The Evolution Theory is a Myth Equivalent to the Flat Earth Theory

I'm going to read his article but I haven't yet. My guess is that the people who did the experiments weren't looking for what he sees in them.

Without reading the article, you might as well guess that Rumpelstiltskin made up the Theory of Evolution out of straw. Don't forget the peer reviewers. And all of the other scientists who have studied the results and given up their chance at a Nobel Prize for proving evolution wrong.No doubt there's a giant conspiracy of people refusing to acknowledge what one little goober could figure out with nothing but a pencil, a piece of paper and a grudge.

I don't think there is a conspiracy, I think there is a habit of thought that is reinforced from many angles. I do think you all could do better at trying to understand what this guy is trying to say instead of piling up the straw man misinterpretations, and that IS what you all are doing. He's the first creationist I've personally ever seen here who is arguing in a way I can follow and appreciate so I'd like to see him last a while. However, I also think there are plenty of creationists who have proved the ToE false.

Please bear in mind hat he hasn’t got around to presenting an argument here, his last attempt was horribly mistaken, and that mistaking an analogy for a straw man doesn’t exactly inspire confidence in his ability to argue a case.

I don't even know why you're responding to me. I only summarized what everybody else in this thread was saying - and judging by the number of cheers it seems that my summary was accurate.I haven't expressed an opinion on whether or not forexhr's calculations are correct - but even IF they are, they pose no threat to evolution. You can't calculate reality away. The strawman is his. Yes, it is unusual to find two creationists who can agree on anything.

Yeah, you think a lot of stuff.

A lot of it true too.

Well, let's take a look at the article. This should be fun . . .Here is the first section that stood out:

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The longest empirical observation of this rearrangement process is the E.coli long-term evolution experiment (LTEE). In this experiment, Richard Lenski has been tracking genetic changes (which are essentially rearrangements of molecules — i.e., nucleotides) in 12 initially identical populations of asexual Escherichia coli (E. coli) bacteria since 24 February 1988. After three decades the experiment has rolled through more than 67,000 generations of E. coli, which the researchers note is equivalent to over one million years of human evolution. Regarding this comparison to human evolution, we must note that human population sizes are much smaller than that of E. coli. In the LTEE, the size of each population fluctuates daily between about 510^6 and 510^8 (Richard E. Lenski, 2004). On the other hand, the effective ancestral population size for Homo sapiens was in the range of 8,000 — 10,000 individuals (Chen FC and Li WH., 2001). Meaning, there have been much more molecular rearrangements in three decades of E. coli evolution than in a million years of human evolution. For this reason, the comparison of E.coli and human evolution only through generations is imprecise and it goes in favor of the evolution theory. But we will use it anyway to give the advantage to the theory.
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There are several problems here. First, the author is assuming that the per base mutation rate and recombination rate are the same in E. coli and in mammals. I know for sure that the substitution rates in wild type E. coli in normal growth conditions are much lower than in humans, but this is also complicated by the emergence of hypermutators in Lenski's experiments.Nonetheless, there needs to be some math to show how genetic change (substitution and recombination rates) in Lenski's experiment is greater than or lesser than that seen in other populations.I think I will break this down into several posts so that it isn't one big wall of text.Edited by Taq, : No reason given.

Here is the next section:

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Now, the question we are interested here is what did Richard Lenski discover in his experiment with regard to the idea we mentioned at the beginning? Did he discover that all those molecular rearrangements resulted in new biological functions? Well, the answer is: not at all. The largest and the most important study of evolutionary processes in action has demonstrated that after more than 67,000 generations, and after billions upon billions of molecular rearrangements, this processes resulted in a total of 0 — zero new functions.

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I really want to see the experiments that Lenski or anyone did to determine that these bacteria had no new biological functions. From what I have read, they were focused on the emergence of aerobic citrate metabolism. That is the only function they were looking for. I don't see how any of their experiments could have ruled out any new biological function. The author needs to explain the methodology used for determining the lack of new biological function in these evolved E. coli strains. Lacking such methods or results, no one can claim that there are no new functions in these bacteria.

It doesn't really matter how much mutation there is. Mutation can only change the particular phenotype that is the product of the genetic sequence it alters.I don't know why forexhr thinks this experiment proves anything, I hope he will come back and explain, but his opening statements seemed clear enough that neither mutation, nor gene migration, nor natural selection nor genetic drift has the capacity to produce new features or function, which is essential if the ToE is true.Mutation is the only one of the four that could possibly produce change anyway, but it can't because it only changes whatever trait the genetic sequence governs that it alters. If you want to claim that something new can actually be produced you'd have to focus on major structural traits and forget about everything else, but even then it's not going to be possible to change those outside the parameters already dertermined by the range of possibilities governed by whatever sequence is affrected by the mutation.At least that's what I got out of his opening statement.

I suppose a definition of new function is needed but I think he made the point with his general statement anyway, anything new is impossible through the processes of evolution. All you can get is variations on whatever trait the gene governs.If it's a gene that governs fur color you can only get a fur color, maybe a "new" fur color though I'd guess it was an old one that had disappeared that the mutation revived, but only a fur color, you will not get a different fur type, only a fur color if that is what the gene produces, you will not get eye color, you will not get six toes, you will only get a varation in fur color. OR nothing at all. OR the mutation if it changes the sequence too much can even just make the gene unfunctional or dead.. Edited by Faith, : No reason given.

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One of those changes involves 60 de novo (orphan) functional protein-coding genes on the human lineage that are not found in chimps (Dong-Dong Wu et al. 2011). These genes are called orphan, because they do not have homologs in the ancestral species, or in other words, they are without any trace of evolutionary ancestry.

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This is a mistake that I see a lot of creationists make. They tend to confuse homologous gene with orthologous DNA. Those are not the same thing. A gene is a stretch of DNA that is transcribed into RNA. A stretch of DNA that is not transcribed into RNA is not a gene, but it is still DNA.The vast majority of human orphan genes I have seen do have evolutionary ancestry. You can find the same DNA in chimps, the difference being that the DNA is not transcribed in the chimp genome and is therefore not a gene in the chimp genome. Something as simple as a single substitution mutation can produce a promoter region in the human genome and result in previously untranscribed DNA to suddenly be transcribed. This is further supported by one of the references used by the author:

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One of those changes involves 60 de novo (orphan) functional protein-coding genes on the human lineage that are not found in chimps (Dong-Dong Wu et al. 2011).

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If we go to the Don-Dong Wu (2011) paper, we find this quote:"The origin of genes can involve mechanisms such as gene duplication, exon shuffling, retroposition, mobile elements, lateral gene transfer, gene fusion/fission, and de novo origination. However, de novo origin, which means genes originate from a non-coding DNA region, is considered to be a very rare occurrence. Here we identify 60 new protein-coding genes that originated de novo on the human lineage since divergence from the chimpanzee, supported by both transcriptional and proteomic evidence."So these orphan genes did have evolutionary ancestry as non-coding DNA, contrary to the author's claims.On the same subject matter:

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What are these numbers telling us? Well, they tell us that there are hundreds of new biological functions in both chimps and humans, which are coded with those genes. The logical repercussions that follow from that are pretty obvious: if the evolution theory is true, all those functions had to be produced by evolutionary processes in the last 200,000 generations. But, the longest empirical observation of these processes in action (the LTEE) has shown that they have been unable to produce even a single such function in more than 67,000 generations.

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For the purposes of the emergence of orphan genes in non-coding DNA, the human and E. coli genomes are not comparable. The E. coli genome is 4.6 million base pairs. The human genome is 6+ BILLION bases, more than a thousand times larger than the E. coli genome. On top of that, the vast majority of the E. coli genome is made up of actual genes and their promoters. Like other bacteria, the E. coli genome has very little junk DNA. The vast majority of the human genome is junk DNA, some 90% of it.Therefore, there are several orders of magnitude more DNA where orphan genes can arise in the human genome as compared to the E. coli genome. You can't compare them side by side. On top of that, I haven't seen Lenski or anyone else looking for orphan genes in the evolved E. coli strains, so the author needs to explain how he determined that there were no new orphan genes in these evolved strains.

If there is a duplication of a gene you can keep the old phenotype with one of the duplicates and evolve an additional phenotype with the other duplicate. The problem is that there isn't any evidence to back this claim. That is yet another claim that you need to support with evidence.

What evidence do you have to back this claim?

From the article written by the author in the opening post:

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The next thing we need to know is the functional space size of gills. This size represents the number of all possible molecular arrangements (gene variants) that will provide underwater respiratory function. We can get this number through the parameter that we will call the deformation tolerance. What does that mean? Well, if we presuppose the existence of fully functional primitive gills, and we start to deform them by randomly rearranging their molecules, then obviously, at some point, we will destroy their ability to provide underwater respiratory function. In other words, gills, just like all other biological structures, have some deformation tolerance. Let’s be very conservative and assume the deformation tolerance of 50 percent. In terms of genes, such deformation tolerance means that 50 percent of base pairs in a gene that codes for primitive gills can be random, and this will still retain the ability of this structure to provide underwater respiratory function.

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This demonstrates a complete lack of understanding about the relationship between genotype and phenotype.1. There isn't a gill gene. All anatomical structures are the result of many different genes interacting with each other.2. Not all mutations are the same. A single mutation can cause no change while another single mutation can cause a massive change in an anatomical feature.The idea that there is a 1:1 ration between nucleotide change and anatomical change is ludicrous.