The department faculty, then, are unequivocal in their support of evolutionary theory, which has its roots in the seminal work of Charles Darwin and has been supported by findings accumulated over 140 years. The sole dissenter from this position, Prof. Michael Behe, is a well-known proponent of "intelligent design." While we respect Prof. Behe's right to express his views, they are his alone and are in no way endorsed by the department. It is our collective position that intelligent design has no basis in science, has not been tested experimentally, and should not be regarded as scientific.
For those joining in, Intelligent design, or ID, is a modern form of creationism built up to circumvent the teaching of religious views in the science classroom. Included in its dogmas are ludicrous ideas that the Earth is about ten thousand years old. Because explicit references to God got them into trouble the first time around, God has been replaced with a savvy sounding "intelligent designer." They also say that some features of life are too complex to have evolved, and so required intelligent designer based intervention.
Salvador Dali, Hommage a Newton, Bronze with brown and green patina, 1969, 52" high
Evolution like we all know takes place though natural selection, genetic drift and random variations of genets generated by mutation. Mutations in the DNA sequence that make up the genome results in an alteration of the protein sequence, expression, and/or function. When protein sequences are altered either in response tot he environment or randomly, certain combinations of mutations interact symbiotically with the environment to give the organism undergoing the mutation a significant advantage helping it to adapt better to a changed circumstance. Very briefly that is the essence of evolution.
It is the last aspect with which Mr. Behe has the biggest problem with... Mutations. Behe tries to claim that random mutations cannot possibly be the building blocks of evolution. The cornerstone of his argument involves malaria, in particular the evolution of humans to resist infection by malaria, and the evolution of the malaria parasite itself to counteract the evolution of human resistance and the development of anti-malarial drugs.
Norman Rockwell, Returning From Camp, 1940, Oil on Canvas, 38" X 30"
I quoted the following from the New Republic as they have done a superb job of explaining malaria, mutations and natural selection.
Malaria actually provides a superb example of natural selection, and its story has some intriguing quirks. The disease is caused by a protozoan carried by mosquitoes, who act as flying syringes that inject the microbe into the human bloodstream. There it takes up residence in the liver and then in the red blood cells, multiplies prolifically, and can ultimately cause anemia, kidney failure, hemorrhage, and death. Residence in red blood cells and the liver is adaptive for the parasites, because in those spots they are hidden from the immune system that usually destroys invading microbes. Yet the human spleen can also detect and destroy circulating parasite-laden cells. To counter this tactic, the malaria parasite secretes proteins that cause its carrier blood cells to stick to the walls of blood vessels, avoiding the spleen (this sticking is what causes hemorrhage).
Here, then, is an arms race between a blood-loving parasite and a human body seeking to destroy it. Yet the story is even more complicated and interesting. In sub-Saharan Africa, where malaria is rampant, a mutation has arisen in the gene producing hemoglobin that helps ward off malaria. The striking thing about this mutation, known as the sickle-cell mutation, is that it somehow reduces the chances of contracting malaria when its carriers have one copy of the gene (like most organisms, we have two copies of every gene, one on each of our two sets of chromosomes), but it causes sickle-cell anemia when the carriers have two copies. In sickle-cell anemia, the red blood cells form clumps because of the altered hemoglobin they carry, causing a syndrome of complications that invariably cause death before adulthood.
Thus we have the unusual situation in which heterozygotes, or individuals carrying both one "normal" and one "mutant" hemoglobin gene, are fitter than homozygous individuals, who carry either two "normal" genes (more susceptible to malaria) or two mutant genes (death from sickle-cell anemia). Evolutionary genetics tells us that in a case such as this one, both forms of the gene will remain in the population, ensuring some protection against malaria but also the continuing production of babies with sickle-cell anemia. Africans would be better off if everyone were a heterozygote, but that is impossible, because the two gene copies separate at reproduction and unite with other copies, necessarily producing some deleterious homozygotes.
This example above goes to show that natural selection is not the best alternative sometimes and it works with whatever mutations arise to create the best possible situation given the available raw material and the constraints of genetics. In addition, though the malaria parasite has been unable to evolve resistance to heterozygotes for the sickle-cell gene, it has through mutation, evolved resistance to various anti-malarial drugs devised by us (as is clearly documented).
According to Behe, malaria shows that random mutation is insufficient to explain biological complexity. He disparages the defensive sickle-cell mutation and similar mutations, saying that they "are quintessentially hurtful mutations because they diminish the functioning of the human body" (does successfully resisting malaria really diminish the function of our body?) and that they are "not in the process of joining to build a complex, interactive biochemical system." And although the parasite and the humans are in the process of trying to outwit each other in an evolutionary arms race (including the development of drugs), Behe notes that this arms race has not prompted the evolution of biological complexity. Instead Behe sees the malaria/parasite battle as a mere "trench war of attrition."
August Strindberg, Flower of the Moor, 1901, Oil on Paper, 18" X 11"
When someone can write a book and refer to evolutionary changes as 'trench warfare' and accuse mutations of causing 'broken genes', I would just aver to say that this person is simply telling lies and at a broader level engaging in sophisticated trickery towards the readers of his book.
I hope the booksellers see through this sophistry and re-classify the book as fiction.
2 comments:
The malaria gene "stuff" is really fascinating. As for Behe, his rhetoric unfortunately fits right in with the predominant agenda of today which is to conquer and divide...turn everything into a war. It's so infuriating and tragic.
Hopefully blogs can help spread the fact that Behe's work is a work of fiction.
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