
Two weeks ago, I
demonstrated to
Dr. Michael Egnor that his knowledge of early molecular genetics was severely flawed. He
responded yesterday, calling me a "pseudo-Darwinist" because those experiments involved, according to him, "designed" variation and "artificial" selection, not random "undesigned" variation and "natural" selection.
He is of course wrong about the experiments, but his rantings about pseudo-Darwinism bring up an interesting point: Egnor himself is a "pseudo-Darwinist", drawing an absolute dichotomy between natural and artificial selection when it suits him and blurring the two when it doesn't. Eugenics, according to Egnor, is both the "single incontrovertible Darwinian contribution to the field of medical genetics" (
3/28) and the "antithesis of Darwin's theory" (
4/9). But such rhetorical contradictions are what we have come to expect from creationists and ID activists.
For a more detailed trip to the woodshed you can read the following two posts.
My "
Backed into a Corner, Egnor Cannot Keep His Arguments Straight"
Orac's "
Irony meter about to explode. Must. Escape"
10 Comments
raven · 10 April 2007
raven · 10 April 2007
I put "evolution medical genetics" into the pubmed.gov NLM search box. Got 526 hits. One such abstract is below. Of course evolution has contributed to medical genetics. It is likely to do so more and more in the future with the human diversity project. Doesn't this clown read the scientific literature and know how to use a search engine and a library?
Hum Mutat. 2006 Jan;27(1):44-54. Links
Mutation, selection, and evolution of the Crohn disease susceptibility gene CARD15.King K, Sheikh MF, Cuthbert AP, Fisher SA, Onnie CM, Mirza MM, Pattni RC, Sanderson J, Forbes A, Mansfield J, Lewis CM, Roberts RG, Mathew CG.
Department of Medical and Molecular Genetics, Guy's, King's and St. Thomas' School of Medicine, King's College London, London, United Kingdom.
Three common mutations in the CARD15 (NOD2) gene are known to be associated with susceptibility to Crohn disease (CD), and genetic data suggest a gene dosage model with an increased risk of 2-4-fold in heterozygotes and 20-40-fold in homozygotes. However, the discovery of numerous rare variants of CARD15 indicates that some heterozygotes for the common mutations have a rare mutation on the other CARD15 allele, which would support a recessive model for CD. We addressed this issue by screening CARD15 for mutations in 100 CD patients who were heterozygous for one of the three common mutations. We also developed a strategy for evaluating potential disease susceptibility alleles (DSAs) that involves assessing the degree of evolutionary conservation of involved residues, predicted effects on protein structure and function, and genotyping in a large sample of cases and controls. The evolutionary analysis was aided by sequencing the entire coding region of CARD15 in three primates (chimp, gibbon, and tamarin) and aligning the human sequence with these and orthologs from other species. We found that 11 of the 100 CD patients screened had a second potential pathogenic mutation within the exonic and periexonic sequences examined. Assuming that there are no additional pathogenic mutations in noncoding regions, our study suggests that most carriers of the common DSAs are true heterozygotes, and supports previous evidence for a gene dosage model. Four novel nonsynonymous mutations were detected, one of which would produce premature termination of translation c.2686C>T (p.Arg896X). Two potential DSAs--c.2107C>T (p.Arg703Cys) and g.2238T>A (c.74-7T>A)--were significantly associated with CD in the case control sample. Analysis of the evolution of CARD15 revealed strong conservation of the encoded protein, with identity to the human sequence ranging from 99.1% in the chimp to 44.5% in fugu. Higher primates possess an open reading frame (ORF) upstream of the putative initiation site in other species that encodes a further 27 N-terminal amino acids, while four regions of high conservation are observed outside of the known domains of CARD15, indicative of additional residues of functional importance. The strategy developed here may have general application to the assessment of mutation pathogenicity and genetic models in other complex disorders. 2005 Wiley-Liss, Inc.
Jeffrey K McKee · 10 April 2007
raven · 10 April 2007
raven · 10 April 2007
David Stanton · 10 April 2007
Once again Egnor opens his mouth and ignorance comes out.
First, Darwin did not know the origin of the variation on which natural selection acts and that source is irrelevant. As long as there is variation that is not neutral in a given environment, selection will act. Historically, the source of that variation has been sexual reproduction and random mutations. If you increase the rate by using mutagens, the mutations are still random and will still be selected on. If you specifically genetically engineer an organism, then the variation is not random but it can still be selected on. Regardless, the principles first outlined by Darwin still apply.
Second, selection can be natural or artificial. In either case selection still acts. It still has predictable consequences and it still has limitations. This doesn't really change, no matter what the selection agent. Darwin knew all about artificial selection in pigeons. That is one of the lines of evidence he used in developing his hypothesis. It's still selection even if not "natural". By the way, sexual selection also works. I wonder when Egnor will get around to denigrating that.
Third, just because we can take the principles elucidated by Darwin and use them in "designed" and "artificial" ways, doesn't mean that there is anything wrong with the principles. In fact just the opposite is true. If the principles were unsound then they would not be useful. Atomic theory is not incorrect just because you can build a working atomic reactor. Calling it pseudo-Darwinism or whatever doesn't mean anything. As Reed correctly points out, Egnor isn't undermining anything but his own ignorant argument about eugenics.
Don't worry, I'm sure that realpc will be along any minute now to tell us what Egnor really meant. He didn't mean "designed" in the sense of nonrandom and he didn't mean artificial in the sense of not natural. Evolution doesn't violate the known laws of nature, only the unknown ones!
raven · 10 April 2007
What is this word pseudodarwinist, ism etc..? I've never heard of it before. Seems to me if one is going to make up words, they should define them. Pseudo means false or pretend. So, what is a pretend or false Darwinist?
I think he just made up some words to confuse the issue, bafflegab. PseudoDarwinism is evolution when you see it, know it exists, even know it is a serious problem in medicine and agriculture....but you don't believe in evolution.
Chris Noble · 10 April 2007
HAART (triple cocktail) is formulated to keep virus titers very low so there is less chance for mutations to drug resistance.
It explains the failure of monotherapy and why double therapy and triple therapy are better. It should be pointed out that the same pronciples are important for other diseases such as malaria. The current strategy for malaria is to uses arteminsin only in combination with other anti-malarials precisely in order to prevent arteminisin resistance developing.
Anton Mates · 10 April 2007
Henry J · 11 April 2007
Re "The result is not death to the unsuccessful competitor, but few or no offspring. Sexual selection is, therefore, less rigorous than natural selection."
Well, natural selection can operate when the only effect is fewer or no offspring, as well, rather than early death of the organism.
Henry