I have been doing these articles for some time on my website, and, although people read them, they had never previously replied to any of my articles...until yesterday. Yesterday, from the time of me writing this, a critic who I often have run-ins with, replied several times to my post on this site on chromosome 2 fusion, a subject we've had debated before through email. You can find our discussion on alleged Chromosome 2 Fusion on this site here. He didn't understand my arguments then, and he doesn't understand my arguments now. Only now I think he's intentionally trying to not understand my arguments.
When someone engages me in a debate I try really hard to get them to focus on the arguments and to understand my position and the arguments I am making. However, since I had engaged Glenn before now, I know how these discussions will end. He'll try very hard to resist acceptance of my position and arguments, and we'd ultimately "give up" on trying to convince each other. It was getting late, nearing suppertime for me, I was getting hungry, and I had grown tired of trying to convince someone who didn't want to be convinced. So, ultimately, I told him what I thought, told him I was leaving the conversation, and I said "God bless!" to him which is how I usually tell people "good bye" whenever I was done speaking.
However, this did not stop him from replying as I knew he would, even after I had already clicked off the post. My email always send me alerts whenever someone replies to one of my posts, but does not tell me what they said. It just provides me the link that enables me to go to the exact page where someone had replied. Since I was done with the conversation I didn't bother to click the link nor raise up my site to see what he had said. I didn't care, because I knew his last words would result in more misrepresentations of my arguments or more hot air being thrown at me. I didn't want to continue dealing with someone who wasn't even making any rational and reasonable effort to understanding my arguments, plus nothing he said so far hurt, injured, or even destroyed any of the four premises in my argument.
In my argument I had four premises. You can review my argument here. My argument was a deductive argument, as I said in my article. In a deductive argument if the conclusion is valid and the premises are true, then the conclusion must be true. My conclusion flowed logically from my premises, so it was a valid argument. This means that the only way to challenge my argument is not to challenge the conclusion, but the premises. Glenn followed suit with this, and, in the comment section of my article, he started challenging the premises of my argument. The first premise he challenges not at all but this might be due to his misrepresentations of my argument throughout the course of his responses, but most of his attacks appears to be on Premises #2 and #3, with Premises #1 and #4 being entirely ignored.
We'll see how Glenn Williamson's arguments fair against what I had argued in the article. Our arguments were all over the place because Glen had responded several times, and every time I responded to a post, and went to respond to others, Glen responded several more times. To make this article coherent I need to express my replies in my own words, while Glenn's wording will be verbatim, and reorder the series of attacks by Glenn the best I can. Glenn's arguments, statements, and responses will be in red, while mine will be in blue. My conclusion will be in black.
Glenn: “In the mouse example, the telomere-telomere fusions were only shortened by 100 bp.”
How did you come to that conclusion, when the paper says:
“In human primary fibroblasts that lack detectable telomerase activity, telomeres shorten by about 100 bp per cell division.”
First of all, it’s referring to HUMAN cells, and secondly it’s PER CELL DIVISION. So first of all, we don't know whether that 100 base pairs applies to mice, and secondly, the fusions started happening in the mice in the second GENERATION. There are probably hundreds of cell divisions in that time.
Brian: Glenn is referring to a mistake I had made in my original blog. Since then, it has been corrected, but at the time he'd written this it had not. Since I am the only one that works my ministry, and because I was really focused on my YouTube channel lately, I hadn't had time to correct the mistake. Since then, however, it has been corrected. It was pointed out to me by a friend of mine who I had made a video with on chromosome 2 fusion awhile back. I had referenced the 100 base pairs but missed the part about the "per cell division."
He also said this is for human cell division, which, after going over the paper with him, I agree with him on this, but 100 base pairs/cell division is still low for human standards. However, since evolutionists regard humans as mammals, the context indicates this apply to all mammals, which includes mice. So my mistake, notwithstanding, would still hold true to mice. However, a much more precise passage is given later on in the paper, and this one refers directly to mice:
These cultures revealed a significant decrease in TTAGGG hybridization signal with increasing mTR−/− generation. The rate of telomere shortening was 4.8 ± 2.4 kb per mouse generation. This value was calculated by comparing the mean of the TFU distributions for the p arm, the q arm, and for all ends between wild type and mTR−/− G2, G4, and G6. Representative FISH images from wild-type mTR−/− G2, G4, and G6 MEF cultures are shown in Figure 6. Strikingly, no TTAGGG signal was detected on chromosome ends in 5% of the chromosomes in G6 cultures (Figure 6D and Table 2) (María A. Blasco, Han-WoongLee, M. Prakash Hande, Enrique Samper, Peter M. Lansdorp, Ronald A. DePinho, Carol W. Greider, Telomere Shortening and Tumor Formation by Mouse Cells Lacking Telomerase RNA, found at: https://www.sciencedirect.com/science/article/pii/S0092867401800064#BIB13, accessed at 11/12/2023.)
According to this paper, 4.8 kb ± 2.4 kb/mouse generation had degenerated, so the claim there "was hundreds of cell division by that time" by Glenn is false. The abbreviation, "kb", stands for "kilobase"--a "kilobase" in genetics is equal to a 1000 bases, so 4.8 kb is 4,800 bases! DNA is double stranded, so to find out how many bases is in a base pair, divide by two. In other words, 4,800 bases is really 2,400 base pairs (bp)! However, if we add 2.4 kb to it, that would be 2,400 bases or 1,200 bp! This would give us a maximum of 6,000 bases or 3,000 bp! In a minute this will be important.
However, keep in mind this is in a single generation (that's the "per generation" that it's referring to). How long can a mouse live. Typically, most mice live about seven years, but they have children a lot. I think it is safe to say that a mouse generation is about seven years long. This means in one generation it degenerated roughly 3,000 bp at most! Wait a minute! How long are telomeres again? They are anywhere from 5,000 bp to 15,000 bp long, and so between two telomeres that are fusing, we'd expect the alleged fusion site to between 10,000 to 30,000 bp long. However, in the mouse paper that Glen referred to, only about 3,000 bp had even degenerated! That's still not a lot of base pairs degenerating.
However, even if we grant that the mouse paper was correct, these are still far too examples of alleged telomer-telomere fusions happening. Remember, my arguments isn't arguing against the impossibility of telomere-telomere fusions happening, but the improbability of telomere-telomere fusion happening. Having only less than a small handful of examples only further makes my point. This is the point that I think, I daresay deliberately, Glenn is missing to begin with! Also, the lab example is an example of telomere-telomere fusions being induced and, thus, unnatural. If I was arguing for the impossibility of telomere-telomere fusions happening, then bringing up these lab results, but, as it were, I am not. I am arguing for the improbability of this even not its impossibility. Again, Glen is missing the point of my argument and failed to dismantle my premise.
Glenn: "We're talking a degeneration of anywhere between hundreds of thousands to millions of base pairs long."
Right! Perhaps read and understand the paper before commenting. The scientists made dicentric chromosomes, and then observed the deactivation and REDUCTION IN SIZE of the deactivated centromere. Exactly what we see in chromosome 2.
Brian: No, Glenn assumes that it happened with Chromosome 2. No telomere-telomere fusions involving Chromosome 2 has been observed. Glenn is arguing in a circle. Centromeres, themselves, are between 250,000 to 5 million base pairs long (Tomkins, "Chimps and Humans", p. 59)! The problem is wrongly understood by Glenn. It's not the fact that degeneration had happened (assuming a fusion event that is), but how much degeneration would be required for this to be true. The mouse paper does not report this amount. I did read the paper, but the problem is Glenn is attacking and focusing on the wrong thing.
Glenn: "This alleged "second centromere" is supposed to be evidence of a deactivated centromere accept it is found in a highly functional protein-coding (and non-coding) gene"
When you say "highly functional", what do you mean? "highly functional" relative to an "average" gene? Can you point me to a gene with "low" functionality?
Brian: By "high functionality" they mean a gene with lots of functions. This is the more humorous portions of Glenn's arguments. He tries to nick-pick at words, and then tried to play them off other genes as if my statement "highly functional" is meant to be a comparative statement to other genes. However, by "highly functional" is meant to be an expression of "very functional" not a comparative statement. By nick-picking at words here, Glenn is, once again, missing the point. Telomeres are never located in functional genes, but the supposed fusion site is in the middle of the DDX11L2 gene which has lots of functionality, both expressed and co-expressed. I have heard anywhere between 255 to 1,000 functions. In my interview with Donny Budinsky on alleged Chromosome 2 Fusion, he gave me several examples. However, how many functions is not as important as the fact that it is functional in the first place. How could this be a fusion site of two telomeres fusing together if there is a functioning gene that the supposed fusion site is right in the middle of it in the first place?
The supposed second centromere is also located in functioning protein-coding and non-coding gene. Again, the same problem occurs as it does with the supposed fusion site. Centromeres are never found this way. Once again, Glenn misrepresents the argument, and tries to focus, instead, on how the argument is worded, rather than the fact that this should not be so if this is truly a deactivated centromere.
Glenn: Okay, but that obviously doesn't answer the question. You're implying now that there are genes that are NOT "fully functional". What does that mean? What does a gene that is NOT fully functional look like?
Brian: Glenn is replying to my comment that I had made him that "I think they mean it's fully functional" and so he responds accordingly. However, Glenn is missing the boat again. Evolutionists will often label genes that they think are non-functional (possessing no biological function) as pseudogenes. YECs often reject the notion of pseudogenes, but evolutionists believe in them because in their paradigm they would assume that there would be leftover genes from our supposed evolutionary development. So, anytime they find a gene where it either has low functionality or they are unaware of its functionality, they label them "pseudogenes." However, many supposed pseudogenes are being discovered to have lots more functionality than is claimed by the evolutionary community. DDX11L2 gene is what they would call a "pseudogene" but it has been discovered that it has lots of expressed and co-expressed functions. This is why we use the phrase "highly functional" as opposed to what evolutionists think on alleged pseudogenes. Somehow Glenn has missed the memo at the annual evolutionary convention on that one. He doesn't understand why we use that particular phraseology.
However, all of Glenn's direction here is irrelevant. The point is that it has functionality, but a telomere nor centromere can exist within a functioning gene. Telomeres are made up of entirely of repeats. Same thing is true for centromeres. They can't exist in functional genes. Glenn is clearly not getting it. His attempt at just focusing on how I word my phrasing was an utter failure!
Glenn: "the fact that it is highly functional at all!"
Please read my comments carefully because you respond. You've again said "highly" functional. "High" relative to what? An "average" gene?
You've thrown two numbers around: 255 and 1,000. Are these numbers "high" relative to other genes? What's the average? What are the equivalent numbers for a "low functioning" gene?
Brian: Once again, he assumes that my use of the word "highly" is meant as a comparative term, but it's actually meant to express a functionality that supersedes evolutionary thinking on claims of a pseudogene. It's not intended comparatively, but to emphasize the point that this gene is very functional. He's focused on the amount instead of the fact that it contains lots of functionality. How many functions it has is just further used to drive the point home, but Glenn has chosen to focus on the numbers whether than the fact that it is a very functional gene and, thus, making it more unlikely that either two telomeres fused together in that spot, or that the spot contains a deactivated centromere in Chromosome 2. This is the whole point, but Glenn is missing it again. You'll find that this will be a constant theme of his of missing the point of the argument, and me constantly accusing him of this. I think he's intentionally trying to miss the point, whether than understand the argument that was being made.
Glenn: "Let's take the word "highly" out of it."
Agreed. You cannot claim that DDX11L2 and ANK30RDL are "highly functional".
"The fact that a functional gene .."
What does DDX11L2 DO? We all agree it's transcribed - is that "functional" in your assessment? You throw some numbers around - like co-expression, and cell-type expression, but refuse to contrast those numbers with any other gene.
Brian: First, Glenn takes me out of context. My statement of "let's take the word 'highly' out of it" is meant for me to try to get Glenn to focus on the main point that had been emphasized, not suggest that it was an inappropriate use of wording, which it was not. Secondly, he tried to use that to deny their functionality altogether which is a non sequitur. It would be like saying if my car isn't colorful then it must have no color at all. However, this doesn't follow logically. This also shows, in truth, Glenn understood the point I was making here, but was intentionally arguing previously as if he didn't understand. His arguing like he didn't understood my point was done intentional, so he could deny the point without any real logical basis for denying it. It obviously has functionality.
Thirdly, again, he acts as if the point is to compare this to other genes, but it's not. The point is that it contains a lot of functionality when it shouldn't contain any, or, at least, not very much, and this gene, DDX11L2 gene, does a lot. Dr. Jeffrey Tomkins, a geneticist, writes:
My research showed it is expressed [DDX11L2 gene] in at least 255 different cell or tissue types. It is also closely co-expressed (turned on at the same time) with a variety of other genes around the genome and is connected to processes associated with cell signaling in the extracellular matrix and blood cell production. The location of the so-called fusion sequence inside a functional gene associated with the genetics of a wide variety of cellular processes strongly refutes the idea that it is the accidental byproduct of a head-to-head telomeric fusion. Genes are not formed by catastrophic chromosomal fusions!
The purported fusion site is itself functional and serves an important engineered purpose. My research showed that the fusion site actually serves as a switch for trolling gene activity. In this respect, a wealth of biochemical data showed that 12 different proteins called transcription factors bound to this segment of the gene. One of the proteins that bind to it is none other than RNA polymerase II, the main enzyme that copies RNA molecules from DNA in a process called transcription. Backing up this important discovery is additional data that I uncovered showing that the actual process of transcription initiates inside the region of the so-called fusion site.
Technically speaking, we would call the activity in the alleged fusion site a promoter region. Promoters are the main switches at the beginning of genes that turn them on where the RNA polymerase starts to create an RNA. Many genes have alternative promoters like the DDX11L2 gene inside the gene in the first intron. As mentioned, there are actually two areas of transcription factor binding in the DDX11L2 gene. The first is in the promoter directly in front of the first exon, and the second is in the first intron corresponding to the fusion site sequence. This duel promoter scenario, along with the fact that the DDX11L2 gene produces RNAs with two or three exons, indicates that the gene undergoes a process called alternative transcription. Not only it the gene itself complexly controlled, with the alleged fusion sequence playing a role, but even the transcripts produced are very complex. My research also showed that the RNAs themselves contain a wide variety of binding and control sites for a class of small regulatory molecules called microRNAs (Tomkins, Chimps and Humans: A Geneticist Discovers DNA Evidence that Challenges Evolution, pp. 55-57).
So, yes, the DDX11L2 gene contains high functionality. This is not a comparative statement necessarily, but it does mean that this gene has significant function within the genome. Glenn agrees that it's transcribed, but he questions whether this transcription represents functionality, but it does. Transcription is a process, and through this process we get the necessity on the creation of RNA, and ultimately even, microRNA as well. However, it has more than just transcription factors as indicated by the quote. Even the alleged fusion site has lots of gene activity going on.
Glenn: "In my video with Donny he went over many of these functions."
Yup, so something like co-expression of DDX11L2: are there genes that AREN'T co-expressed with other genes? Is there "high" correlation of co-expression for DDX11L2?
"I'm tired of this back and forth."
Yup, it's certainly frustrating when I have to repeat the same question over and over because you refuse to give a straight answer. I think we both know why you can't. Or more accurately, WON'T.
Brian: Again, Glenn is treating this like it's a comparative thing, but it isn't. The point is that it is a functional gene which the alleged fusion site is found within. If the supposed fusion site is the results of two telomeres fusing together, telomeres are never found inside any functional gene. This is the point Glenn is intentionally missing. It is a point that I had repeated several times in our conversation, but Glenn is either not getting it, or he's trying really hard to not get it.
His second part of his statement whereby I said I was tired of the back and forth, and that I was done with our conversation on this because he didn't seem to want to understand what I was arguing as I had mentioned previously in the introduction. I had answered each and every question, but his questions was based upon misrepresentations of my position or arguments. I had, also, point this out each and every time. It's a lot more frustrating when I have to repeat the same points I was actually making, but Glenn continues on in his misrepresentations as if I didn't explain my arguments to him! What more can I do when he refuses to understand? I can't force comprehension in him!
Glenn: "there is no known present observable examples of them happening outside of Cancer, indicates that these do not occur normally in nature"
You have been given three examples - Hartmann's Zebra, Jack Jumper Ant and the Domestic Pig - where the karyotype analysis shows that a telomere-telomere fusion has occurred, and in the case of the Jack Jumper Ant, is CURRENTLY in the process of becoming fixed in the population. You also have the mouse paper that shows that when telomeres are depleted then they fuse together.
On what grounds do you reject these examples? Please contrast that with evidence you WOULD accept for a telomere-telomere fusion.
Brian: Again, Glenn further misrepresents my argument here. This is the reason I referenced the word "present" in my statement here. The Zebra, Ant, and pig were all apart of papers that assumed that this happened in the past. I was referring to observable examples in the present that can be observed happening in the present outside of a situation involving Cancer where everything's going crazy. Why do they think a telomere-telomere fusion happened? Because of how the alleged fusion site looks whereby they assumed a telomere-telomere fusion had happened, then these papers are used to affirm a telomere-telomere fusions in humans in the distant past. This is circular reasoning.
However, I granted the possibility that these papers were correct, and my argument in Premises 1 and 2 still stands. Since I was arguing for the improbability of this event not its impossibility. I repeated this over and over to him, but he continue to assume that if he could point these few examples that would dismantle it. However, since I granted it for the sake of argument, he didn't touch my argument any.
The ant population which has a specific chromosomal count from the other ants was currently being fixed in the population, not that the fusion event, itself, was currently happening. This was what we hadn't observed happening in the present. I had told him this in my reply to him.
Glenn stated that: "You also have the mouse paper that shows that when telomeres are depleted then they fuse together." The mouse paper showed that the fusion was induced under laboratory conditions instead of it happening on its own in nature which is my argument. The fact that degeneration must occur is not my argument, nor anyone else's, it is the amount that needs to be degenerated that's the argument. He has misrepresented my argument again. Also, I had went over the mouse degeneration. Too little would be degenerated from the mouse. Even under lab conditions not enough base pairs are degenerated in the mouse paper. Only 3,000 bp per generation, once the math is done, that had degenerated in the mice that had been tested. This is not enough.
Again, I don't reject these examples. I questioned their veracity, but my arguments do not rise or falls on the veracity of these papers. I am willing to grant their accuracy for the sake of argument to emphasize my point: too few examples are given, so even if telomere-telomere fusions were possible, they are highly rare occurrences, making them improbable events. The problem isn't the examples in the papers, it is the amount of examples that's the problem. To prove that this is something quite frequent (evidentially speaking), you'd have to need far more examples than you have. My argument is a probabilistic argument. I am only arguing for the improbability of the event itself. Since my argument is focused on the rarity of telomere-telomere fusion as part of an argument that is arguing that this event probably didn't occur, then this is the point I am making here which Glenn is misunderstanding.
Glenn: "and we don't even observe them happening in nature today"
What do you mean by this? I'm trying to extract from you what you think it would look like - in practical terms - a telomere-telomere fusion happening "in nature" that is somehow not satisfied by the three examples you've been given. What extra evidence are you expecting for you to conclude that they ARE happening "in nature" today?
Brian: Here, Glenn is focused on the "in nature" part of my argument. His argument is two-fold: 1) What do I mean by "in nature" and 2) what would such an example look like? By "in nature" we mean happening on its own occurred, or something observable outside of the laboratory. If it was induced to happen in a lab example, then the telomere-telomere did not happen on its own. However, within the evolutionary paradigm, it's not like the lab-coated scientists can stand around as the first humans are branching out from our alleged "ape-like" ancestors to induce a fusion event between two chromosomes. Thus, if the event happened, it did so without the direct interference of the lab-coated scientists. We need present, observable examples of its happening on its own.
What about his second question: what would such an example look like? I would be an example in which the scientist can observe happening on its own in nature. In my response to Glenn I gave him an example. I will convey that example below, verbatim:
You could, in theory, point to a scientist who observe a particular species, but that species was known to have a certain amount of chromosomes, but after taking a blood sample, he discovered that two telomeres from two different chromosomes had started to fuse and even degenerate as it reduced in size. He watched and observe them for the next several years, drawing blood to see where the chromosome fusion was at, and he discovered that every few months it'll degenerate even more. After a few years or so, the two chromosomes are completely fused. All this time he's making notes, recording data, and taken pictures, or recording his progress via video camera (from my reply to Glenn Williamson).
This is what I mean by "in nature" as something happening on its own under normal circumstances. In other words, the fusion event isn't being forced to fused, it's doing so without compulsion. Glenn Williamson will start developing a view that is a little weird to me. He'll assumed that these are unhealthy cells that are fusing, except evolutionists, as I understand it, marks this as part of supposed evolutionary development. If the organism was sick when fusion occurred, then this would mean that it didn't survive. If it didn't survive then how did this chromosome number solidified in the rest of the human race? What about inheritance? Why didn't this disease pass to its children with this new chromosomal count? This is an unusual argument, one in which we'd explore more in a bit.
Glenn: "You must observe telomeres fusing under normal conditions and without interference from you forcing them to fusion together. In other words, it happening on its own."
Okay, and how is this NOT satisfied with the ant, the pig and the zebra? This is so puzzling. Like are you expecting the scientists to take their microscopes out in the field, do some spreads while sitting next to an ant colony and literally have video of two chromosomes joining up in real time .. ? Please be more specific about what you are expecting.
I seem to be repeating a lot of my questions, because you're not giving satisfactory answers. Please READ the questions carefully.
Brian: Did Glenn observed a telomere-telomere fusion in an ant population, or did any scientists observe this? Was this observed in the present, or did this allegedly happened in the past? It's not puzzling if Glenn to take a moment and try to understand. We're talking about present examples of telomere-telomere fusion events being observed in the present. None of these papers satisfies that.
His statement "Like are you expecting the scientists to take their microscopes out in the field, do some spreads while sitting next to an ant colony and literally have video of two chromosomes joining up in real time .. ?" is conflating the study of the thing being observed, with lab experiments forcing, or inducing, this even to occur. I am speaking of experiments where, under controlled circumstances, a telomere-telomere fusion happens, but, even if that was the case, it's not a natural occurrence, and, once again, I'm not arguing against the impossibility of telomere-telomere fusions, but the improbability of telomere-telomere fusions happening in nature.
Anyhow, a scientist can still use instruments to measure and study these things, and a scientist already takes microscopes out in the field to study some piece of interest. It's like he's expecting the scientists, out in the field, to be void of any equipment at all. Then how could they do any tests, measurements, or to follow the day-to-day routines of an animal they mean to track?
I am being specific, very specific. This is why I bold, underline, capitalize, and italicize words. It so I can make myself as clear as possible. However, Glenn has to make an effort too. He needs to read my responses and arguments carefully, and try to understand them. As it is, he is not even trying to understand them.
No, he's repeating himself, because you don't have better responses. I'm repeating myself because he's not even bothering to try to understand what I am arguing. My answers are satisfactory, but his lack of agreement with them doesn't change that. What he really wants me to tell him is that he's right, but that's not the case, and I am not in the habit of telling people what they want to hear. I will always tell you the truth, even if that's not what you want me to say. By the way, I read the question careful, but it just wasn't the answer he wanted me to give. Sorry, but I can't change what's true. I know what I was arguing, and that is what I am trying to explain to Glenn, but he keeps misrepresenting my arguments.
Glenn: "... two different chromosomes had started to fuse ..."
This is a puzzling phrase, and I think it explains why you're having trouble answering the question. Chromosomes are either fused or they are not fused. There is no "starting to fuse". It's like being a "little bit pregnant".
Maybe you're referring to a population where some individuals have fusions and others don't, and that's exactly what's happening with the Jack Jumper Ant. It *IS* happening in nature, right now.
Brian: Here I was referring to the process of fusion. Fusions wouldn't be instantaneous. It's not like one second they weren't fused, and then the next second they were. You could say at the start of the process they weren't fused yet, but I wasn't referring to the completed process. In his pregnancy's example, for example, you could liken my statement to the fertilization of the egg which leads to pregnancy. He apparently confused my statement with the completed process, which took my statement out of context.
In his second example, once again the process of "fusion", if any fusion had happened, has already ended. They are a population of ants that have that chromosomal count. However, we didn't observe this process. Instead, what he is referring to is a population of ants with one chromosomal count which is being "fixed" in a group of ants with other chromosomal counts at present, but this is not what I am referring to. Here, Glenn is making the fallacy of irrelevant thesis. It is irrelevant to what I was arguing on how a particular chromosomal count had gotten "fixed" into a population of ants since this has nothing to do with the process of a telomere-telomere fusion happening in the present and being observed in the present.
Glenn: "Telomeres are generally 5,000 to 15,000 base pairs (bp) long."
Right, HEALTHY telomeres in humans are 5k - 15k long. Healthy telomeres PREVENT fusion. The claim of a 10k to 30k signature is nonsensical, because it implies that you are expecting HEALTHY telomeres to fuse.
The mouse paper shows very clearly that DEPLETED telomeres fuse together, because they are missing that 5k - 15k of telomeric repeats. The mouse paper states: "We estimate that those ends lacking telomere signals have <0.2 kb TTAGGG repeats"
Brian: My statement here was referring to how long telomeres at the end of chromosomes were in order to show how much would need to be degenerated, not to do some sort of circular argument in my statement. I think he misunderstood me here. His statement, "The claim of a 10k to 30k signature is nonsensical, because it implies that you are expecting HEALTHY telomeres to fuse" is false. I am not expecting any telomeres to fuse in the first place, he is. Remember he's making the claim, and so the burden of proof is on him. However, the "10k to 30k" is referring to two telomeres that are fusing (that is their combined base-pair lengths) so it's not "nonsensical" since this has to happen. It's almost like he's expecting under unhealthy situations that telomeres degenerate before fusion ever began, but my understanding from the other side, even from previous discussions with Glenn, they think the degeneration happen because of the fusion event, so it is only "nonsensical" to assume that some kind of degeneration happened to the telomeres prior to the alleged fusion event, even in a situation involving diseases like Cancer that can cause a telomere-telomere fusion to happen.
The mouse paper had claimed degeneration as a result of the fusion event, but degeneration is not prior to it, but a direct result of it:
Telomerase-deficient cells could be immortalized in culture, transformed by viral oncogenes, and generated tumors in nude mice following transformation. Telomeres were shown to shorten at a rate of 4.8 ± 2.4 kb per mTR−/− generation. Cells from the fourth mTR−/− generation onward possessed chromosome ends lacking detectable telomere repeats, aneuploidy, and chromosomal abnormalities, including end-to-end fusions (María A. Blasco, Han-WoongLee, M. Prakash Hande, Enrique Samper, Peter M. Lansdorp, Ronald A. DePinho, Carol W. Greider, Telomere Shortening and Tumor Formation by Mouse Cells Lacking Telomerase RNA, found at: https://www.sciencedirect.com/science/article/pii/S0092867401800064#BIB13, accessed at 11/12/2023, from abstract, bold added for emphasis.)
So even if I accepted the mouse paper's conclusion, a telomere-telomere fusion is included in it. I think he's misunderstanding the paper. The paper isn't claiming that the unhealthy chromosomes' telomeres degenerated first, and then fusion happened, but that fusion happened, along with other stuff, including degeneration. Interesting, I had already dealt with this above. Once the math is done this comes to about 3,000 base pairs per generation at most. Of course, we'd have to guess at how many generations we're talking about. However, this doesn't seem like a lot. However, all you'd need to do is read the abstract and you can see that the scientists in question are making this happen instead of it happening on its own. We'll deal with his claim of this supposed fusion event happening as a result of "unhealthy" telomeres here in a moment.
Glenn: "I'm not, you are."
WOT. No, YOU are expecting a signature of 10k to 30k. That implies that HEALTHY telomeres are fusing. I'm claiming that DEPLETED telomeres fused, because healthy telomeres PREVENT fusion. I'm expecting a much smaller signature, because I don't expect healthy telomeres to fuse, I expect depleted telomeres to fuse.
So I'll ask again, why are you expecting HEALTHY telomeres to fuse?
Brian: No, again, I am not got any expectation of a kind. The burden of proof is on Glenn, not me. 10 to 30 thousand base pairs is a reference to how many base pairs, on average, exist within 2 telomeres coming together. This includes healthy or unhealthy telomeres. The fact that you are sick, even with Cancer, doesn't guarantee a telomere-telomere fusion. If this was the case, then every Cancer patient would be having telomere-telomere fusions happening quite frequently, and quite possibly on every chromosome in their bodies. Telomeres on average are 5,000 to 15,000 bp long, and that's a fact. Two telomeres fusing together would mean a combination of these numbers: 10,000 to 30,000 bp long. This does not assume a degeneration of these base pairs, nor does it assume that these base pairs can't degenerate. It just doesn't assume one or the other. To do so for either of us would be circular, which is why I don't assume that this number can't degenerate. My argument here is only intended to point out how much base pairs would need to degenerate to get down to the 798 bp alleged fusion site claimed by the other side. Once again, he's misunderstood my argument on this.
Glenn stated: "I'm claiming that DEPLETED telomeres fused, because healthy telomeres PREVENT fusion. I'm expecting a much smaller signature, because I don't expect healthy telomeres to fuse, I expect depleted telomeres to fuse." Telomeres don't stop fusions because of how long they are. They stop fusion because of how they are and the fact that they are made up of telomeric repeats. Glen is hoping by reducing the number of base pairs in degeneration he can than make a fusion event more likely. However, how long telomeres are is not what prevents fusions. Plus, it's the fusion itself that causes chromosomal degradation. Glenn is trying propose that some other problem resulted in the degeneration of base pairs, that resulted in a fusion event, however, he's placed the cart before the horse. Even if degeneration occurred beforehand, that would not caused a fusion event, unless we're talking about both telomeres being completely wiped away, but then there would be no telomeric signatures at all if that was the case.
Let's deal with Glenn's "unhealthy telomeres" argument a bit better. I agree that only in situations involving Cancer do we observed telomere-telomere fusions happening. I've repeatedly told him this. However, evolutionists believe that a specific telomere-telomere fusion happened either when humans alleged split off with their common ancestor with great apes, or shortly thereafter. As far as I can tell, none have ever suggested that unhealthy telomeres had fused, but they just claim that in our alleged evolutionary past, a telomere-telomere fusion had occurred between two chromosomes of the great ape. I can't remember what these were originally called, but evolutionists renamed the two chromosomes in the great ape that they think had fused together as "Chromosome 2A" and "Chromosome 2B" because of how much they believe this event had happened.
Glenn knows that we only observe situations like Cancer and the lab example with mice (although the later is not a natural example since it's being induced in lab-controlled environment rather than it happening on its own) for such fusion between two telomeres to occur. Obviously, this must be a rare occurrence at best or it'll be happening all of the time. So, you'd only find an example in an unusual occurrence that is not a normal situation. Glenn knows this, so he tries to argue that this is occurring unnaturally through a situation where the telomeres are unhealthy.
You've got to hand it to Glenn, if it wasn't for the fatal flaw in this argument that I am about to go into you'd think his argument was brilliant. Just argue from a situation that we can agree on that would, possibly, cause a telomere-telomere fusion. However, there is one fatal flaw in his argument here: how do you get this new chromosomal count, post-fusion, to get fixed in a population if the organism had caught Cancer and died from the disease?
Not just any disease would cause a telomere-telomere fusion. It'll have to be something that causes the cells to go hog-wild. Cancer is the only thing that would cause this, and Cancer is fatal and hereditary. To get Cancer to affect the telomeres in this way, it can't be Cancer in its first stage. It would have to be advance stages of Cancer to cause this type of reaction.
However, evolution, in the Darwinian sense, is all about "survival of the fittest" which means only the "strongest" survive. In evolution, death is the hero of the story, weeding out the "weak" from the population. However, if our prehistoric alleged ancestor had gotten Cancer, then how did they survive to give this new chromosomal count to the next generation? Did they have children while dying of Cancer? Did they also catch Cancer as they are passing it to their kids? If this situation is going on, then how did most of the newly evolved homo sapiens wound up with the new chromosomal count so it could get "fixed" into 100% of all human beings? This whole thing don't make since in light of Glenn's evolutionary beliefs. This is having those who are not fit to survive surviving! This is inconsistent with Glenn's own evolutionary views!
That last question he asked there commits the fallacy of the complex question, also known as the fallacy of the loaded question. The fallacy of the complex question is, essentially, a circular question. It is two questions built in while making a circular assumption about the thing in question. For example, if I asked you, "Have you stop beating your wife yet?" and you say "yes" then this would assume that you use to beat your wife but now you've stopped, but if you say "no", then this means you are still beating your wife. The person must assume spousal abuse in the past or present in order for them to ask that question. Similarly, by Glenn asking me why am I expecting healthy telomeres to fuse, assumes that this is what I expect. In reality, I don't expect that, and I've told him this several times, including in the reply that he's responding to. He's merely assumed his position, and then intentionally straw-mans my position. Once again, I make no assumptions about the conditions of the telomeres. There's no way to do that without arguing in a circle, as he has done, so I make no assumptions about the conditions of its nature, but if Glenn wants to continue to argue that the organism that the chromosomes 2A and 2B had fused together got sick with some type of Cancerous disease, then the burden of proof is on him. Simply citing a paper which studies telomere-telomere fusion in mice won't do, he'd need evidence that this happened in homo sapiens' supposed evolutionary past. Simply assuming it happened isn't enough.
Glenn: The question is about what we should expect at a possible fusion site. You are claiming that we should expect a signature between 10kbp and 30kbp. Your basis for this is that HEALTHY telomeres are between 5kbp and 15kbp each. What has been shown in many scientific experiments is that healthy telomeres PREVENT fusion, and depleted telomeres ALLOW fusion.
So please address the simple question: why are you expecting HEALTHY telomeres to fuse?
Brian: Again, he's making a strawman argument and confusing the facts again, not to mention the circularity of his argument. My argument, regardless if we are talking healthy or unhealthy telomeres, pre-fusion event, is that on average telomeres are between 5,000 and 15,000 bp each, and this is a fact. Since a fusion event involves two chromosomes being fused together, this would then double this number. There is only one type of unhealthy condition known that can cause a telomere-telomere fusion event, and that's Cancer. Even if degeneration occurred, it isn't just happening because someone got sick with Cancer, it would be because a fusion event occurred that caused degradation. That's always possible for a Cancer patient. I know telomeres prevent fusion, this is the very thing that would make telomere-telomere fusions so rare in the first place.
His statement "What has been shown in many scientific experiments is that healthy telomeres PREVENT fusion, and depleted telomeres ALLOW fusion" is simply false. Telomeres prevent fusions. However, how many base pairs it has (how long it is) is not the reason that it prevent fusions, so trying to shorten it does not cause fusions. Interestingly, he claimed "many scientific experiments" confirm this, but he's only ever presented to me a single study, and this paper, itself, references the fusion event. I agree that in a situation like Cancer you might get a telomere-telomere fusion, but I am not arguing against its impossibility but its improbability. The 10,000 to 30,000 bp was just way to indicate how much it would have to degenerate from. I am not arguing against degeneration, but the amount of degeneration that would need to occur in order to get down to the 798 bp length alleged fusion site. He simply doesn't understand my argument.
Glenn: "No, your "expectations" are circular."
Again, this question is about YOUR expectation. YOU expect a signature of 10kbp to 30kbp, right? That implies that healthy telomeres have fused, as opposed to depleted telomeres.
Please stop avoiding such a simple question: why do you expect HEALTHY telomeres to fuse, when healthy telomeres PREVENT fusion? The fact that you have to constantly dodge the question tells me you know the 10kbp to 30kbp signature claim is nonsense.
Brian: No, it is not about my expectations. Glenn is the one making the argument, not me. He has the burden of proof, not me. I have no expectations of the conditions of the organism(s) that a telomere-telomere allegedly happened in. Neither of us can do that without making a circular argument, so I have no presuppositions regarding the nature of the alleged organism that the alleged fusion event happened in. Glenn is trying to force me to make a circular argument just as he has made.
Again, he has misrepresented my argument. I am not saying I expect it to fuse with 10,000 to 30,000 base pairs, but that prior to the fusion event, this is the average that it would be. Simply claiming that this number would degenerate due to a telomeres alleged "unhealthy" state won't do unless Glenn assumes that this organism has been "unhealthy" all of its life. Was there ever a point where the organism was healthy with 5,000 to 15,000 bp/chromosome? Saying 10,000 to 30,000 bp is its starting point prior to fusion. This avoids me making a circular argument. However, Glenn is straw-manning my argument here. It's like he's assuming that I think that the entire time "fusion" is going on, the telomeres remained 10,000 to 30,000 bp, but that's not my argument nor focus. My argument and focus here is that the 10,000 to 30,000 bp is what it would have to degenerate from! The alleged fusion site is only 798 bp long. To go from 10,000 bp to 30,000 bp a lot of degeneration would need to take place. That's anywhere from 9,202 bp to 29,202 bp that would need to be degenerated. Nothing in the mouse paper would suggest a degeneration that could degenerate that many base pairs in the amount of time that it would take for a fusion event to occur.
He said: "Please stop avoiding such a simple question: why do you expect HEALTHY telomeres to fuse, when healthy telomeres PREVENT fusion?" Once again, the fallacy of the complex question. This is another constant theme in his argumentation, he keeps accusing me avoiding/not answering questions, when that's not the case. However, in the fallacy of the complex question situation it doesn't matter which way you answer, the question, itself, is circular. He's assuming his position and ask the question according to that assumption. However, my answer is always the same, you're misrepresenting my position, Glenn. I have told him this repeatedly. I make no assumptions about the nature of the telomeres (healthy or unhealthy), but he is! At this point, his misrepresentations of my positions was getting frustrating. In this case, his strawman argument was intentional which makes this a very deceptive argument as a result. Also, again, I agree that the only situation that can cause a telomere-telomere fusion is Cancer. So, again, he keeps arguing this as if I never even referenced this statement, even though I repeated in my original article, in my previous emails to Glenn on this subject matter, and to Glenn in the comment section, but still he repeats it as if I never said it. This is a very deceptive way to argue.
Glenn said there at the end, "The fact that you have to constantly dodge the question tells me you know the 10kbp to 30kbp signature claim is nonsense." Again, I didn't "dodge the question" but his question assumed a position and an argument I don't have and was not making! I had told him this several times. It's like he wants me to confess to a view that I don't carry. When I refuse to do that, he then accuses me of avoiding the question, which is not what I was doing at all. This is terrible rhetoric, and very dishonest of Glenn. The 10,000 to 30,000 bp is not nonsense since that would be the normal lengths of two telomeres, prior to any fusion event. My argument was simply to focus on the amount that would need to degenerate. I think Glenn is intentionally misrepresenting my argument. As they say in philosophy, "It is easier to tear down a 'strawman' than to deal with the actual argument." Glenn found it easier to assume that I was arguing something that I was not arguing in order to show how bad that misrepresented position/argument was, except, that's nor my argument nor my position, and given the fact that I told him this several times, this would mean that he's purposefully misrepresenting my position and argument on this. This would also make this deceptive.
Another thing to keep in mind, as stated previously, Glenn is being inconsistent with his own views on evolution since, assuming that this was an unhealthy telomere, then this assumes Cancer for the organism whose telomeres fused. How did the organism survived long enough to get the chromosomal count "fixed" into the population post-fusion? How was he/it able to mate with its/his body being a weakened state? Didn't he pass along his lethal disease to its/his children? How did they survive long enough for it to get "fixed" at a largescale population of evolving humans so that 100% of all humans can have 46 chromosomes? Wouldn't evolution weed out the "weak" from the population? Wouldn't this be the opposite of what evolution claimed? Overall, I find his arguments on this both circular and self-refuting. He's obviously be inconsistent to his own position.
Glenn: "Human centromeres are huge, spanning out between 250,000 to 5,000,000 base pairs long! However, this alleged second centromere is only 41,608 bp long!"
Right! When there are two centromeres, one of them is necessarily deactivated, and in that process, "it was observed that the alpha satellite array of the inactive centromere became reduced in size after centromere inactivation" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3557915/)
The cryptic centromere being reduced in size is EXPECTED.
Brian: Again, Glenn is making another strawman argument. Just like with the telomere-telomere degradation, I am not arguing against centromeric degradation, but I am arguing against the amount that is needed to degrade! This was my whole point of bringing up the amounts in the first place. Glenn seems like he's feeling that he needs to prove that degradation is inevitable if such an event occurred, but none of this affects what I am actually arguing. Even if you expect it to reduce in size, it is having to reduce a lot more than any experimental data would indicate.
In addition to that, even the paper itself in the context of the citation Glenn is quoting tells us that it is speaking of a deactivated centromere in fish, not humans. In fact, it was right before Glenn's initial starting point for his quote which he conveniently left off. The paper also gives other reasons for a centromere being reduced in size, apart from its deactivation:
[C]entromere inactivation could be explained by removal of the CENP-A chromatin portion of the array. Indeed, decreases in alpha satellite array size at inactivated centromeres have been suggested from studies of patient-derived dicentrics (Fisher et al. 1997; Maraschio et al. 1990). In the remainder of induced dicentric fusions with inactive centromeres, there was no evidence of centromeric deletion, suggesting that similar to the engineered i(Xp)s, epigenetic mechanisms are also involved in centromere inactivation (Fig. 2b) (Kaitlin M. Stimpson, Justyne E. Matheny, and Beth A. Sullivan, Dicentric chromosomes: unique models to study centromere function and inactivation, found at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3557915/, accessed at 11/14/2023.
The paper gives other reasons that can attribute to this, not just its inactivation. Of course, Glenn is still missing the point. The focus of my argument is on how much of the base pairs would need to be degraded, not on the fact of the degradation. I also found it a bit hypocritical of him to chastise me for my mistake with the "100 bp per cell cycle is in humans" thing, but then failed to take into account that this was a study done on fish centromeric DNA, not humans. The authors referenced that right before Glenn's starting point for his quote, which Glenn, conveniently, cut off at the start.
Glenn: "We're talking a degeneration of anywhere between hundreds of thousands to millions of base pairs long."
Right! Perhaps read and understand the paper before commenting. The scientists made dicentric chromosomes, and then observed the deactivation and REDUCTION IN SIZE of the deactivated centromere. Exactly what we see in chromsome [sic] 2.
Brian: I did read and understood the paper, but Glenn has, once again, failed to understand my argument. My argument is not against degradation, but against how much degradation would be required in order to be true. This was my whole point of bringing up the numbers is that I was focused on the amount of degradation involved. Glenn is attacking an argument that I am not making. Centromeres are anywhere from 250 thousand to 5 million base pairs long but the alleged deactivated centromere is only 41,608 base pairs long. This means that the amount that would need to degrade is between 208,392 and 4,583,392 base pairs that would need to degrade. None of the experimental evidence we have shows a degradation of this latitude. Thus, this is not what we see in the alleged deactivated centromere, despite what he says on this.
CONCLUSION
Before I give an overall evaluation of Glenn's arguments, challenges, and attacks on my own argument, I first want to give a recap on the argument that I made in my previous article on this that Glenn is responding to. The full article with my initial argument is linked in the Introduction to this article above.
Here's my four-premise argument, but without the expansion of the details:
P1: Telomere-telomere fusions are improbable, although not impossible.
P2: The evidence against a specific fusion event occurring in chromosome 2 is strong.
P3: The evidence in favor of a Chromosome 2 Fusion is weak.
P4: If a fusion event occurred in the past then the Biblical model could explain and account for it better than the evolutionary model.
C: Chromosome 2 Fusion happening in the past is improbable, but if it did happen, it would still not prove relationship between chimps and humans, nor common descent.
I often wonder what it would look like if someone tried to challenge my argument here. Would my argument hold its own against being challenged? How strong are the arguments are when faced with criticisms? I originally proposed this argument at the end of me and Glenn's original conversation over this, so I never gave him a chance to respond. I often what his response to these arguments would look like, and now I know. Let's evaluate them overall to see how my premises held up when Glenn made his attempt to challenge them.
However, before we go further I feel I must pay Glenn a few compliments. The argument above is what's called a deductive argument, as I had mentioned both in my original article and in my original email to Glenn. In a valid deductive argument if the premises are true, then the conclusion must be true. The only way you can attack a valid deductive argument is, not by attacking the conclusion, but by attacking the premises. The above argument is valid because the premises follow logically to the conclusion. Glenn knew this, so instead of attacking my conclusion, which would've been idiotic and pointless, he attacked my premises. Bravo, Glenn, well done.
Secondly, I want to thank Glenn for raising the "100 base pairs per cell cycle in humans" thing to my attention in the mouse paper he sent me. I already knew about the 100 bp/cell cycle. This was pointed out to me by Donny from Standing for Truth ministry. I had just not noticed it when I had written the original article. Since then it has been changed on my article. The one contribution that Glenn did make to this was the fact that he pointed out that the context indicated that this was in humans not mice. The writers did make a later statement concerning the degradation of the telomeres in mice later on in the paper, which was referenced by both me and Glenn. However, I did find it interesting that when referring to the degradation of centromeres, the context in his paper indicated that it was talking about fish, not humans, which was what Glenn was talking about. I think that's the reason he started after the paper referenced "fish" even though it was apart of the same statement and Glenn, conveniently, started after the paper told us what it was referring to. I think he'd knew that I'd focus on that just as he focused on it with the mouse paper.
However, the degradation doesn't seem like a lot. Nevertheless, there's a number of uncertainties involved with both of the papers regarding these statements. With the mouse paper, how many cell division are we talking about in humans? Glenn assumed that it would be a lot because he claimed that it was "on the second generation" but that doesn't tell me anything. The cell divisions were in the human telomeres being studied, and the paper doesn't tell us how many cell divisions were involved. Both me and Glenn speculated in favor of our own position, but that's all it were, speculations. There's no way for us to know for sure since neither papers gives that information. The centromere paper that he had linked claimed "per generation" but failed to tell us how many generations were involved. So, once again, we simply don't know for sure. We can at least assume one cell division and one generation being studied at minimum, but this would not be a whole lot of degradation, which was my point.
Whenever I had calculated the numbers that were used for the mouse paper in regards to how much degradation had occurred, it calculated to 3,000 base pairs per generation. This is not a lot. Keep in mind, though, it doesn't just have to degrade to where it is now, there would need to be enough time for the present size to integrate and be "fixed" in the entire population of humans for all present-day humans to have the same-sized alleged "fusion site" and for the same-size alleged "second deactivated centromere" and so if these degraded to this number over time, especially lots of it, then we'd expect different humans to have different-sized "fusion sites" and different-sized "second deactivated centromeres" in various humans across the planet, but we do not see this. This is a very heavy problem for Glenn's view on this. You would need the telomeric fusion to cause its degradation and the degradation of the centromere to happen to its present number over a much shorter timespan! That's a lot that would need to degrade over a short amount of time. This is just not what we observe in any of these experiments.
As far as the premises are concerned, Premise #1 and #4 remained untouched throughout the course of Glenn's arguments. In the email he tried to respond to my argument on Premise #4, but it was defeated, and the refutation of which was also in the original article. However, in Glenn's counter-arguments and responses, he never challenge Premise #4.
Premise #1 wasn't just not responded to, he'd ignored entirely, even as he gave his responses to various things that I had said. If he had considered Premise #1, he'd not made a lot of the mistakes that he'd made. A lot of them came because he'd ignored the fact that this was a probability argument and I wasn't arguing against the possibility of these things, but only the probability of it. Since this was a deductive argument, I was going from generalities to generalities. This was intended as a probabilistic argument. So, show something could happen doesn't dismantle my argument. Most of his attacks failed on the mere basis of him misrepresenting my arguments. Thus, there was a great deal of strawman arguments made in many of his responses.
He does attack Premises #2 and #3 really strongly. He makes a strawman argument regarding my alleged assumption of "healthy telomeres fusing" which I was not making. I was not claiming anything about the natures of the telomeres prior to it allegedly "fusing" together. To do so would be a circular argument. I told him this repeatedly. This makes his claim on this also an intentional strawman argument, which is deceptive of him. In addition to that, I agree that this is the only time you'll ever see telomere-telomere fusions happening is in Cancer patients. I had also told him this repeatedly.
However, there is one fatal flaw in his "unhealthy telomere" argument. If the organism was dying of Cancer, then how did the chromosomal count, post-fusion event, get "fixed" in the population of humans whereby 100% of all human beings have 46 chromosomes? How would they have the strength to mate and to procreate? Wouldn't their children inherit their disease? How did they survived to populate the chromosomal count to the point where it was possess by all human beings on Earth present-day? If Glenn ever responds to this argument, I imagine his argument would be circular: assuming that it must've happen because it happened previously in the populations of other organisms that other peer-review papers have written on. However, the argument then becomes circular. How does he know that they did experience a telomere-telomere fusion event?
Overall, and one-by-one, my premises stood against every attack, many of which never got touched by his arguments since he was misrepresenting the arguments themselves, and my position. Because of the misrepresentations, the evidence I had provided in my original article and argument on this also didn't get touched. Overall, Glenn's counter-responses were a bit disappointing, and very weak at best. He spent too much of his time misunderstanding my arguments, or trying really hard not to. There was even times that I thought his misrepresentations were deliberate or purposeful. I tried really hard to get him to understand, but I think his lack of comprehension he was forcing onto himself.
Our conversation ended like many of our debates, with me having to end it abruptly and Glenn trying desperately to cling onto me with weak arguments. After all of this time spent waiting to respond to my argument on this, I was very disappointed. However, I was really impressed with how my arguments withstood Glenn's "best" that he could throw at it. I'll pray for Glenn, but I think Glenn's position on this cannot hold its own once the facts are examined. God bless!
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