Darwin got some very important points correct but was wrong on other important points about evolution. Experimental evidence shows that Darwin was correct about biological competition and descent with modification but incorrect about universal common descent. Should Darwin’s ideas be tossed out because he was wrong about universal common descent when his other ideas explain how drug resistance evolves?
Hello Alan, welcome to the forum.
Modern evolutionary studies incorporate much of Darwin’s ideas, especially fitness effects on differential reproduction, but the current theory is much more comprehensive. Common descent is accepted by the scientific consensus, and is strongly supported by many lines of evidence, so that could be considered a validation of Darwin’s work.
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Hum. I read people state all the time on YEC sites about how Darwin was wrong, usually referencing things they grossly distort and are actually not correct themselves. He certainly missed the mark on some things, but usually those things represent the state of knowledge at the time of how things worked. And he did not appreciate factors other than natural selection that are in play, again do the limited knowledge of the time. But, I don’t think universal common descent was one of them. Any support for that statement?
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Hi Ron,
Many of Darwin’s ideas should be incorporated into evolutionary theory because they correctly describe what is observed empirically and experimentally. They explain how drug resistance evolves. But universal common descent is not experimentally verified, in fact, it is contradicted. Two important biological evolutionary experiments, the Kishony Mega-Plate experiment, and the Lenski Long Term evolution experiment contradict universal common descent. This is due to the laws of physics and how they apply to biological competition and descent with modification operate. It takes huge populations for descent with modification and adaptation to occur. Humans and chimpanzees have never had population sizes anywhere near necessary for these two species to come from a common ancestor.
Hi Phil,
I’m not arguing about YEC, that is not my area of study. I’m writing about the physics and mathematics of biological evolution and why this physics shows that universal common descent is not possible, no matter how much time you give. It is all about the size of the population needed for descent with modification and adaptation to operate. Humans and chimpanzees don’t have the population size for natural selection to operate for any more than a handful of adaptive mutations.
Even with smaller populations, modification and adaptation is not only possible, but inevitable. The variety of lemurs on the constrained island of Madagascar, which most creationists insist represent a single kind, is one of innumerable examples.
This paper Variation in the molecular clock of primates utilizes molecular clock data and reasonable population sizes to place the human - chimpanzee split within accepted anthropological timelines. There are large uncertainties associated with molecular clocks, but all within the framework of evolutionary time.
With these considerations in mind, we reestimate the divergence and split times of humans, chimpanzees, and gorillas, using substitution rates estimated only at CpG transitions. Assuming the per year mutation rate for CpG transitions obtained in ref. 10 (SI Appendix, Note S1), we estimate that humans diverged from chimpanzees ∼12.1 Mya and from gorillas ∼15.1 Mya (Fig. 4). Assuming further that the effective population size of the human–ape ancestor was five times the current population size (as estimated by refs. 43, 44), the human–chimpanzee split time is ∼7.9 Mya, and the human–gorilla split time is 10.8 Mya. We note that there is substantial uncertainty in estimates of ancestral population size of apes, with previous estimates ranging between 50,000 and 100,000 (43–45). Accounting for this uncertainty provides estimates of human–chimpanzee split time in the range of 6.5–9.3 Mya, and human–gorilla split time in the range of 9.4–12.2 Mya. Reassuringly, these estimates are similar to those obtained by explicitly modeling the dependence of replicative mutations on life history traits in hominines (33). Moreover, they are in broad agreement with evidence from the fossil record, which suggests a human–chimpanzee split time of 6–10 Mya and a human–gorilla split time of 7–12 Mya (46–51). Thus, within hominines, there is no obvious discrepancy between phylogenetic and pedigree-based estimates of mutation rates, once the effect of life history traits on mutation rates is taken into account (33).
It takes huge populations for descent with modification and adaptation to occur.
Ron, that is not what the experimental evidence shows. Experiments such as the Kishony and Lenski experiments show why. These experiments show that natural selection takes about a billion replications for each adaptive mutation to a single selection pressure. The reason why is that the mutation and selection problem is a variation of a binomial probability problem where the mutation is the random trial and the possible outcomes for that trial are a mutation occurs or a mutation does not occur. The probability of a mutation occurring is given by the mutation rate and for those experiments, the mutation rate is about 1E-9. The mean value for this binomial probability problem is 1/(mutation rate), the probability of success in a single trial. These experiments are demonstrating evolution to a single selection pressure. The probability becomes exponentially lower when evolution must occur to multiple simultaneous selection pressures. A good empirical example of this is the successful use of 3-drug therapy for the treatment of HIV even though the virus can evolve resistance to a single drug very quickly. Do you understand why?
Humans and chimpanzees have not achieved the population sizes necessary to evolve from a common ancestor even if you want to assume this evolutionary process only involved a single selection pressure.
Sure it does. Pedigree mutation rates in Primates, most especially in humans, have been measured.
While I disagree with your assessment of Kishony and Lenski, I have no interest in discussing the applicability of prokaryote evolution when there is more pertinent data available, such as the paper I referenced.
Descent with modification and adaptation works the same for eukaryotes as prokaryotes. Do you think that recombination can create new alleles? If so, how? Why do combination herbicides and pesticides work? These replicators are eukaryotes.
For a time.
In any event, the paper I cited is pertinent and direct evidence that common descent of humans and chimpanzees are compatible with known molecular clocks and population sizes, which addresses your objection.
Why do combination herbicides and pesticides work?
They work because it takes mutations to adapt to these selection pressures. These mutations occur with replications and replications determine population size. Experimental studies show that it takes many replications to get a single adaptive mutation. If a variant must get two mutations to improve fitness, that probability will be much lower because of the multiplication rule of probabilities. That is what these real, measurable, and repeatable experimental examples of biological evolution show. People say all kinds of things but can you verify your claims with experimentation? Does your paper explain how drug resistance evolves?
The full paper, which is open and not fire walled, relates real and measurable observations concerning your statement.
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Darwin never took a position on universal common descent, so it’s hard to see how he got it wrong.
This is the very last sentence from “On the Origin of Species”
He clearly states that life could have started out as one form or as a few forms. He never stated that life had to have a universal common ancestor and left the possibility open of separate common ancestors.
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You have quite a few wrong assumptions. Here are two major ones:
- There is only a single mutation in the entire genome that can be advantageous at any one time.
- You ignore sexual reproduction which combines advantageous mutations within the population into a single genetic background.
Take lactase persistance in humans as an example. There are several different mutations that all confer lactase persistance.
This advantageous trait was found independently several times in recent human history.
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How does a lineage accumulate a set of adaptive mutations? Do you think that humans and chimpanzees have the same reproductive fitness?
Darwin also did not know what DNA evolution is or that DNA even existed.
How do two or more possible adaptive mutations change the mathematics? Does each of those variants follow the same evolutionary trajectory? Or do you now have two or more different lineages following different evolutionary trajectories?
Recombination can increase the reproductive fitness of an offspring under specific circumstances. What is the probability of that happening? For example, HIV does recombination but 3-drug therapy still works. Why can’t HIV recombine adaptive mutations and defeat 3-drug combination therapy? Why do combination herbicides and pesticides work?
Humans have had sufficient replications for mutations to occur at every possible site in the genome, but that’s a different matter than a lineage accumulating a set of adaptive mutations. Do humans have greater reproductive fitness than chimpanzees and if so, what adaptive mutations do humans have that chimpanzees don’t have?
Two things. First, Darwin reported data and developed ideas from those data. He is not an end point, nor a starting point. Many of his ideas are based on the statements from the Reverend Thomas Malthus. It is a stream of thought and that Darwin got some things wrong is normal and natural in the development of ideas. Second, why to people from Kenya keep winning the Boston Marathon?
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One at a time?
@T_aquaticus example of lactose persistance is a good example of a late selective pressure due to domestication of cattle.
Fitness is contextual to environment, and at some point that diverged between humans and chimpanzees. Humans are enormously successful due to the unique capacity to manage and regulate environmental factors, and therefore reduce coupling to environmental constraints.
If you have to ask this then you don’t understand your own mathematics.
If there are 1 million possible advantageous mutations it would obviously take fewer offspring to get an advantageous mutation than if there was only 1 possible advantageous mutation in the whole genome.
The population follows the same trajectory because they are all interbreeding.
Drug resistance in HIV is not universally applicable to all species in all environments.
If you want to claim that humans could not evolve from a common ancestor shared with chimps then you need to show us the probabilities for humans, not HIV.
If you are using asexual species as your model you are going to continue to get the wrong answers.
Compare the genomes. Amongst those differences are the advantageous mutations that humans have. The same for chimps.
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That depends on whether the population is asexual or sexual.
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