It may very well be invalid. But since there's no other data to work from it's kind of a moot point, no?[/quote[
There is no data to work with because the kinds of changes that would have had to occur for humans to evolve from apes has no genetic basis.
I have no idea what you are babbling about. Yes, 1.6 mutations occur per sexual generation (i.e. per offspring). I'm not saying all of them become fixed. Where do you keep getting this idea?
You said 1.6 per genome per sexual generation assigning a period of 20 years and you used that to account for 68,000 indels that are fixed in the two comparative genomes. You said that you were going to focus on the effective genome but never accounted for the effects of mutations on protein coding genes. At any rate when you used the 1.6 figure I thought that you got it from this:
"Under conservative assumptions, we estimate that an average of 4.2 amino-acid-altering mutations per diploid per generation have occurred in the human lineage since humans separated from chimpanzees. Of these mutations, we estimate that at least 38% have been eliminated by natural selection, indicating that there have been more than 1.6 new deleterious mutations per diploid genome per generation. Thus, the deleterious mutation rate specific to protein-coding sequences alone is close to the upper limit tolerable by a species such as humans that has a low reproductive rate"
High genomic deleterious mutation rates in hominids
You still haven't demonstrated that these are errors. You harp on about the difference between humans and chimps, but you're fixated on the difference between the total genomes, which is something I never set out to address. You are also fixated on the deleterious effects of mutations, but you've never demonstrated that this is a problem with respect to an evolving population.
Number one, you did cite and link the chimpanzee/human chromsome comparison paper where it explicitly described a 5% divergance not 2%. For another thing you have completely ignored the fact that 80% of the mutations effecting the amino acid sequences are deleterious. Now you want to account for these mutations, using statisitics of fixed differences but you don't want to talk about how changes are fixed in overall genomes, particulary to the effective genome. Nothing in your post addresses the effective genome and all of your statistics are either unbiased, with regards to the protein coding genes in primates, or obscure generalities concerning bacteria.
And when I ask you to back it up by doing your own math (to estimate mutation rates and human/chimp divergence), you claim it's impossible to do so.
6 billion times nothing is still nothing. I have repeatedly showed you the overall changes noted in genetic research and their influence on the effective genome. You have yet to demonstrate how a single beneficial effect can be derived from mutations in the protein coding genes.
There were other examples given. I still don't know why you are pretending otherwise. In fact, here are some now.
Oh good, more anecdotal evidence
Another polymorphism for humans:
Polymorphisms and mutations found in the regions flanking exons 5 to 8 of the TP53 gene in a population at high risk for esophageal cancer in South Africa.
Slight selective advantages for a small minority, for a short time:
"The frequency of the Ser447-Ter genotype in GG and CG was significantly lower in CAD than in the controls (11.9% vs 26%, odds ratio = 0.38; 95% confidence interval, 0.18-0.81; p<0.02). "
Maybe
"This mutation may have a protective effect against the development of CAD via its favorable lipoprotein profile."
Same thing here:
"As compared with controls, the frequency of LPL genotype CG (heterozygous Ser447Ter mutation) was lower in ischemic stroke patients (10.4% vs. 21.4%, p<0.05), and was not significantly different in hemorrhagic stroke patients (15.6% vs. 21.4%, p>0.05). The LPL G allele frequency was also lower in ischemic stroke patients (5.2%) vs. controls (10.7%, p<0.05)."
and here:
"CONCLUSIONS: Patients with ischemic stroke have a lower frequency of the LPL Ser447Ter mutation, which indicates that this mutation may have protective effect on ischemic stroke."
I'm not even sure this is a mutation, it sounds like a gene variation, not a spontaneous mutation.
Ter447 variant was negatively associated with neuropathologically verified brain infarcts (P = 0.006), and even more strongly with small brain infarcts (P = 0.004).
The rest of the anecdotal evidence show no improvement of vital organs or anykind other then a slight selective advantage for a short time.
And like it or not, the homozygous genotype for the CCR5d32 mutation does prevent people from developing AIDS (based on HIV-1). So it's definitely beneficial in that context.
No, it does not prevent people from getting full blown AIDs it just hinders the outset of it.
Slight selective advantages, to a small minority, for a brief period of time is neither evolutionary adaptation nor a genetic basis for major morphological innovation. Its called equivication Pete and its a fallacy:
"Equivocation is the type of ambiguity which occurs when a single word or phrase is ambiguous, and this ambiguity is not grammatical but lexical. So, when a phrase equivocates, it is not due to grammar, but to the phrase as a whole having two distinct meanings.
Of course, most words are ambiguous, but context usually makes a univocal meaning clear. Also, equivocation alone is not fallacious, though it is a linguistic boobytrap which can trip people into committing a fallacy. The Fallacy of Equivocation occurs when an equivocal word or phrase makes an unsound argument appear sound."
http://www.fallacyfiles.org/equivoqu.html
There is an old adage in evangelical theology, 'a text without a context is a pretext'.
Grace and peace,
Mark
