Talk:Skepticism about science

OK, for this to fly we need to research and footnote my wild assertion in paragraph 3 human be in 00:53, 6 September 2007 (CDT)
 * Well, there's | this, but I'm not sure if it's quite what you are looking for. I think the development of the flagellum will remain hypothetical, at least for a while.  I'm pretty sure most of the development happened without being fossilized, and is not recurring for the same reason we don't see new "versions" of DNA/RNA occuring.  I suppose I could be wrong about that, though, and would be very interested to find out I am. -Smyth 12:00, 25 September 2007 (EDT)
 * To be honest I've never even understood what BEhe was trying to get at with his malaria Guff. But this looks good as a rebuttal: | rebuttal.  Hey that's weired it doesn't' come up now.  I've copied it below as I had the tab open.  Feel free to zap it.--Bob's your uncle 12:58, 25 September 2007 (EDT)

In a series of rather disconnected and scientifically dubious arguments, Behe tries to claim that random mutations cannot possibly be the building blocks of evolution. His main 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.

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). advertisement

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 shows that natural selection does not necessarily produce absolute perfection; it works with whatever mutations arise to create the best possible situation given the available raw material and the constraints of genetics. And finally, although the malaria parasite has been unable to counter-evolve resistance to heterozygotes for the sickle-cell gene, it has evolved, through mutation, resistance to various anti-malarial drugs devised by humans. This resistance has become so strong that some strains of malaria are completely resistant to drugs--yet another example of successful natural selection.

Malaria, then, shows evolution acting on a number of levels. So how can it disprove Darwinian evolution? 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."

In the end, after pages of rather tedious detail about malaria, Behe dismisses the evolutionary aspects of malaria as "chaotic and tangled," which, while showing random mutation and natural selection, are irrelevant to his main concerns: "In this book we are concerned with how machinery [i.e., complex organisms] can be built," he writes. "To build a complex machine many different pieces have to be brought together and fitted to one another." Behe buttresses his conclusion by describing how the AIDS virus evolved to outwit not only the strategies of the human immune system but also powerful anti-viral drugs. Again he sees little evolution of complexity: "HIV has killed millions of people, fended off the human immune system, and become resistant to whatever drug humanity could throw at it. Yet through all that, there have been no significant basic biochemical changes in the virus at all."

In light of evolutionary theory, these conclusions are truly bizarre. No sane evolutionist has ever claimed that an adaptation of a parasite to a host will produce complex biochemical changes. Evolutionary theory predicts only that parasites will adapt, not how they will adapt. In fact, both the malaria parasite and the HIV virus have undergone sufficient "biochemical change" to make them almost completely adapted to withstand both human drugs and the immune system. And humans have, through the sickle-cell mutation and other changes in hemoglobin, become somewhat resistant to malaria. Beyond that, what does Behe expect? A red blood cell with hands to throttle the parasite? A malaria parasite with a cunning brain to outwit the sickle-cell protein? HIV and malaria are doing pretty well at reproducing themselves--sans new complex systems--in their present environments. That is all evolution can do.

So what if the malaria parasite has not completely outwitted the sickle-cell mutation? No biologist, least among them Darwin, ever claimed that adaptation is always perfect. Every infection by a parasite, every disease, and every species that goes extinct represents a failure to adapt. Sometimes the right mutations do not arise or cannot arise because of the constraints of development; sometimes they do arise, but produce an imperfect adaptation. In his book The Causes of Evolution, the British biologist J.B.S. Haldane addressed this problem with tongue in cheek: "A selector of sufficient knowledge and power might perhaps obtain from the genes at present available in the human species a race combining an average intellect equal to that of Shakespeare with the stature of Carnera. But he could not produce a race of angels. For the moral character or for the wings, he would have to await or produce suitable mutations."

By disparaging the malaria system as mere "trench warfare" and characterizing the mutations involved as "not constructive" and causing "broken genes," Behe not only engages in sophistry, but shows an almost willful misunderstanding of Darwinism. Natural selection is not a one-way path to more complex adaptations or organisms. Organisms adapt to whatever environmental challenges they face, and those changes could require either small biochemical adjustments (as in the case of malaria), more extensive changes that require complex adaptation (as in the evolution of amphibians from fish), or even the evolution of less complexity. The tapeworm, for example, is considerably simpler than its ancestor: it has lost its nervous system, its digestive system, and most of its reproductive system, becoming in effect an absorptive sack of gonads. But it is nevertheless well adapted to its novel intestinal niche, where it can dispense with unnecessary features (its food, for one thing, is pre-digested). Using malaria and HIV to argue that random mutations cannot fuel the evolution of complexity is like displaying a crudely built footstool to prove that it is impossible to build a house with lumber, hammer, and nails.

IV.

The general reader, at whom The Edge of Evolution is aimed, is unlikely to find the scientific holes in its arguments. Behe writes clearly and engagingly, and someone lacking formal training in biochemistry and evolutionary biology may be easily snowed by his rhetoric. The snow falls most heavily when Behe writes about the complex biochemical adaptations of animals, such as the structure and the operation of cilia. Cilia are small, hairlike structures whose rhythmic beating propels microorganisms; they also help move things along in other species (cilia line the fallopian tubes of mammals, for example, where they sweep the egg into the uterus). Each cilium is built from more than two hundred different proteins, including those making up its structure and "motor proteins" that make it move. Moreover, when a cilium is damaged or a new one is built, an equally complex system of intraflagellar transport uses sixteen other proteins to bring new material from out of the cell for repair, rather like a molecular assembly line.

This description is entertaining and instructive, and those unacquainted with molecular biology will be wowed by the elegance of this adaptation. Indeed, such complex features were what lured many of us into biology, hoping to explain their evolution. But the purpose of Behe's exercise, beyond pedagogy, is simply to overwhelm the reader with nature's complexity, hoping to raise the question of how mutation and natural selection could possibly have built such a feature--as if being wowed were the same as being persuaded. As Behe says, "The point is to see how elegant and interdependent the coherent system is--to see how different it is from the broken genes and desperate measures that random mutation routinely involves." ("Broken genes and desperate measures" refers to the simple adaptations of the malaria parasite and its human opponent.) Surely, says Behe, a better theory is that cilia were created by the Intelligent Designer.

In Darwin's Black Box, Behe made exactly the same argument to show that a similar structure, the flagellum (a larger cilium that propels microorganisms), could not have evolved by natural selection. But in this case Behe's claim that no intermediate stages could have existed was refuted. Ken Miller, a biologist at Brown University (and an observant Catholic), showed how flagella and cilia could have had their precursors in mechanisms that the cell uses to transport proteins, mechanisms that are co-opted to construct flagella. Indeed, the whole problem of the evolution of cilia was argued before Judge Jones in Harrisburg, who ruled that there was no convincing evidence that evolution could not have produced this structure, making legal doctrine from something biologists already knew. In his new book, however, Behe simply ignores his critics, repeating his bankrupt claim that there is "no Darwinian explanation for the step-by-step origin of the cilium."

If ID were science, we could make an equivalent demand of its advocates. We could ask Behe to produce a complete step-by-step accounting of what God (sorry, the Intelligent Designer) did when He designed the cilia. And of course Behe would not be able to do that--nor does he even try. IDers never produce their own "scientific" explanation of life. They just carp about evolution. And as evolutionists explain one thing after another, IDers simply ignore these successes and move on to the ever-dwindling set of unsolved problems in which they continue to see the hand of God.

Behe's arguments from the gaps in scientific knowledge are fatuous. It is certainly true that we do not yet understand every step in the origin of the cilium, but these are early days. Molecular biology is a very young field, and molecular evolutionary biology is even younger. The way to understand the evolution of cilia is to get to work in the laboratory, not to throw up our hands and cry "design." Perhaps we will never understand every step in the evolution of a complex feature, just as we cannot know everything about the development of human civilization from archaeology. But is the incompleteness of our knowledge a reason to invoke God? The history of science shows us that patching the gaps in our knowledge with miracles creates a path that leads only to perpetual ignorance.


 * Sounds like his typical crap: It's too complicated for me to understand it, therefore it's beyond the ability of science to explain it and we must bring in supernatural entities. The strangest thing about his arguements, to me, is that they always seem like fairly clear examples that argue in favor of evolution.  Maybe if his arguements weren't so anecdotal. -Smyth 13:19, 25 September 2007 (EDT)

Hmmm....
We might want to rethink this article. Skepticism about science is a legit thing. (Think cold fusion or arsenic-based life forms.) I think this is referring to JAQing off or skepticism to create doubt (there is controversy about global warming....). sterilesporadic heavy hitter 15:20, 4 September 2012 (UTC)