Also, incidentally, exponential population growth is a realistic parameter. It’s typically how populations grow: expontentially, until they hit environmental carrying capacity.
IS there ANYTHING you aren’t wrong about?
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Which is it?
Both. Literally both. It is a realistic parameter for a population to grow exponentially. In my model, however, population size remains constant which is ensured by half of offspring dying every generation.
So both, clown. Both.
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Your model is not realistic because it assumes deleterious mutations kill an animal before they can reproduce. Where is your evidence supporting this?
There are many unrealistic things about that model. The model is the way it is partly because you specified some of the parameters (the mutation rate, that 1 mutation accumulates in every offspring every generation), and I in turn tried to bring it towards more realism to make it obvious why selection, offspring numbers, and population size, matters, while also being able to work out it’s entailments easily in our heads. Well, some of our heads.
You’re welcome to modify the probability of death of offspring to be proportional to the net effect of selection coefficients of carried mutations, and include realistic (measured distributions of fitness effects of mutations) and then run the simulation. Remember to show your work.
Also, it would be more realistic to have expected number of offspring be defined by a probability distribution, which would also be influenced by the net effect of carried mutations, instead of just having every individual produce 1, 2 or whatever, every time. So carriers who had accumulated more deleterious mutations (some would build up to a certain point, here or there) would be significantly more likely to die, and had fewer offspring on average, which is how selection would ultimately remove them from the population. But you’re too stupid to work this out, so we made it simple. For you.
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Bill, please quote exactly where Behe “is very clear what his model is and is not” on the subject of “existing variation in nature”.
If you cannot do this, your above statement is clearly false, and will be taken as further evidence of dishonesty.
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I agree completely.
Bill, kindly point us to where (the exact words) Behe is very clear about ignoring existing variation in natural populations. If you can’t, you should retract your false claim.
I’m all but certain that your claim is a deliberate fabrication. If you don’t think it is, show us where he was very clear about omitting existing variation.
Do you not see the utter mendacity of Behe claiming to be tearing down Darwin?
Darwin based everything on his observations of existing heritable variation, while Behe’s silly model pretends that none of what Darwin observed exists.
Behe’s not even trying to include the most important parts. IMO, he’s trying to omit them to get the answer he hoped to get and to avoid embarrassment. I think you are too. As soon as you are taught why you are wrong, you saunter over to a new falsehood.
Yep, and both of us are pointing out very important things that Behe has omitted.
How can underestimating the magnitude of variation in a population by a million-fold add to the accuracy of a model that allegedly addresses variation and selection?
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I think @colewd is less interested in making a coherent or credible argument, on the original topic of this conversation or anything else, than in establishing his undying fidelity to Michael Behe.
I can see no other reason to be harping on and on about a single, discredited, 17yo model by a mediocre biochemist and his partner, neither of whom have any expertise (nor, as far as I can ascertain, even competence) in population genetics, when there are presumably dozens (hundreds?) of more competent models produced by scientists with real expertise in that field.
It is not that Bill has any credible claim that it is a good model – it is that it is Behe’s model – so must be defended until the heat-death of the Universe (or at least until some moderator comes along and puts this misbegotten thread out of its, and our, misery).
Bill’s entire contribution to this thread could be summarised by the following:
I pledge allegiance to Michael Behe, and to the Designer for which he stands, one model under God, indisputable, with deleterious mutations for all.
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Your ‘model’ is even less realistic, because it assumes that deleterious mutations have no effect whatsoever.
Where is your evidence supporting this?
(I know, you haven’t got any evidence, and hadn’t even realised that in your ‘model’ deleterious mutations aren’t deleterious. So I don’t expect a sensible answer, I’m just giving you another chance to demonstrate how incompetent you are.)
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Isn’t that a bit like giving the Pacific Ocean another chance to prove that it’s wet? 
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My model has nothing to do with the effect of deleterious mutations. It simply is a model of how deleterious mutations accumulate in a population.
I agree at some point they will stop accumulating in the population but at that point the neutral mutations on that specific gene that occurred with equal probability will also stop accumulating.
John your whole argument here is a logical fallacy (ad hominem) and has no basis in reality. He clearly defines his starting point what it includes and what it does not and why. He also is very clear about the strength and weaknesses of his assumptions.
If they have no effect, how are these mutations deleterious?
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Pointing out a false statement is not fallacious.
Show us where Behe was very clear about omitting existing variation.
Show us where Behe was very clear about not including existing variation.
Then show us where Behe was very clear about assuming that variation doesn’t already exist, a huge weakness.
Or, keep digging…
Hi John
You need to read his paper carefully. He is very clear his model starts with duplicated genes already in the population.
The starting point of the simulation (see Materials and Methods for a more complete description) is a population of organisms that already contains N exact duplicates of the parent gene, which then begin to undergo mutation
I have. You need to understand how bad the paper is, as it has no basis in reality.
But there are no variants of either of those genes, which represents an enormous weakness that he neither explains nor addresses. He doesn’t address it in his books either. Thus, your claims:
…are objectively false.
Why would the genes only begin to vary after duplication? Why would any population of meaningful size have zero polymorphism for either gene? How would the duplicate gene be distributed throughout all members of the population with zero mutations occurring?
Behe doesn’t say, and there’s zero basis for making that assumption–other than that he doesn’t get his desired result.
How do you propose he would add the variants to his model? If the variants are neutral how does this reduce the time to fixation of the MR feature?
What you are discounting is Mike starting the simulation with a pre existing duplicated gene.
Regardless of whether Bill understands or admits this, Michael Behe does:
Our paper (Behe and Snoke 2004) contains one simple result. When reasonable parameters are used with our model to estimate actual time scales or population sizes for the evolution of multi-residue (MR) protein features, they are unrealistically large. This implies that the model we chose, which is restricted to point mutations and assumes intermediate states to be deleterious, isn’t a plausible evolutionary pathway. One must therefore look about for a new model. We did not rule out such a possibility; in our original article, we explicitly stated, “we should look to more complicated pathways, perhaps involving insertion, deletion, recombination, selection of intermediate states, or other mechanisms, to account for most MR protein features.”
A response to Michael Lynch - Behe - 2005 - Protein Science - Wiley Online Library
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And Lynch did not. Yet his model still showed that “conventional population-genetic principles embedded within a Darwinian framework of descent with modification are fully adequate to explain the origin of complex protein functions.”
Really not much wiggle room for you there. Eh, Bill? And, yet, you wiggle the best you can. If you refuse to accept reality, what other option do you have?
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Is there anything about Lynch’s model that might make you skeptical of the above statement?