I will leave much of the post alone as others have already addressed those points. I would however like to correct a few errors that you have made w.r.t. ascorbic acid biosynthesis and how it makes portions of your arguement invalid.
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I checked one claim about the GLO pseudogene (the gene that catalyses the final step in vitamin c synthesis) that has been inactivated in the same spot in primates and is taken as proof for common ancestry. And, indeed a superficial look would immediately convince any evolutionist. However, if you have a careful look at the presented sequences you will discover that the replacement of nucleotides is not at random between the distinct species.
OK, leaving aside your rather spurious dig concerning the ability of the evolutionists on this board to properly read data, I have to say that you are in error here. Ohta's paper clearly shows RANDOM mutations (other than the frame shift) in exon X between four species. I would like to see a fuller sequencing so that this gene could be used in the construction of a phylogenic tree for comparison to other phylogenic trees as internal controls.
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Secondly, you will discover that it does not make a difference for the mutation rate of this gene whether it is functional or not, in contrast to what evolution theory would predict.
Did you get this from another reference. I do not remember it from Ohta's paper.
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Thirdly, it violates population genetics: why would the inactivated gene become fixed in the entire population, while the active gene conveys longivity.
This error is based on a misconception of Hardy-Weinburg genetics. A gene which is environmentally silent, as this one is in most primate populations due to a diet which circumnavegates the genetic and phenotypic flaw, can spread through drift. Genetic bottlenecks then often do the redt.
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In addition, evolution never compensated for vitamin C uptake in the gut,
I doubt that this is or would be neccessary. The only papers that I have on hand indicate to me that this is not neccessary, in humans at least:
Just a moment...Please note that the bioavailability is roughly 100% at ranges sufficient to prevent scurvy. This is expected for nutrients takeup by sodium co-ports
Flavonoid inhibition of sodium-dependent vitamin C transporter 1 (SVCT1) and glucose transporter isoform 2 (GLUT2), intestinal transporters for vitamin C and Glucose - PubMedand
PubMed
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and, finally, the gene is redundant anyway since the third step in vit c synthesis already yields vitamin C by spontenaous oxidation and is sufficient to avoid vit c deficiency.
Sorry but this is flat out wrong, at least in its implications in deficiency. While the conversion of L-xylo-hex-3-ulonolactone to L-ascorbate is spontaneous the missing enzyme causes the conversion of L-gulonolactone to L-xylo-hex-3-ulonolactone concurrent with the reduction of oxygen to hydrogen peroxide. This step requires an enzyme and is not spontaneous. It is simple, no enzyme, no vitamin C biosynthesis.
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Also not unimportant, at least 2 primates are able to synthesise vitamin c in the liver, indicating the presence of an intact GLO gene .
I would like a reference for this one for two reasons,1) so I can compare these "primates" to a phylogenetic tree and 2) to ensure that what was being observed was not just storage of ascorbate as the liver is the bodies reservoir for ascorbate for ALL primates.
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(I once had a discussion about this gene with Dr D. Theobald (Talk Origin) so I know a bit about pseudogenes
Oh, and I used to work in a lab which did ascorbate nutritional studies so everything I have said is pretty much accurate (I left that lab about 7 years ago to work in industry so I may have forgotten a few things).
At least with respect to vitamin C the data here supports NS or descent with modification in the neo-darwinian sense far more than it does ID.
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"Chance favors the prepared mind." L. Pasteur
Taz
[This message has been edited by Dr_Tazimus_maximus, 08-22-2002]