Evolution will fall not because of creationism's triumph, but simply because the mechanism is seriously flawed and cannot produce the complexity and vast amounts of information on our planet.
That's a really funny thing to say. You
do know that engineers and programmers are employing that exact mechanism - actually, those exact two mechanisms, random mutation and natural selection - to create circuits and designs vastly more complicated than intelligence is able to do on its own, right?
They're not "seriously flawed", they're more than sufficient to create complexity; we use them to do specifically that for our own ends.
Suppose a DNA sequence which specified some trait were laid out as follows. IWILLCREATEAHAIRFOLLICLE.
That's not how DNA sequences are laid out, however. They're laid out like this:
5' ACGTATATGCAT 3'
Now suppose that mutates, so that you have
5' CCGTATATGCAT 3'
Is that new genetic information? Obviously, it is. That's a novel sequence that the organism did not possess, so naturally, it must be new information.
Please point me to one of those "beneficial" mutations.
J Clin Invest. 1980 Nov;66(5):892-900.
A-IMilano apoprotein. Decreased high density lipoprotein cholesterol levels with significant lipoprotein modifications and without clinical atherosclerosis in an Italian family.
Franceschini G, Sirtori CR, Capurso A 2nd, Weisgraber KH, Mahley RW.
quote:
Significant hypertriglyceridemia with a very marked decrease of high density lipoproteins (HDL)-cholesterol levels (7-14 mg/dl) was detected in three members (father, son, and daughter) of an Italian family. The three affected individuals did not show any clinical signs of atherosclerosis, nor was the atherosclerotic disease significantly present in the family. Lipoprotein lipase and lecithin:cholesterol acyltransferase activites were normal or slightly reduced. Morphological and compositional studies of HDL in the subjects showed a significant enlargement of the lipoprotein particles (approximately 120 vs. approximately 94 A for control HDL) and a concomitant increase in the triglyceride content. Analytical isoelectric focusing of HDL apoproteins provided evidence for multiple isoproteins in the apoprotein(apo)-A-I range, with nine different bands being detected instead of the usual four bands observed in normal subjects. Two-dimensional immunoelectrophoresis against apo-A antiserum indicated a clear reduction of apo-A in the alpha electrophoretic region, with splitting of the protein "peak." The observation in otherwise clinically healthy subjects of hypertriglyceridemia, reduced HDL-cholesterol, and marked apoprotein abnormalities, without a significant incidence of atherosclerotic disease in the family suggests this is a new disease entity in the field of lipoprotein pathology, very probably related to an altered amino acid composition of the apo-A-I protein (see Weisgraber et al. 1980. J. Clin. Invest. 66: 901-907).
Evolution is directional.
Yes, it is. And that direction is "outward" - that is, increasing diversity. It's not a surprise that we see more complex organisms; when you're at the bottom of the simplicity scale, but diversity is increasing, there's only one direction to go.
But it remains the case that no matter how you measure them, the vast, vast majority of life on Earth is extraordinarily simple; the complex stuff is so rare it barely rates mention. Except, of course, for the anthrocentric fact that we belong to that extremely small group.
You don't just reconstitute new DNA structures by random processes and create meaningful information.
Actually, you can. It's really not all that hard to generate a sequence of DNA that can be transcribed into a protein; about one-half of all random amino polypeptides exhibit ATP-binding activity. The rate at which random mutation generates new, useful genetic information is drastically improved, of course, when you add selection into the mix.
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