Hans Blaster
On August Recess
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If you are going to argue that humans and chimpanzees evolved from a common ancestor, then some type of adaptive mutations must have occurred because humans have much greater reproductive fitness than chimps (7 billion humans today vs about 300,000 chimps). What gave humans the reproductive advantage over chimps. If you believe it is explained by genetics, what mutations give humans this marked reproductive advantage.
The best-measured examples in controlled experiments are of course the Kishony and Lenski experiments, you know, the experiments you can't explain. Then there is the combination therapy for the treatment of HIV and all the measured clinical success in suppressing the adaptive evolution of this virus. Then there are the many examples of the successful use of combination herbicides, pesticides/insecticides in suppressing the evolution of adaptive evolution. Don't forget the use of combination therapy for the treatment of cancer, something that will probably be necessary for the successful use of targeted cancer therapy. Now, find a real, measurable, and repeatable example of adaptive evolution that doesn't work the way math I've presented. You won't.Well if you don't like that one, what are the five examples you find so valuable?
The best-measured examples in controlled experiments are of course the Kishony and Lenski experiments, you know, the experiments you can't explain. Then there is the combination therapy for the treatment of HIV and all the measured clinical success in suppressing the adaptive evolution of this virus. Then there are the many examples of the successful use of combination herbicides, pesticides/insecticides in suppressing the evolution of adaptive evolution. Don't forget the use of combination therapy for the treatment of cancer, something that will probably be necessary for the successful use of targeted cancer therapy. Now, find a real, measurable, and repeatable example of adaptive evolution that doesn't work the way math I've presented. You won't.
You must have missed Edward Tatum's 1958 Nobel laureate lecture:When are you, your basic argument was shot down 50 years ago.
You really need to expand your reading list beyond your so-called "on topic" journals. It was Edward Tatum's observation that made me aware of the effect of the multiplication rule on adaptive evolution. And that was more than 50 years ago.In microbiology the roles of mutation and selection in evolution are coming to be better understood through the use of bacterial cultures of mutant strains. In more immediately practical ways, mutation has proven of primary importance in the improvement of yields of important antibiotics – such as in the classic example of penicillin, the yield of which has gone up from around 40 units per ml of culture shortly after its discovery by Fleming to approximately 4,000, as the result of a long series of successive experimentally produced mutational steps. On the other side of the coin, the mutational origin of antibiotic-resistant micro-organisms is of definite medical significance. The therapeutic use of massive doses of antibiotics to reduce the numbers of bacteria which by mutation could develop resistance, is a direct consequence of the application of genetic concepts. Similarly, so is the increasing use of combined antibiotic therapy, resistance to both of which would require the simultaneous mutation of two independent characters.
It is still not clear to me. Which came first, lactase persisters or those who can't produce lactase as adults.No, I think the *ability* to metabolize lactose in adulthood is a potential improvement. It gives me access to more food sources, and did so for my ancestors for many generations. Did it allow them to survive to reproductive age better? Probably. One thing I do know about my ancestors is that all of them lived long enough to reproduce.
What question? Detrimental mutations occur and someone who is a lactase persister can have an offspring with a mutation that prevents them from being a lactase persister. Is this your idea of adaptive evolution?Dodging the question, again?
More ducking and dodging. You already admitted that you only have an ad hoc explanation, though you do not know it. And those are worthless in the world of science.Do you speak chimpanzee? Perhaps they can explain to you how DNA adaptive microevolution works.
Would you like to explain the microevolution of lactase persistence? Let us see how your explanation lines up with evidence.It is still not clear to me. Which came first, lactase persisters or those who can't produce lactase as adults.
All the mathematical and empirical evidence gives that there were about 1 billion humans that lived before 10,000 years ago. From 10,000 years to today, about 99 billion people of which about 7 billion are alive today. That's the population size you have to work with to give a lineage that accumulates a set of adaptive mutations. If you believe that humans and chimpanzees evolve from a common ancestor, what mutations could account for the difference? Why can humans do industrial agriculture, build aircraft, make computers,... and chimps cannot? What mutations account for this?None of these are in humans. The question was about adaptive mutations in humans.
Don't forget, I have the mathematical and empirical evidence. Of course, you don't understand the math.More ducking and dodging. You already admitted that you only have an ad hoc explanation, though you do not know it. And those are worthless in the world of science.
No Alan, you don't, as I tried to explain to you the reason nobody takes your math seriously is that it does not extrapolate from the very limited circumstances that you used to generate it. It is not us that does not recognize the dangers of extrapolation.Don't forget, I have the mathematical and empirical evidence. Of course, you don't understand the math.
That's not difficult, if individuals have the genetics for lactase persistence, they will pass on those genes to their offspring with a probability of mutations in that gene equal to the mutation rate for a single replication. If there are a billion replications and the mutation rate is 1e-9, there will be on average one individual in that population with a mutation in one site in that gene. If there are 500 bases in that gene, there will be on average 500 individuals in that population of a billion with a mutation in one of the sites in that gene. Now, if you apply Edward Tatum's principle and compute the probability that one of those 500 individuals also gets a sickle cell trait mutation, you have to use the multiplication rule.Would you like to explain the microevolution of lactase persistence? Let us see how your explanation lines up with evidence.
I'm not doing extrapolation, if I were, you could post an empirical example that contradicts this math, you don't.No Alan, you don't, as I tried to explain to you the reason nobody takes your math seriously is that it does not extrapolate from the very limited circumstances that you used to generate it. It is not us that does not recognize the dangers of extrapolation.
How old is the earth? How long have humans been living in Africa vs Europe? Is it possible that these genes could evolve separately and recombine later or do you still think they must me multiplicative. Are you a homeschooled virgin?That's not difficult, if individuals have the genetics for lactase persistence, they will pass on those genes to their offspring with a probability of mutations in that gene equal to the mutation rate for a single replication. If there are a billion replications and the mutation rate is 1e-9, there will be on average one individual in that population with a mutation in one site in that gene. If there are 500 bases in that gene, there will be on average 500 individuals in that population of a billion with a mutation in one of the sites in that gene. Now, if you apply Edward Tatum's principle and compute the probability that one of those 500 individuals also gets a sickle cell trait mutation, you have to use the multiplication rule.
That's not difficult, if individuals have the genetics for lactase persistence, they will pass on those genes to their offspring with a probability of mutations in that gene equal to the mutation rate for a single replication. If there are a billion replications and the mutation rate is 1e-9, there will be on average one individual in that population with a mutation in one site in that gene. If there are 500 bases in that gene, there will be on average 500 individuals in that population of a billion with a mutation in one of the sites in that gene. Now, if you apply Edward Tatum's principle and compute the probability that one of those 500 individuals also gets a sickle cell trait mutation, you have to use the multiplication rule.
I'll leave the speculation to the believers in macroevolution. I'll stick with real, measurable, and repeatable experimental evidence. The evolution of drug resistance is too important a topic to be left to speculators.How old is the earth? How long have humans been living in Africa vs Europe? Is it possible that these genes could evolve separately and recombine later or do you still think they must me multiplicative. Are you a homeschooled virgin?
Do you think that the joint probability of those mutations being on an individual is not computed using the multiplication rule?Do you know *where* lactase persistence and the sickle cell trait are found? (Hint: It's not the same place.) Why should we multiply the probabilities of those traits if the are established in different populations?
Do you think that the joint probability of those mutations being on an individual is not computed using the multiplication rule?
Do you think that the joint probability of those mutations being on an individual is not computed using the multiplication rule?
If they are particular mutations, yes, the multiplication rule must be used.If joint probability is the appropriate concept, of course, but have you shown that it is appropriate here?
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