"In most animals, including apes, the surface of every cell, except brain cells, carry glycoproteins that contain one particular member of a family of sugar molecules called sialic acid. In humans, this sugar is not present in any cell other than red blood cells. Evolution decided to remove this [sugar] from humans and found a way for our chemistry to keep up with such a [dramatic] change? Insanity. " --micah1116
Firstly, there was no "decision" to remove anything—that isn't how biological change works. Secondly, arguing that humans never had the same sialic acid N-glycolylneuraminic acid (Neu5Gc) production observed in many other animals is an untenable position. This is for two reasons:
- The gene that encodes the enzyme—cytidine-5'-monophosphate-N-acetylneuraminic acid hydroxylase (CMAH)—to metabolize Neu5Ac into Neu5Gc has already been identified. In humans, this gene is a pseudogene, due to an inactivating frame-shift mutation caused by a 92-bp exon deletion when an AluSq was replaced with a human-specific sahAluY in our last common ancestor (Chou et al., 2002).
- Humans have high levels of a vast array of heterophile antibodies that detect Neu5Gc (Padler-Karavani et al., 2008).
As for the assertion that the loss of Neu5Gc production caused by the deactivation of CMAH gene would be so devastating that the hypothesis that such an event could be survived is "insanity;" that claim just doesn't hold up to scrutiny, in light of the research done on that very event:
The CMAH gene has been deactivated in mice, and the effects observed in vivo. The result was the same Nue5Ac accumulation present in humans, as well as the appearance of problems common in humans; diminished acoustic sensitivity and startle response threshold (relative to normal mice), hearing loss in old age, and skin healing delay in adulthood (Hedlund et al., 2007).
To recap, we know that humans have a wide range of anti-Neu5Gc antibodies, and once had a Nue5Gc synthesizing CMAH gene, but lost it due to a frame shift mutation. We also know that CMAH deactivation is observed to cause effects inherent to humans.
The idea that human Neu5Gc deficiency indicates separate creation is simply incorrect.
Chou, H. H., T. Hayakawa, S. Diaz, M. Krings, E. Indriati, M. Leakey, S. Paabo, Y. Satta, N. Takahata, and A. Varki. "Inactivation of CMP-N-acetylneuraminic acid hydroxylase occurred prior to brain expansion during human evolution." Proc Natl Acad Sci U S A. 99.18 (2002 Sep 3): 11736-41. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC129338/?tool=pubmed>.
Hedlund, M., P. Tangvoranuntakul, H. Takematsu, J. M. Long, G. D. Housley, Y. Kozutsumi, A. Suzuki, A. Wynshaw-Boris, A. F. Ryan, R. L. Gallo, N. Varki, and A. Varki. "N-glycolylneuraminic Acid Deficiency in Mice: Implications for Human Biology and Evolution." Mol Cell Biol 27.12 (2007 Jun): 4340-6. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1900035/?tool=pmcentrez>.
Padler-Karavani, V., H. Yu, H. Cao, H. Chokhawala, F. Karp, N. Varki, N. Varki, X. Chen, and A. Varki. "Diversity in Specificity, Abundance, and Composition of Anti-Neu5Gc Antibodies in Normal Humans: Potential Implications for Disease." Glycobiology 18.10 (2008 Oct): 818-30. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2586336/?tool=pmcentrez>.
(The phylogenetic tree was generated with the NCBI's BLAST program, using nucleotide sequences obtained from their Entrez Nucleotide database. The multiple sequence alignment was generated with the ClustalW2 program on the EMBL-EBI's website.)