Wow.
FYI, I’m a virologist.
Perhaps you should follow my advice and not regurgitate Sanford’s false claims about virology.
Or, you could examine the evidence for yourself instead of dealing entirely in hearsay.
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That’s not how I approach such questions. If there is broad consensus among experts in a field which is based on objective and verifiable evidence, I presume that these experts know what they are talking about and simply accept that consensus. If it is a subject about which I have a particular interest, I will try learn about the evidence on which the consensus is built. However, if that evidence is not convincing to me, I will assume that this is the result of my lack of expertise in the area leading me to misunderstand the evidence, and will try harder to learn more, or simply accept that the subject is beyond my current capabilities. I will not conclude that I am some brilliant, unschooled genius who has managed to find a flaw that somehow escaped all the world’s experts.
But that’s just me.
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A genome wherein no gene would be defective
How do you determine that a gene is not “defective”?
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Without a functional definition of defective, that can only be a circular definition, as in “not defective = perfect”, “defective = not perfect”.
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None of those fit Gil’s position. He’s convinced that the experts are wrong, but he did not come to that conclusion from the evidence. If I think that an expert consensus is wrong, I deal ONLY in evidence.
I think that on some level, @Giltil knows he’s not correct. That’s why he stays so far away from the evidence and just pretends to be familiar with it using hearsay.
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I’m not trained as such, but I do play one in the scientific literature.
Start with the question I asked previously: “In order for very slightly deleterious mutations to dominate in sites like this, there has to be some mechanism to get the sequence into the preferred state to start with. What is that mechanism?” Why would someone like Graur think that the human genome would be in a state such that very slightly deleterious mutations were much more common than very slightly beneficial ones?
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Do you agree with Sanford that 6000 years ago human genes were “perfect”?
You didn’t supply any commentary on the hominid genomes much older than that, going back to the 430,000 year old one I linked to. How does GE explain all the earlier hominid data?
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Is the presumed rate of GE constant? If so, we ought to be able to compare contemporary human genomes from those a few centuries old and see less disorder and be able to map a nested hierarchy of genetic breakdown.
I’m guessing Sanford has not done this, nor plans to.
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In his book, he plots the ages of specific patriarchs in the Bible, along with average Roman lifespan, to produce this curve and say it’s significant. Accordingly, most of us should probably be dead by now.
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Yes - according to Sanford’s equation, the average lifespan now should be just 21. This is incompatible with reality. Furthermore, because it’s an exponential curve, lifespans would have been in the low 20s since before the industrial revolution, so modern medicine and technology can’t be used to excuse the discrepancy.
There are other obvious problems. First, Noah should still be alive, since he has an infinite lifespan. If Noah’s wife was born within a century of Noah, she should still be alive too.
Anyone born before Noah would have had an imaginary lifespan, which is possibly the only correct result obtainable from this graph.
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He should plot the birth dates of the oldest trees. But then he’d have to extend the left side of the plot quite a bit. I don’t think it would fit his timeline.
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But the mutation load includes effectively neutral deleterious mutations, doesn’t it?
It does in the case that effectively neutral deleterious mutations outnumber effectively neutral beneficial mutations, which will generally only be the case after a population size reduction. Graur isn’t considering such mutations, in any case – that’s clear from the fact that he treats synonymous mutations as ones that can be ignored. Synonymous mutations are easily the most studied class of very nearly but not quite neutral mutations.
(I don’t actually buy Graur’s argument in this paper, by the way, since I think it mixes relative and absolute fitnesses.)
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IIRC (and I may not) Fisher made simplifying assumptions, and didn’t attempt to account for a changing environment. In this setting a population ought to reach equilibrium, rather than increase indefinitely. Sanford might be correct in this sense - However, I seriously doubt Fisher intended his result to be interpreted as an unending increase in fitness in a fixed environment.
I didn’t attempt to follow the math past that point because I was informed the population geneticists had work out this difficulty long ago.