Morphy: “Well, if a red blood cell is malaria resistant what is it if not improvement???”
To which, I reply: Broken. Also:
A dead blood cell is malaria resistant. That’s not an improvement.
A quadriplegic is resistant to tennis elbow. Ditto.
A disease that preempts a worse disease is still a disease.
Morphy: “If you give me detailed genetic codes of all human ancestors from the first alive, primitive prehistoric cell to the human genome I won't resort to diseases. …positive mutations are extremely rare, like 1:1.000.000? Or maybe even rarer.”
Yes, I guess you could get one out of a million, considering that you morph a mutation-caused disease into something positive.
Morphy: “If you add that there is natural selection - then it is enough to prove there is evolution.”
Morf, you’re describing change, not Darwinian evolution. Darwinian evolution is not a synonym for the word change, it is a claim that a certain type of change has occurred, namely a change that adds genetic information to produce increasingly complex organisms. (It seems as though the evolutionists in this thread have gone senile, forgetting that Darwinism is supposedly PROVED by the evolutionary progression of SIMPLE to COMPLE organisms).
If you had a lot of evidence for evolution, you could easily concede our point that disease is not excellent evidence for molecules-to-man evolution. But because of the absence of “excellent evidence” for evolution, you guys parade around evidence for de-evolution. News flash: Both sides believe in mutations, and that they often cause changes, including disease and death.
To provide evidence for molecules to man evolution, you’re going to have to show mutations that increase the information content of a genome, NOT evidence of disease, because that’s just too funny and easy for us creationists to explode.
And finally, you asked about drug resistance, which results from different known mechanisms including mutations, transfers, etc. I’ll describe a common mechanism, which is a mutation and a loss of information. The streptomycin antibiotic is a three-dimensional molecule that interlocks with a bacteria's ribosome (as in Mycobacterium tuberculosis), interfering with its protein synthesis and thus killing the bacteria that causes tuberculosis. If Mycobaterium has a ribosome mutation (breakage), and therefore its ribosomes are deformed and become less effective at assembling proteins (this actually happens), then the streptomycin molecule cannot attach as it did to the healthy ribosome because it's shape no longer fits into the deformed shape of the mutated ribosome. We call this a resistant strain, which it is, although at the cost of a broken ribosome which is fortuitous to the antibiotic, bad for its host, and making all a little bit worse off for the mutation. I realize you asked for more particulars, but I suggest you read Spetner’s book. If you’d like, I’ll mail you a copy. By the way, he was with the Applied Physics Laboratory at John Hopkins University and in the Hopkins biophysics department.
And Morphy, since you invited me, I’ll post a defense for my Evolve.exe evolution refutation program. Coming soon to a thread near you!
-Bob Enyart
