Why you should stop believing in evolution

My apologies for the delay in responding, we've had security software hang-ups that were blocking this post and it took a while to find the specific problem and resolve it. Here it finally is:

Arlen, you are passing judgement upon things of which you have no knowledge. Evolution is taught as a stand-alone class, as is genetics, in college. Once you get to graduate school, it gets more intensely interwoven, and I can assure you that I have had both levels of education, and done primary research directly dealing with genetics.

Here are a couple of my scientific publications, if you'd like verification:
Fine Mapping of an Amyotrophic Lateral Sclerosis Modifier Locus to a Single BAC

Mutations in the Cu/Zn superoxide dismutase (SOD1) gene are responsible for 15-20% of familial amyotrophic lateral sclerosis (FALS) cases. Severity of the ALS phenotype is dependent on genetic background for mice carrying the mG86R SOD1 transgene. A BAC (149m19) containing several candidate genes (Serf, Smn, Naip2 and Naip5) and derived from 129Sv genomic DNA was used to investigate whether these genes partially rescue the mG86R SOD1 (FVB/NJ) ALS phenotype by delaying ALS onset. Two single-insertion BAC lines were produced and both mRNA and protein for BAC genes were shown to be elevated. Mice heterozygous for mG86R SOD1 and BAC149m19 in the FVB/NJ background were shown to have significantly delayed ALS onset compared to mG86R SOD1 controls. BAC 149m19 did not significantly delay ALS onset for mice carrying the human G93A SOD1 mutation in the FVB/NJ background. Delayed ALS onset for BAC/mG86R mice was not due to reduced SOD1 expression. Overexpression of one or more of the BAC genes appears to be linked to the severity of ALS phenotype in mice, but in a mutation specific manner.

The Genomic Organization of the Gene Encoding the Vanilloid Receptor: Evidence for Multiple Splice Variants

Characterization of the genomic structure encoding the 5′ portion of rat Vr1 confirmed that VR.5′sv is derived from the VR gene; however, SIC seemed to be derived from two related but independent genes. We also deduced the genomic organization of the human gene VR1. Comparative studies of rat and human VR genes showed substantial conservation in genomic organization. The splice site flanking exon–intron 7 in rat and human VR1 diverged from the expected consensus sequence; this may help to explain the skipping of exon 7 within VR.5′sv and other VR splice variants.

Now, on to the definition of mutation . Sorry, but a "principle" of mutation is not that it must be harmful. A mutation is merely a sequence alteration - it can be beneficial, neutral/cause no change, or harmful.

Definition: Any alteration in a gene from its natural state; may be disease causing or a benign, normal variant.
A mutation is a change in a DNA sequence. Mutations can result from DNA copying mistakes made during cell division, exposure to ionizing radiation, exposure to chemicals called mutagens, or infection by viruses. Germ line mutations occur in the eggs and sperm and can be passed on to offspring, while somatic mutations occur in body cells and are not passed on.

And sorry, but Punctuated equilibrium does not "get around" Darwin's idea of accumulated change, nor does it have anything to do with "inbreeding". It says that change does not occur in a smooth, even pace, rather it can happen in "spurts" followed by periods of little change. It does not preclude gradual change occurring during "stasis" periods. For more on the subject, read Stephen Jay Gould's books - he's one of the scientists who came up with the idea and was its most vocal proponent. Brilliant man, egotistical and arrogant as all get out, but brilliant.