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Biologist Paul Ewald Says Genes, Not Germs, Cause Most Killer Diseases by Steve Sailer UPI, December 2, 2000 |
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Not genes but germs cause most chronic diseases. So argues respected evolutionary biologist Paul W. Ewald in his new book, Plague Time: How Stealth Infections Cause Cancers, Heart Disease, and Other Deadly Ailments,"(Free Press, 282 pp, $25.00). The Amherst professor is attempting to drag the medical establishment into the Darwinian age. Although it's trendy today to blame most major long-term diseases on inheriting bad genes, Ewald contends that today's "Human Genome Mania" often violates the fundamental principle of biology, Darwin's Theory of Natural Selection. Darwin argued that families with harmful hereditary traits will die out over time. They would be replaced by lineages whose hereditary constitution better enables them to survive and reproduce. Although Ewald is attempting to revolutionize the practice of medicine, he has made sure that lay readers will find his book interesting and intelligible. He believes that patients are often more open-minded than their doctors. In an interview, Ewald claimed that the health benefits of the Human Genome Project are over hyped because "Most diseases aren't genetic." He claimed that spending on improving antibiotics would bring greater payoffs than spending on the glamour field of genetic research. Ewald, who is not a medical doctor, said, "My goal is to bring into medicine all of biology, especially evolution." So far, he has had more success persuading other biologists than the medical establishment. The late William D. Hamilton of Oxford, who is considered by Edward O. Wilson and Richard Dawkins to be the most important evolutionary thinker of recent decades, commented on Ewald's theory, "It opens our eyes to many quite weird possibilities about disease that most medical scientists, tending to be unaware of current evolutionary thought, don't think of." Ewald contended that there are only three fundamental causes of disease. First, he noted, there are nonliving environmental agents like radiation, poisons, and nutrition. Too many cigarettes cause lung cancer; too little Vitamin D causes rickets. In the early days of the environmental health movement, scientists quickly identified extremely dangerous chemicals like mercury, lead, DDT, and tobacco tar. This important process appears to have run into somewhat diminishing returns lately, as researchers now argue endlessly over whether ambiguous substances like coffee are bad for you. Second, Ewald continued, there are infections. Long ago, people figured out that smallpox, measles, and chicken pox passed from one person to another. Since then, an ever-growing number of diseases have been shown to be induced by bacteria, viruses, or protozoa. For example, in the early Eighties, to prove that the H. pylori bacteria caused stomach ulcers, researcher Barry Marshall drank a test tube full of the germs. Just as he had predicted, he developed gastritis. Then, he cured himself with an antibiotic. Even this dramatic stunt did not grab the attention of doctors, however. The medical profession cured few peptic ulcers until patients who had read an accurate 1990 National Enquirer article entitled "Breakthrough Pill Cures Ulcers" began demanding antibiotics from their doctors. Historically, infectious agents have been harder to identify than nonliving poisons as the cause of diseases because germs can evolve ways to hide. Simple chemicals cannot. Third, and trendiest, there are hereditary causes. The Human Genome Project has been widely advertised as eventually leading to cures for many diseases, such as breast cancer. Ewald observed, though, "If one identical twin gets breast cancer, the other's likelihood of contracting it is only around 10% to 20%. This suggests that genes are not the whole story." But there's a more basic logical problem with Human Genome Mania, argued Ewald. According to Charles Darwin's Theory of Natural Selection, Ewald said, "A disease-causing gene that reduces survival and reproduction would normally eliminate itself over a number of generations." This reasoning was forcefully introduced to Ewald in the early Nineties by a letter from a physicist named Gregory M. Cochran. After America won the Cold War, this New Mexico rocket scientist had turned to developing formulas for estimating which diseases are hereditary and which are infectious. The key number proved to be the ailment's "reproductive fitness burden." In other words: Compared to a healthy person, how many fewer descendents will a sufferer procreate? The tendency of people with healthy genes to reproduce more than people with sick genes, Cochran and Ewald determined, makes it unlikely that there are many hereditary syndromes that are both widespread and significantly damaging to their victims ability to reproduce successfully. But, you might wonder, can evolution work fast enough to get rid of bad genes? According to standard genetic math, yes, it can. If you have a genetic flaw that reduces your expected number of surviving children by just 1%, that bad gene will likely kill itself off within a few thousand years. And the human genetic code has been around much longer than that. Further, if the natural tendency of bad genes is to die out, Ewald asked, "How would the killer genes spread widely in the first place?" We can evolve new defenses against both bad genes and bad germs. What makes infections more dangerous than genes, however, is that germs can fight back. They can counter our new resistance strategies by evolving news methods of attack against us. As a close analogy, consider one of our artificial defenses, penicillin. It is less effective today than in 1950 because today's germs tend to be descended from the germs that had the right stuff for surviving onslaughts of penicillin. Most diseases that are both widespread and nasty, like AIDS, malaria, and syphilis have already been identified as infectious. Yet, suspicions have only recently turned toward infections as the origin of some of the most devastating chronic diseases, such as atherosclerosis (heart disease) and breast cancer. Ewald admitted, though, that there are numerous hereditary diseases. Yet, the ones produced by spontaneous mutations tend to be quite rare since the bad genes quickly get weeded out of the gene pool. Duchenne's muscular dystrophy may be the most widespread example of a spontaneous mutation. It only afflicts 0.02% of the populous. Still, it's possible for more common hereditary diseases to survive down through the generations if they are a defense against something worse, such as an infectious disease. The best-known example is sickle-cell anemia. This severely sickens a few percent of all children of West African descent. The sickle-cell gene is an awkward defense that evolved, possibly only recently according to biologist Chris Wills of U.C. San Diego, to help the lucky possessors of one copy of the gene survive the brutal falciparum malaria. Children who inherit two sickle-cell copies, however, tend to die young, unless they get modern medical care. A spokesman for the National Human Genome Research Institute responded diplomatically to Ewald's charges that research dollars invested in genetic research would save more lives if devoted to infectious diseases instead. He suggested, "This shouldn't be a zero sum fight. As promising new areas come along, the government should spend more on health research in general." The spokesman also argued that when the Human Genome Project eventually maps the variations found among a large number of individuals, it will help us understand why some people have better resistance to particular germs. For example, he said, there are certain East African prostitutes who appear to be immune to HIV. Understanding their genetic peculiarities might well help us fight this horrendous infectious disease. Nonetheless, Ewald's "Plague Time" may someday be remembered as a landmark in the development of more effective treatments for killer diseases. Steve Sailer (www.iSteve.com) is a columnist for VDARE.com and the film critic for The American Conservative.
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