Intelligent Design, the best explanation of Origins

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Intelligent Design, the best explanation of Origins » Theory of evolution » Behe, the edge of evolution

Behe, the edge of evolution

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1 Behe, the edge of evolution on Tue Feb 13, 2018 2:40 pm

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Behe, the edge of evolution

Recall the example of sickle cell disease. The sickle cell mutation is both a life saver and a life destroyer. It fends off malaria, but can lead to sickle cell disease. However,hemoglobin C-Harlem has all the benefits of sickle, but none of its fatal drawbacks. So in western and central Africa, a population of humans that had normal hemoglobin would be worst off, a population that had half normal and half sickle would be better off, and a population that had half normal and half C-Harlem would be best of all. But if that’s the case, why bother with sickle hemoglobin? Why shouldn’t evolution just go from the worst to the best case directly? Why not just produce the C-Harlem mutation straightaway and avoid all the misery of sickle? The problem with going straight from normal hemoglobin to hemoglobin C-Harlem is that, rather than walking smoothly up the stairs, evolution would have to jump a step. C-Harlem differs from normal hemoglobin by two amino acids. In order to go straight from regular hemoglobin to C-Harlem, the right mutations would have to show up simultaneously in positions 6 and 73 of the beta chain of hemoglobin. Why is that so hard? Switching those two amino acids at the same time would be very difficult for the same reason that developing resistance to a cocktail of drugs is difficult for malaria—the odds against getting two needed steps at once are the multiple of the odds for each step happening on its own. What are those odds? Very low. The human genome is composed of over three billion nucleotides. Yet only a hundred million nucleotides seem to be critical, coding for proteins or necessary control features. The mutation rate in humans (and many other species) is around this same number; that is, approximately one in a hundred million nucleotides is changed in a baby compared to its parents (in other words, a total of about thirty changes per generation in the baby’s three-billion-nucleotide genome, one of which might be in coding or control regions). In order to get the sickle mutation, we can’t change just any nucleotide in human DNA; the change has to occur at exactly the right spot. So the probability that one of those mutations will be in the right place is one out of a hundred million. Put another way, only one out of every hundred million babies is born with a new mutation that gives it sickle hemoglobin. Over a hundred generations in a population of a million people, we would expect the mutation to occur once by chance. That’s within the range of what can be done by mutation/selection.

To get hemoglobin C-Harlem, in addition to the sickle mutation we have to get the other mutation in the beta chain, the one at position 73. The odds of getting the second mutation in exactly the right spot are again about one in a hundred million. So the odds of getting both mutations right, to give hemoglobin C Harlem in one generation in an individual whose parents have normal hemoglobin, are about a hundred million times a hundred million (10^16). On average, then, nature needs about that many babies in order to find just one that has the right double mutation. With a generation time of ten years and an average population size of a million people, on average it should take about a hundred billion years for that particular mutation to arise—more than the age of the universe. 

Hemoglobin C-Harlem would be advantageous if it were widespread in Africa, but it isn’t. It was discovered in a single family in the United States, where it doesn’t offer any protection against malaria for the simple reason that malaria has been eradicated in North America. Natural selection, therefore, may not select the mutation, and it may easily disappear by happenstance if the members of the family don’t have children, or if the family’s children don’t inherit a copy of the C-Harlem gene. It’s well known to evolutionary biologists that the majority even of helpful mutations are lost by chance before they get an opportunity to spread in the population. If that happens with C-Harlem, we may have to wait for another hundred million carriers of the sickle gene to be born before another new C-Harlem mutation arises.

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