Rebuttal To Creationists - "Since We Can't Directly Observe Evolution..."

We can do some back of the envelope calculations. There are about 40 million mutations that separate humans and chimps, so we can split those between the two for 20 million each.If we go with a high estimate of functional sequence at 10% of the human genome, then that puts us at 2 million mutations in functional sequence. If 10% of those are beneficial, then we are at 200,000 beneficial mutations. This would include indels, both large and small. These numbers exclude genomic arrangements which aren't massive in numbers, but could be important.

Ultimately, the energy source is the fusion of hydrogen and helium in the Sun. Energetic photons are released by the Sun due to fusion, those energetic particles drive the formation of sugars and higher energy metabolites in plants, and those energy containing molecules (e.g. glucose and citrate) are fed to the bacteria.

How else would you explain the physical differences between chimps and humans? If our physical differences are not due to differences in the sequence of our genomes then please tell us what causes those physical differences. They are among the 40 million differences between our genomes. We conclude that humans and chimps share a common ancestor because of mountains of evidence.

E. coli won't replicate in warm distilled water, or even warm saline.We all agree that it takes energy to reproduce. What are you on about?

What physical process isn't?Is your grand contribution to biology the rather obvious observation that resources are limited? If so, you are a bit late to the game.

The mutation rate is significant. Why wouldn't it be? What is demonstrated by single drug therapy? Does mutation rate matter?

Do you think a polar bear is well adapted to the Arctic? Do you think a polar bear is well adapted to the Sahara desert?

Compare the human and chimp genomes. Find the differences. Compare the descendants' genomes to the ancestral genomes. Find the differences. The process of running a refrigerator is a 2LoT process, and yet it moves along just fine. Since there is ample energy available to biology to drive negative entropy it isn't a problem. The error you are making is in assuming every adaptation is as stringent as that seen in either the Lenski or Kishony experiment. There is no reason to think that the number of mutations necessary for an arboreal ape to adapt to a savanna is as few as the number of mutations that can confer antibiotic resistance or aerobic citrate metabolism. Not all adaptations are equal. Compare the human and chimp genomes. Find the differences.

You don't even have to accept common ancestry in order to stumble on the stupendously obvious answer.Do you accept that chimps and humans are physically different because the sequence of their genomes are different? If yes, THERE IS YOUR ANSWER. Are you aware that mutations happen? It's really a thing.Even more, we have mountains of evidence that the same process that produces mutations in both chimps and humans right now, in the present, is the same process that produced the differences between their genomes through evolution and common ancestry.Do you understand the difference between transitions and transversions?Transitions vs transversionsWhat we observe is that transitions are much more common than transversions due to the fact that transitions occur between bases that are more similar to each other. We can also measure the bias towards transitions in real time. When we compare the rates of transitions and transversions between the human and chimp genomes it is an exact match to the observed rate at which these mutations occur.Human Genetics Confirms Mutations as the Drivers of Diversity and Evolution – EvoGrad The mutation rate is about 50 mutations per person per generation. With a constant population size of 100,000 that would be 5 million mutations per generation. Over 5 million years you would get 200,000 generations with a generation time of 25 years. That would be 1 trillion mutations that happened in the human population with just a population of 100,000 people. We only needed to keep 20 million of those mutations, or 1 out of every 50,000 mutations. I really don't see a problem with that.

Yes, I understand it just fine.Where is the problem? Wrong on both accounts. I never assumed that all mutations are neutral nor did I claim that 10% of all mutations are beneficial. First, I said that only 10% of fixed mutations would occur in functional DNA which means only 10% of fixed mutations would have a chance of being beneficial (assuming de novo gene production is rare). Of those fixed mutations I said maybe 10% are beneficial as just a guess. 10% of 10% would be 1% of all fixed mutations could be beneficial. Again, I stress the word fixed.I am not saying that 10% of even 1% of all mutations are beneficial. We are talking about the fixed mutations. And wouldn't you know it, beneficial mutations have a much higher chance of reaching fixation than neutral ones on a one-to-one basis. If you want, we could say that 0.1% or even 0.0001% of fixed mutations between humans and chimps are beneficial in humans, if you want.You are also edging closer to the Sharpshooter fallacy where you assume that the genomes we get at the end were the only possible outcome. What you ignore is the many different paths that could have been taken. Epistasis is also a very real thing. Interaction between mutations can have a profound effect on what paths evolution can and does take. A seemingly neutral mutation can actually influence the fitness impact of future mutations, making a future mutation either beneficial or detrimental where it would have been neutral without the preceding mutation. There is more than one road that leads to Rome. I already know how they work.

Because of the stringency of the fitness landscape. There are only 1 or a few mutations that will allow adaptation to the new conditions. In the Lenski experiment it required a very rare recombination event to evolve aerobic citrate metabolism. In the case of antibiotic resistance there can be as few as 1 mutation that confers resistance. Some adaptations are just harder to come by than others.On top of that, bacteria are asexual. A lack of recombination in each generation limits the mixing of different mutations and different alleles.

I don't see why the speed of the experiment matters. It does.

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Human immunodeficiency virus (HIV) is a diploid virus: each virion carries two complete RNA genomic strands. Homologous recombination can occur when a cell is coinfected with two different but related strains. Naturally occurring recombinant HIV strains have been found in infected patients in regions of the world where multiple genotypic variants cocirculate. One recombinant HIV strain has spread rapidly to millions of persons in Southeast Asia. Recombination is a mechanism whereby high level and multidrug-resistant strains may be generated in individual treated patients. Recombination also poses theoretical problems for the development of a safe HIV vaccine. Certain features of HIV replication, such as syncytium formation and transactivation, may be best understood as components of a sexual reproductive cycle. Recombination may be an important HIV evolutionary strategy.
Recombination in HIV: an important viral evolutionary strategy. - PMC

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Mathematics is meaningless unless you understand the process you are applying it to. From what I can see, you simply don't understand how evolution or biology works.

I am claiming that the beneficial mutations for the adaptation they are studying are rare. That is the stringency I am talking about.For the Lenski experiment, they had no idea how long it would take which was part of the experiment. It could have taken just a few days, but it didn't. In the case of the Kishony experiment they would have known the rate of adaptation for the conditions they put the bacteria under so that they could get the results they wanted within the experimental design. The same can be said for classical experiments like the Luria-Delbruck fluctuation experiment and the Lederbergs' plate replica experiment. What does that have to do with human evolution?To use an analogy, you are pretending that the odds of winning the lottery can be applied to flipping a coin.

You are again assuming all adaptations are the same. They aren't. Let's take a look at a classic paper, the Lederbergs' plate replica paper:

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The culture is fully sensitive to the phage T-1, as well as to streptomycin, and like most E. coli strains gives rise to resistant mutants at rates of approximately 10^-7 and 10^-10 per division, respectively.
REPLICA PLATING AND INDIRECT SELECTION OF BACTERIAL MUTANTS - PMC

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That's a thousand fold difference between beneficial mutation rates for different adaptations. The mathematics are different for each species and each fitness landscape. That's what you can't seem to understand. For some adaptations there might only be a handful of beneficial mutations possible. For a different adaptation there may be thousands of possible beneficial mutations.Added in edit: How many possible evolutionary pathways are there for an arboreal ape to adapt to an open savanna? I would think there are many, many, many possible pathways. Wouldn't you agree? So it would be incorrect to say that the mathematics for calculating a winning lottery ticket does not apply to the odds of flipping heads?This same thing applies to different adaptations.

Edited by Taq, .

What does the Kishony and Lenski experiments have to do with the evolution of an arboreal ape into the the human species we see today?