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

If they are at different genes then they are no longer mutually exclusive.

Any relationships that do exist are rather mundane. Even Darwin recognized the impact limited resources would have on evolution, and one could say that is tied to the 1LoT. It's not that earth shattering, though.What would be interesting is to see where the 2LoT is supposed to fit into the theory of evolution, according to Kleinman. We often see the faulty conflation of entropy and Shannon information. Those are analogous processes, not homologous. Others try to say that species should "breakdown" over time because the 2LoT demands it. These are the types of people who don't understand that negative entropy is a thing. If it weren't, their refrigerators wouldn't work. They seem to forget that an input of energy into a system can reduce entropy.There really isn't any solid tie between 2LoT and genome sequences. The replication of DNA itself requires a net reduction in entropy to start with, so I really don't see how the order of bases really matters with respect to 2LoT. I mean, heat moves from hot things to cold things . . . therefore DNA . . . what?

Then your addition rule doesn't apply to any variants in the human genome. A recombination event will put any de novo beneficial mutation into the same genome that contains many, many already existing beneficial variants, and those recombination events occur with every single offspring.You do understand that in sexual species there is a recombination event for every single individual, right?

When faced with evidence, this is the best you can do. Go figure.

Funny how creationists can never understand this simple concept.The best is when they claim that humans couldn't have evolved from a single cell to a complex, multicellular organism because that would violate the 2LoT. You then remind them of how babies are made. You remind them that at one point in time they were a single cell. The responses I have heard after this bit of creationist theatre still make me chuckle. It ranges from "DNA has instructions that allow violations of the 2LoT" to "the womb is protected from thermodynamics". Cheap laughs, but still laughs.

It's a bit ironic given the fact Kleinman is obsessed with poop bacteria like E. coli.

Having worked with MD's, PhD's, and MD/PhD's in a basic science research setting, I thought I might chime in.The biggest hurdle an MD has is a lack of lab knowledge. They may have a good kernel of an idea, but they don't know how it can be tested in the lab or how to design scientifically solid methodologies. MD's are often the "idea person", and they will hire staff to run the lab and teach the MD how their idea can be fleshed out into a real research project. It is extremely rare for an MD to be designing and running the experiments themselves. In fact, it is somewhat rare for PhD's (i.e. the principal investigator) to be running the experiments, but at least they have a good understanding of the lab work that is being done. A career in basic science research is a career of constantly learning new techniques, technologies, and data analysis pipelines which also teaches you how to learn. It is this experience that MD's lack, which is absolutely not their fault. That's why the good MD's recognize their inadequacies, hire staff to fill those holes, and learn where they can. The bad MD's . . . they usually don't get far in research. Large egos get in the way.Clinical trials are a bit different. These are usually sponsored by a pharmaceutical company, so there are already well written and vetted protocols that are FDA approved, so the MD just has to follow the protocol. All of the nitty-gritty details are usually handled by a clinical study nurse with the doctor focused on patient care.

The way you have described these relationships is a bit wonky. For example, the 1LoT says nothing about limited resources, only that energy can not be created nor destroyed. The relationship between DNA sequence and the 2LoT has been a contentious one. Personally, I really don't see how the 2LoT has much purchase in the realm of sequence. Those features are better modeled by different information theories which are only analogous to the 2LoT. It is a bit like someone claiming that a messy bedroom has more entropy than tidy bedroom. That's not really how the 2LoT works.

I've discussed that very thing multiple times now. You are just trying to distract us away from the fact that you are ignoring the evidence for UCD.

It is a solid equation for specific contexts, not any context you decide to apply it in. As I have shown several times now, that equation is for alleles at the same locus, not alleles at different loci. That equation absolutely applies to every population, but it applies to alleles for the same locus. Right back atcha, chief.

They absolutely do. The 2LoT says that the entropy of a system can decrease if energy is added to the system.What we are referring to is the claim that entropy can never decrease in a system. That law only applies to closed systems.

The healthy allele for achondroplasia is at a frequency of 0.99.The healthy allele for cystic fibrosis is at a frequency of 0.99.The frequency of people with neither of those alleles is negligible.0.99A + 0.99B + ~0C != 1Your math fails. Then your equation does not apply to the vast majority of variants in the human genome.You keep touting this equation as the reason why beneficial alleles at different loci can not simultaneously move towards fixation. Remember that? If we add your made up intersection rule, then this allows beneficial alleles at different loci to simultaneously move towards fixation and add up to frequencies that are more than 1.Your equation no longer serves the purpose you thought it did.

You still don't understand evolution in E. coli. You keep touting this "1 in a billion beneficial mutation" claim, even though it is massively wrong. From a previous post:Joshua and Esther Lederberg published a hallmark paper in 1951 titled, "Replica Plating and Indirect Selection of Bacterial Mutants", which can be found here:REPLICA PLATING AND INDIRECT SELECTION OF BACTERIAL MUTANTS - PMCLuria and Delbruck went on to explain the processes that undergirded the Lederberg's results which later won Luria and Delbruck a Nobel Prize.There is one interesting observation in the Lederberg paper:"The culutre 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 10E-7 and 10E-10 per division, respectively."In this example we saw a beneficial mutation rate of 1 in 10 million and 1 in 10 billion to two different selection pressures using the same strain of E. coli.Kleinman is telling us that one beneficial adaptation every billion divisions is some universal constant, or something of the like. It is so universal that it can even be applied to human evolution. However, in another experiment using E. coli we see beneficial mutation rates that are quite different than what Kleinman claims.If Kleinman's math can't even apply universally to evolution in E. coli, what hope does it have of applying to any other species?

If you mean a career as a basic science researcher after acquiring an undergrad degree, I would wholeheartedly agree, at least in my experience. Having trained undergrads in the lab I can also say that it hasn't changed much since the 2+ decades since my undergrad years. You really learn to do research either by learning in the lab or in PhD programs. MD programs are not a good place to learn how to do research.

26 years of lab experience in a basic science research program teaches you quite a bit. Did you ever show that this was actually the case? Is there anywhere in those papers where they give a beneficial mutation rate? Also, in the Lenski experiment they had hypermutators evolve in several of their lineages, so how do you account for that. The Lenski group also saw an asymptotic relationship between time and fitness which would seem to indicate a reduction in the beneficial mutation rate over time.Then we add the Lederberg paper that I have cited several times now. You keep touting this "a billion replications for each adaptive step" but I don't see how it is the universal constant you seem to think it is. It also doesn't apply to sexual populations where beneficial mutations are moved from different genetic backgrounds to the same genetic background without needing to reproduce mutations in isolated lineages.

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As stated above, Haldane (1957) argued that the costs of natural selection accumulate over loci, i.e., the reproductive cost of allele substitution at two loci would be twice the cost at a single locus. Consequently, the time required for substitution should be twice as long. In general, if it takes t generations for a gene substitution at a single locus, it should take Lt generations for substitutions at L loci. Applying this logic to our model, given that it takes 400 generations for allelic substitution at one locus, it should take 40 000 generations for substitutions at 100 loci. This prediction is in stark contrast to our finding that it takes only 400 generations for allelic substitution at all 100 loci (see Fig. 2F). How can we explain this major difference between Haldane’s prediction and our findings?
Canadian Science Publishing

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