That is a great deal of projection, coming from someone espousing (I presume) creation, but I’m afraid it doesn’t hold up.
I’m not really sure where you come up with the idea that evidence can support any theory, which is simply wrong, but perhaps I can give a few examples to demonstrate the point:
The human chromosome 2 shows an exceptional degree of homology to a pair of chimp chromosomes, named 2A and 2B - the same genes we have on our chromosome 2 they have on those two chromosomes, in the same order. In addition, human chromosome 2 has vestigial telomerse (found at the end of chromosomes) inside it, at the point where the genes from chimp chromosome 2A stop and those of 2B begin. Further, it contains a vestigial centromere (each chromosome only contains one normally). Together, this is good evidence for not just sharing a common ancestor with chimps, but is a rather good sign that after divergence, pre-humans underwent a chromosome fusion event that joined two previously separate chromosomes into a single one, which fixed in the population.
There is a gene in most mammals that codes for a protein which allows us to synthesize vitamin C. Humans, the other great apes, guinea pigs, and a number of other species don’t have a working copy, but instead a pseudogene - a region which does not produce a functional protein, but which resembles a gene in other species. The pseudogenes that exist in humans and the other great apes have the same inactivating mutations; they don’t work for the same reason, to say very simply. This is indicative that the inactivating mutations occurred in a common ancestor to the great apes, and has been passed down to humans and chimps and gorillas all, most notably because of the odds of such a thing arising randomly. The guinea pig species also have a pseudogene instead of a working copy, which bears a major resemblance to the copies in numerous mammalian species, but it is - once more - non-functional. In addition, the mutations which rendered it non-functional are shared within the guinea pig family, but are exceptionally different from those that inactivate the gene in the great apes. Together, this is evidence that the gene is shared among mammals because it arose in a common ancestor mammals share, but it has been inactivated multiple times in multiple lineages, further indicating that, for example, humans are more closely related to great apes then to guinea pigs.
This is, of course, the metaphorical tip of the iceberg; we can talk about the genetic histories of just about any gene you’re curious about, and we find similar patterns.
Now, if you’re backing design, you can look at this and say “that’s how a designer made it” - which is an explanation, if a poor one, but does not make any predictions. Evolution, on the other hand, not only provides an explanation, but a consistent explanation for these in conjunction with other phenomena, and predictive power in that we can use it to predict the lineages of other gene families as well.
This is not a manipulation of the evidence to suit a theory; rather, the theory is based upon the evidence; the fact that the theory’s original predictions fit with the those found by genetics is a testament to its accuracy and power.
That’s the coolest thing about science though - if we find a piece of evidence that cannot be explained by the present theories, we change the theories! That’s how Newtonian physics made way for relativity, for example.
As an afterthought, and clarification, creationism/ID is pseudoscience; it is unable to make predictions (and thus not a scientific theory), is based upon fallacious reasoning, and is not supported experimentally.
Again, a whole lot of assuming of evolutionary theory to interpret the evidence to support evolutionary theory.
Here an obvious few counter-question, given predictive value.
Given the presumed survival value of having a working gene to synthesize vitamin C...
1) Was there a triggering event which caused the inactivating mutation to be selected in guinea pigs?
1a) If so, why did it spread, if being able to make Vitamin C is (apparently) so advantageous that most other mammals possess it?
2) If the diet of guinea pigs was so rich in vitamin C that the ability to synthesize Vitamin C was not crucial, how well preserved was the pseudogene?
3) What accounted for the mutation *changing* in the primates or great apes compared to the guinea pig?
4) What is the number of base pairs different to make the Vitamin C gene a pseudogene? How many simultaneous mutations would be required to allow the organism to make Vitamin C again?
5) Given the obvious survival advantages of being able to make Vitamin C, and the fact that people still can't make Vitamin C, this implies that the mutations necessary still haven't happened (punctuated equilibrium yada yada). We are confident that mutations can happen over relatively short time scales (sickle cell anemia).
6) What level of survival pressure, what change in external circumstances, would be "necessary" to restore the ability to create Vitamin C? (trick question on my part to lead ot further discussion)
That’s the coolest thing about science though - if we find a piece of evidence that cannot be explained by the present theories, we change the theories! That’s how Newtonian physics made way for relativity, for example.
You do realize that this contradicts your previous railings about the wondrous predictive capabilities of science, don't you? The classical physicists were certain they had everything nailed down just so, so far were they from predicting new things. (Cue Lord Kelvin's quote ""There is nothing new to be discovered in physics now, All that remains is more and more precise measurement.""
As for Intelligent Design: keep in mind that Windows ME *was* designed. You are not in a position (were there a designer) to know what constraints were imposed in time, cost, choice of materials, or pre-defined design limitations, on either organisms, or the Universe as a whole.
Cheers!
And [macro]evolution is based on fallacious reasoning and is not supported experimentally.