the lottery shows just how poor your understanding of the problem is. You are saying that in a billion to one chance, something has to win, if we give it one billion chances.
Right! In a billion populations where you have ONE allele that is non-citrate metabolizing, and all the rest CAN metabolize citrate, we should only expect the ONE to win once in a billion opportunities. Like if someone plays the lottery a billion times, then maybe they will win it once!
Its not that SOMETHING has to win in a billion to one odds. That’s totally misleading and not applicable here. You have one chance, and the citrate metabolizing bacteria have a billion chances less one! That means most of the time the citrate wins, and in a billion different populations maybe the “non-citrate’ wins once.
Its laughable that you want to say, yes, but what about after you have two, then its a billion less two. And then what about when you have three mutations, now its only a billion less three-see the odds are getting better! That is just so ridiculous.
Of course if you keep saying add another black and take away another color, you will eventually end up with black. But how about if sometimes you add another color and take away one black! Will you still get to black in a billion chances??? I don’t think so!
You can’t only say all variation goes in the direction of black, and none of the black go back to color-that’s patently ridiculous. Likewise you can’t say all the mutations only go towards the “non-metabolizing citrate allele” and non of the mutations go back towards the “metabolizing citrate allele.” This is where you screw up. You only want to the mutations to go one direction. You want only the ones you like to get lost in the population, so you end up with the ones you want. You don’t want any of the ones you don’t want (the non-blacks or the citrate alleles) to ever be able to return. They only get eliminated, they never get added.
Surely somewhere here besides yourself is clever enough to see the ruse in your game.
I haven’t been following closely but may I suggest that phoodoo consider the niche. In an environment where citrate is available as a food source, the ability to metabolise it is beneficial. In an environment where there is no citrate, it is not. At best it is then neutral. There maybe a cost in carrying genes for citrate (the cost of manufacturing them at least) which renders those alleles slightly deleterious.
We’ve been trying to explain that the probability that such a thing happens is 63%. It’s simple math, you’re such a pathetic ignoramus
Your first source of confusion phoodoo, relates to probabilities, and how these things scale. We have tried to explain to you on previous threads that the rate at which neutral mutations fix (per generation) is equal to the rate at which they occur (per individual, per generation), irrespective of the size of the population. This is high school math.
But there is a second source of confusion:
Here we see your second source of confusion. As others have noted, there are many more ways of not-metabolizing-citrate than there are ways of metabolizing-citrate. This fact is, after all, the starting point for all CSI-type calculations. Absent selection, then <insert adaptation here> is vanishingly unlikely.
Try to think about it this way: you start with a bag of (replicating) white M&M’s. Every minute, one of the M&M’s mutates color. There are thousands of colors. You are saying “What is the chance that black becomes fixed? It is the same as the chance that white becomes fixed!” which is true, but irrelevant.
Given thousands of colors, the chance that the bag stays lily-white over the long haul approaches zero. Geometrically. The p(lily-white) declines e-fold for every N mutations that occur in a population of N M&M’s (because the probability that any one particular mutation fixes is 1/N. We’ve been over this before…)
phoodoo,
phoodoo, you are forgetting that there are many more possible alleles that cannot metabolise citrate than those that can. Almost all mutations will be of the non-metabolising kind. This, for fuck’s sake, is what the ‘islands of function’, ‘brittle protein’, ‘genetic entropy’ and ‘mutations are always damaging’ arguments rely on.
If you remove the selective pressure, each novel non-metabolising allele has a chance p of drifting to fixation, and therefore a chance 1-p of being lost. Chances are multiplicative. t alleles have a chance that ALL of them are lost equal to (1-p)^t
So when t=1 (1 black M&M), the chance that it is lost in a population of a million is 99.9999%. When t=2 (2 black M&M’s have occurred, independently) the chance is 99.9998. When t=10,000 the chance is 99%. So far, your intuition seems OK. Let’s keep going.
With t=500,000, the chance is 60%
t=1,000,000 the chance is 37%
t=2,000,000 the chance is 13%
t=3,000,000 the chance is 5%
t=4,000,000 the chance is 1.8%
t=5,000,000 the chance is 0.6%.
and so on.
With continued production of new mutations, the chance of none fixing diminishes rapidly. Exponentially in fact. Of course this is a simple model that assumes each new one is run to completion before the next. That’s not what happens in real life. But what happens in real life is even more damaging to the chances of retention.
Either way, citrate metabolism, when the selective pressure has been removed, is continually being shot at, your intuitive textual gibbering notwithstanding.
DNA_Jock,
The mutation that caused the bacteria to be able to metabolize citrate actually knocked out a function of the gene, it did not create a new function. You have it backwards as usual.
It is the entropy that enabled the bacteria to utilize citrate, because e. coli is already capable of utilizing citrate as an energy source under anaerobic conditions. The mutations just blocked the regulation of the operons, so that it could also use it in aerobic conditions.
Go do some reading how about Jock?
phoodoo,
In fact according to you Jock, e.coli should never be able to utilize citrate even under anaerobic conditions, because the number of mutations that could knock that out must be numerous right, so it should already be knocked out.
I think you should recheck your source. Wikipedia:
The researchers also found that all Cit+ clones had duplication mutations of a 2933 base pair segment that were involved in the gene for the citrate transporter protein used in anaerobic growth on citrate, citT. The duplication is tandem and resulted in two copies that were head-to-tail with respect to each other. This duplication immediately conferred the Cit+ trait by altering the regulation in which the normally silent citT gene is placed under the control of a promoter for an adjacent gene called rnk. The new promoter activated the expression of the citrate transporter when oxygen was present, and thereby enabled aerobic growth on citrate.
Worth a look and also following links to the primary literature.
As I say, you might like to look at the primary sources.
That’s absolutely correct phoodoo, if and only if the E. coli are grown in an environment where a citT knock-out is under no selective disadvantage whatsoever.
Given the role of citT in succinate, fumarate and tartrate transport, you might find it difficult to create such an environment for your experiment. OTOH, you clearly have the plenty of the requisite starting material: give it a go!
DNA_Jock,
Your theory would only make sense if one couldn’t name at least ten traits in any organism that are no longer selectively necessary and yet are not knocked out by mutations. Like virtually every neutral mutation that is preserved.
Like eyebrows, or the ability to get calluses. Useful? Sure, but selectively favored? I hardly think so.
LOL (I shouldn’t but I couldn’t help it!)
Wonderful!
1) You jumped from a discussion of genes to a discussion of traits. You should read up about the genotype/phenotype distinction and what a spandrel is.
2) You imply that you can name at least ten traits in any organism that are no longer selectively necessary yet are not knocked out by mutations. Did you mean “genes” that “confer no selective advantage” and yet “are preserved”? Cool.
Please provide your list for S. cerevisiae.
3) Your (best?) examples are eyebrows and the ability to get calluses. Say what? You can read up about the functions of eyebrows, or just think about the advantages of being able to form calluses.
Here’s what you are missing: if, as you admit, they are useful, then they are going to be somewhat favored.
(to Alan: I know I shouldn’t too, but sometimes…)
DNA_Jock,
You are complaining that I referenced eye brows and calluses, when your sides entire body of evidence for natural selection is e.coli being able to metabolize citarte in aerobic conditions instead of just anaerobic ones?
Oh that’s cute, you are a satirist.
It should come as no surprise that a satirist like you can imagine a scenario where all the bushy eye-browed folks outcompeted all the hairless browed folks in the ancient savannnah. Way back when there was all the bushy knee folks, and bushy tongued scavengers, and hairy nosed hunters, that all lost the hair sweepstakes to the smart groomed lucky mutational eyebrowed ones.
It was such a crazy time in our history for a while, what with all the unlucky ones with their eyebrows below their eyes, instead of above, and they had to walk upside-down to keep the sweat out of their eyes. That of course led to handstand sex, which left them vulnerable to butt chewing hyenas obviously, and well, you know how the story goes from there….just relics of history now. Long lost fossils.
Thank god natural selection finally sorted it all out, huh Jock?
phoodoo,
You made me smile, phoodoo. You have quite a talent for creative writing.
Again, Phoodoo is real, not a parody and reads Uncommon Descent for ‘educational purposes’.
phoodoo,
It still needs to sort you out of the gene pool, but by all indications that won’t take very long.
keiths,
I reckon intersexual selection can deal with both of the problems that phoodoo presents.
DNA_Jock,
Yea, its really hard for me to find sex partners. I am in great physical condition, I play a sport people love, but gosh, I have really thin eye brows.
Now, if I was a DNA jock-with hair all over my face, instead of , well, a real jock, then it would surely be much easier. Girls love hair anywhere around guys eyes, or nose, or ears.
I am sure even Richardhughes does great, with that hair all over his palms and all, which he uses for wiping his sweaty face.
Btw, I like the gold chain Jock.
OTOH, eye brows can easily be explained by ID: IDiots would look weird when they frown upon evolution without them
phoodoo is indicative of far more than two problems.
100 meter dash away from education?
Freestyle ignoring of evidence?
Blind leap of faith?
A genuine sports person would know it’s about hard work and training. E.G. An education and genuine academic effort.
phoodoo is the equivalent of the ordinary joe turning up with no training and expecting to win gold at the olympics. He’d not expect someone who was playing for the first time to beat him at his sport, yet he expects to be able to best others who actually have the relevant skills.
And as a genuine sports person would know it’s about hard work and training they’d immediately recognise the situation they were in as analogous…
OMagain,
How would you know about what a genuine sports person would know?
Seems I don’t even need to contradict you, when your own words do it for me. You’re neither an expert in biology nor sports, so shouldn’t you be silent right about now?
virtuoso subject-changing?
empty-assertion marathon?
Well, we can perhaps judge the quality of phoodoo’s argument by looking at how widely it’s spread out into the world. If if has convinced many people then there may be something to it after all. Perhaps, perhaps not.
Phoodoo, can you point to a group of people or even a single person that you have convinced of the correctness of your position?