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

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.

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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.

Is this a tacit admission that you have no evidence to back up your claim that mutations can not produce new functions?

That is not common knowledge, and it is wrong. Many traits are the result of many different genes interacting with one another.You have also not shown that a gene can not do something else. It is simply a bare assertion you keep making.

"The ARX gene provides instructions for producing a protein that regulates the activity of other genes. On the basis of this action, the ARX protein is called a transcription factor. The ARX gene is part of a larger family of homeobox genes, which act during early embryonic development to control the formation of many body structures. Specifically, the ARX protein is believed to be involved in the development of the brain, pancreas, testes, and muscles used for movement (skeletal muscles)."
ARX gene: MedlinePlus Genetics What you can't seem to get your head around is that mutations in these genes can change what they govern and change how they function. You seem to have invented these restrictions out of thin air.

I already disproved your claims in previous posts. Perhaps you should check them out. Given your refusal to address posts disproving your claims, it would seem that you have more in common with the flat earthers than we do.

You need some evidence to back up these claims. How is that insufficient for human evolution from a common ancestor shared with chimps?

There are definitely genes. What you can't seem to understand is that many traits are the result of many genes, much like a cookie is the result of many ingredients. Even fur color is the result of many genes. In fact, there are two separate populations of black pocket mice that are black because of mutations in different genes.

Where is the evidence for this claim?Why can't there be a gene duplication event where one copy keeps on doing what it did before, but the other duplicate mutates and starts doing something new and produces a new phenotype?Edited by Taq, : No reason given.

Surely you can understand why your uninformed opinions are not facts nor science?

Bare assertions lacking evidence are also not facts and not science. At least the author of the essay in the opening post attempt to gather some evidence, even if it turned out to be bad evidence in the long run. It is your claim, so it is your burden of proof. I see no reason to disprove a claim that has no evidence to back it.Edited by Taq, : No reason given.