I’ve already answered you fully way back in October, and yet you just pop up again with the same old fallacy, as though you had never been corrected. Don’t you ever learn anything, or are you just so committed to your religious ideas that no reason can get through to you? I will patiently repeat that October post in the faint hope that you will understand it this time:
Fair enough…
This is all reasonably sensible stuff dating back to 1999 that attempts to explain how Hall’s and Cairn’s directed mutations could arise if we consider the cell to be a quantum particle in superposition (although I do think that the idea that cells enter a state of superposition only when they are starving is a little bizarre - most people would say that the suspension of metabolism is a classical effect promoted by enzymes and cell signalling - and nothing to do with quantum superposition).
So here, you have identified two, (not one) perfectly valid different hypotheses…bizarre or not, the quantum evolution hypothesis still remains valid, whether you, or the majority accept it not. I will not get into “cell signalling” because the focus is put directly on the Professor McFadden’s article
pnews.org/ArT/TrU/QuantumEvolution.shtml
But I don’ t think that these explanations are needed.
It’s you’re opinion; and you certainly are entitled in having one.However, your opinion, is just that…an opinion; no more, no less.
As I mentioned in another post, the existance of a different hypothesis does not render McFadden’s
hypothesis invalid. The Big Bang theory and the Steady State theory both exist as plausible hypotheses…one is simply accepted more than the other.
More recent work by Patricia Foster who worked with Cairns (see Foster, Adaptive Mutation in E coli, Journal of Bacteriology, August 2004, p. 4846-4852)
has shown that although the mutational rate goes up when bacteria are starving on a novel substrate, the rate of the beneficial mutation does not go up any more than similar mutations nearby on the genome - there is no “direction” going on.
It seems that McFadden is also aware as he did write:
It is now clear that there were some problems in Cairns original experimental design that meant he missed some of the mutations that did indeed occur in other genes. Yet the phenomenon of adaptive mutations persists and has been detected in a wide range of microbes and even in animal cells.
His approach is more holistic in nature.His focus seems more on trying to explain why there is an increase
in mutation rate in the first place, and why is it dependant on the environment?
What would be your opinion as to why this particular property of mutation exists?
(Quote from the paper:“Fairly early on in our studies, Cairns and I eliminated the hypothesis that mutations were “directed” toward a useful goal.”) It is not true that the cells only acquire the appropriate mutation when lactose is available - it is true that the mutation only fixes and spreads when lactose is available (but that is natural selection in action). The fitness landscape is obviously different depending on which substrate the bacteria grow. In the same way that the most primitive precursor to eyes, a light sensitive patch, would not have been conserved if light had not been available (and animals that adapt to live in darkness often lose their sight and end up with vestigial eyes) - the fitness landscape favours sight if light is available but not in the dark.
this only testifies to what Dr McFadden wrote :
Adaptive mutations is still one of the most controversial topics in genetics and provokes the most heated exchanges at conferences. Many scientists simply refuse to believe in their existence.
Adaptive mutations (a term that is at least 25 years old by the way, not new) are random with respect to fitness. In other words, when the bacteria are stressed all sorts of mutations occur randomly at a higher rate than normal (as my quotation from Patricia Foster shows - the mutations are NOT directed). Those very few bacterial cells that acquire a beneficial mutation (instead of a neutral or deleterious one), are then able to metabolise their substrate and happily return to a state of exponential growth. As far as all the huge quantity of evidence shows, **all **mutations are random with respect to fitness - there are no magic non-random (with respect to fitness) mutations
I am not the one having problems in understanding that different hypotheses exist; it is you who cannot accept that some valid scientific hypothesis exists, pointing to mutation as being non random, which, in turn, would identify Evolution also as being non-random
in essence.
Andre
Hopefully, one day he will be a member of the Pontifical Academy of Sciences. 
The Vatican has their eyes on him. 
