Russell
Posts: 1082
Joined: April 2005
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| Quote | | But what if we find out later that the Milano mutation causes some other problem which outweighs the benefits of reduced risk for heart attacks? Then is it beneficial? No, not any more. We just thought it was at first, but now it's not. |
Right. And what if we don't find out later (as we haven't) that it causes some other problem? Well, then we have no way of knowing that we won't find out still later that it causes some other problem. In other words, it's pointless to argue with you, and it's disingenuous for you to pretend you're open to evidence on a "beneficial mutation", because we can never know whether some deleterious effect will be discovered next year, can we? But you, armed with your biblical understanding of the universe, assume that some such deleterious effect must exist. Well, I think there are generally trade-offs; I wouldn't be terribly surprised if it turns out apo-AIM turns out to cause, say, hypolipidemia on an exclusive diet of anchovies. For you, and maybe for all those who are committed to an exclusive diet of anchovies, that will constitute proof that it's a degenerative change. For the rest of us, I think it would still be a "beneficial mutation".
| Quote | My tentative diagnosis of "seriously delusional" was confirmed last year at the Dover trial.
Really? What specifically made you think this? |
Oh, I don't know. I think it was the fact that he thought he had made a pretty persuasive case after the entire rest of the world was laughing at such gems as "astrology is science", and that there's no research on evolution of the immune system, despite a stack of published literature sitting right in front of him consisting of publications of research on, well, evolution of the immune system. Or the truly comical defense of the rigor of the "peer-review" of Darwin's Black Box.
| Quote | | The facts of biology are that IF these gazillions of details ARE NOT SPECIFICALLY equal to certain values, then the organism will be sick or might die. I have not read many formal definitions of Specificity, but this would be my preliminary defintion. |
Well, let me help you out, then. You see, here we're talking about the binding between a protein and cholesterol, i.e. a biochemical context. In biochemistry, specificity has a much more definite meaning. It would be measured in terms of dissociation constant (Kd) of the complex, relative to the corresponding Kd for other potential candidates for binding. If you're talking about some other definition of specificity, well, you're going to have to define it a lot more precisely than you did here. Because, you see, just like the all-purpose get-out-of-the-argument-free dodge above (i.e. you can never know some serious drawback to mutation won't be discovered... tomorrow), this kind of sloppy, hand-wavy (non)definition of specificity allows you to dismiss any counterexample brought to your attention as - somehow - not matching your goalpost-on-wheels idea of "specificity".
And speaking of mobile goalposts: | Quote | | So ToE really needs something different than "beneficial" mutations in order for the theory to be plausible. What ToE needs in order to get from a "simple" single celled organism up to a complex vertebrate such as a human, is massive increases in specificity. |
Wait a minute. I thought that any increase in specificity was impossible, since, as you know, ToE involves cumulative changes. I.e. unless you can convince anyone that no increase in "specificity" is possible, what's to prevent less-than-massive increases from adding up? So are we wasting our time here talking about specifics, like apo-AIM, or my viral methyltransferases (that you, for some reason, seem to be ignoring)? Does it have be a one step mutation converting a fin into an arm in order to count?
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Must... not... scratch... mosquito bite.
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