 Hey everybody, today we're debating creation evolution and we're starting right now. Ladies and gentlemen, thrilled to have you here for another epic debate as today we have Erika and Standing For Truth joining us for round two. It's going to be an epic one, folks, and want to say if it's your first time here, consider hitting that subscribe button as we've got a lot more debates coming up. In fact, you'll see at the bottom right of your screen, end game, the final chapter between Mark Drisdale and Kent Hovind will be this coming Tuesday. So our last debate between those two gentlemen, as it's always been fun to watch them. And so that's one you don't want to miss. You can set a reminder. So with that, want to let you know we are very thankful to have our guests here. In fact, not only that, but we're also giving a special thanks to Erika. She's a night owl, but nonetheless, it's impressive. She's over in London. Is it London right now? Right? Yeah, yeah. You can see my change of scenery. I'm in my normal living quarters. This is my flat. So I've got all the decorations up. Anybody who's subscribed to my channel, this is a familiar scene. So we've got the whales right here. It's going to be great. I'm ready. Epic, very exciting. So it's going to be a fun one tonight, folks. We are really looking forward to it. And I want to let you know what we are going to do for format. I'm going to pull up on email because I'm trying to remember, unless one of you remembers. But five and five short intros and then open discussion. Yes. Very good memory, Erika. Hey, that's what I do. Got you. Perfect. So it'll be if I understand right, five rounds of five minutes. Is that what you're saying? I mean, I thought of openers and then open discussion. Right. Yeah. No, it's it's five minute introductions and then just open discussion and then in a, I'm guessing. Thanks so much. Appreciate it. Long day already to do it. Anyways, you bet. So we're here for James Stoke for it. Thanks for that refresher and want to let you know, folks, if you have any questions, fire them into the old live chat. I will pull those questions out of the live chat and we'll ask as many as we can at the end of that open discussion section. When we get into Q and A, if you want to do super chat, that's an option as well, in which case it'll push your question to the top of the list for the Q and A and it allows you to make a comment toward one of the speakers. Of course, they'd get to respond to it. And we ask you to be your regular friendly cells for that. And so with that, very excited folks, I am going to set the timer for five minutes and my presumption, because usually it's just the habit. We always have the creation person go first standing for you. Do you want to go first? Or did you already decided that you guys already decided together that Erica would go first? I don't, we didn't have a choice, but I don't care. Yeah, it doesn't matter to me. I mean, to be fair to Erica, she started first last time. So I don't mind starting first this time, but ultimately it's up to you. Yeah, sure. You can start. Yeah, I always start. You start. Only fair. Got the timer set standing for truth. Awesome. Well, thanks so much. Thanks so much for doing this, Erica. The first debate was a blast. So I'm really excited for this one. As in what? James, as always, brother, thanks for setting it up. So before we get started, we all must realize that it's genetics. It's in our DNA where the question regarding ancestry is answered. Genes, trades, genetics is what's inherited sperm and egg. Sperm and egg don't pass on a fossil or a bone. They don't pass on geography or rock. They pass on genetics and trades. And so if we want to find out the history of humanity, this is where we must look. We have clocks in our DNA, for example, that go back just 6,000 years to Adam and Eve. Let's discuss some reasons why, based on genetic data, the Bible's account of human history is true. When we focus on the variation, for example, in the Y chromosome in the world today, we see that Y chromosomes have very little variation. This indicates that we came from a common ancestor in the not so distant past. Interestingly, the Y chromosomes are geographically specific. There exists African Y chromosomes, British Y chromosomes, Chinese Y chromosomes. Why is this? This is because mutations have occurred in the lines after Babel, since God divided the nations based on their Y chromosome. The family lines are based on the male ancestry. These nations were divided across the planet. Is there good evidence for limited ancestry? Or does the evidence tell us that humans did not go back to Adam and Eve, but are actually related to apes, dogs and banana plants? Well, the evidence for the existence of Adam and Eve and limited ancestry is you and me and the genetics of the people in the world today. The genetic structure in humans today speaks to us of a literal Adam and Eve. We have a small DNA compartment called the mitochondrial DNA that we only inherit from our mothers. Everybody on this planet got their mitochondrial DNA from a single woman, who is exactly what we would expect from a biblical Eve. She is quite literally the mother of us all. In a nutshell, we have nearly identical mitochondrial DNA and the very few mutations that differ from Eve's sequence are exactly what would be expected if Eve arose just several thousands of years ago. As I briefly touched on earlier, the same thing goes for the male side. Science tells us that all men have similar wide chromosomes, which is passed down from their fathers and all of male humanity traces back to a single man. This single male ancestor of humanity has all the qualities expected at the Bible were true. The main argument offered, though, by the evolutionist community, especially biologos against a literal Adam and Eve and ultimately limited ancestry has to do with genetic diversity. They will say there exists no real scientific way for two people to generate all the genetic diversity we see in humans today. This main argument is easily refuted and actually reflects a poor understanding of even basic genetics. A man and a woman today could have thousands, even millions of children and no two children would be 100 percent identical. This is because they are heterozygous. There exists built in diversity and millions of sites within the genome of the average person. In the limited time that I have here, the best way I can explain it is if God created Adam and Eve to be heterozygous, which in fact would be optimal design. You could have as much human diversity and more than we have today in their first family. Time is not required for the diversity today because diversity can be designed and built into Adam and Eve. This argument is not even scientifically reasonable. One more line of evidence I do want to point out before we go into the discussion has to do with the HATMAP data. The HATMAP project is what I am referring to. And this very important project was intended to compile a significant fraction of human genetic diversity. They examine millions of variants in thousands of people from around the world and made the data easily available. Dr. Robert Carter puts it perfectly when he states, and I quote, I am quite happy with what we learn from the project. What have we learned? The human genome is young, shared blocks of DNA are large, and there has not been enough time to scramble them to randomness. The human population came from a single source. Most blocks are shared among all world populations. The human genome is falling apart. Deletions tend to not be shared among populations but are unique to subpopulations. This is further evidence for the youth of the genome and that we came from a single source population in the recent past. I've got 10 seconds here. Genetic entropy, orphan genes, the chimp-wide chromosome, endogenous retroviruses, linkage blocks. For example, there's many different lines of evidence we can look to that point to limited ancestry. And I'd be more than happy to discuss any one of these topics with Erica and show her why limited ancestry is true and universal common ancestry is false. Thanks so much. Thank you very much. Standing for truth just several seconds over. We'll give Erica the same leniency. So with that, we will jump over to Erica's opening statement. Thanks again for being here, Erica, especially given how late it is. It's a pleasure to have you. Obviously, don't worry about it. I will, if that's OK, share my screen. I know I normally have my nice monitor up, but I don't have anywhere to put it. Happy to do that. If that's cool, it's just a PowerPoint. I've never done the screen share thing, so bear with me, you guys. Totally. All right, share my screen and then can you guys see that? It's now showing. So let me just squeeze it down to make it fit. And I'll do one of those. Does that work? OK, very cool. Almost there. Three, two, one. OK, and we're set. All right. So biology supports a universal common ancestry. This is the argument that I'm going to make today. Now, generally speaking, when we look at a universal common ancestor, what we're kind of referring to is that all life on earth shares a common ancestor in the form of a single celled organism some 3.8 billion years ago. Now, as Standing mentioned previously, his argument is somewhat different in that he's sort of going for the the creation orchard, so to speak. So if you can see in this picture here, this would be standing creation orchard on the left, or we have several sort of nodes that are acting as creation origin kinds, right, and the diversity within those kinds is stringent and kept separate from one another. Now, of course, my position would be the conventional tree of life, which is here on the right. So the question is, why do all of the fields in biology agree that universal common ancestry is indeed sort of the reality that we live in? And the reason is because, at least in my opinion, in my humble opinion, it is the case. This is, in fact, our reality. We can look to genetic support. We can look to paleontologic support and we can look to morphologic support. Now, as Standing said, we're probably going to be talking mostly about genetics today. So while I included some slides here on paleontology and morphology, which I will skim if I have the time, we're mostly going to be considering genetics. So I've harped on this many times before in other debates and in other conversations. But genetics, by definition, dictates relatedness. This is simply the case. The same sequencing that links humans to all other humans links us to the other apes, all the mammals, all the coordinates, et cetera. So when you look in this picture, again, as I've said multiple times before, the same logic, the same genetic sequencing, the same means by which we develop phylogenetic trees, Standing would would agree within sort of the kinds. Like if they, you know, patients tend to use kinds, the structure, their kinds with genetics as well. The question is, can the lines cross? And my argument here is that there is no empirical reason to suggest that they would. There just isn't. It's a smooth gradient. And I've said this before, too. But the sort of the same process that we use to, you know, allow paternity tests to be considered admissible in court. We used to to reach the 98.8 percent similarity between us and the members of genus 10 and then indeed 92 with the macaques and so on and so forth. So in addition, we could talk about endogenous retroviruses. Now, here I've linked a couple of nice papers that cover the similarities of the RVs between us and the chimps. And we have this nice little quote on the side that you can read if you like, which to summarize it, 99.9 percent of the RVs and humans are at the identical location and are structured identically between us and the chimps. And even when we look at these specific RV insertions, we find that the mutations that those RVs experience in and of themselves are also identical, which means either we're dealing with a completely separate event for every single RV in every single primate lineage, both within and without or outside of the human and the ape kind. And I'm the monkey kind. I'm not sure how standing structures it or we're dealing with a common ancestor. So my question would be, why can creationist not draw these lines between the kinds? Why do we see the smooth gradient that I've been sort of alluding to? You can sort of see the same thing. And when we look into deep homology, which would be kind of the argument that that we're dealing with the same building blocks. So geology and paleontology, of course, continued to confirm a common ancestry. And not just that, they preclude a 6,000 to 10,000 year old earth. Now, I know it might seem sort of, sort of tangential to bring this up in a conversation about genetics, but in genetics, we get sort of divergence times using molecular clocks. And interestingly enough, radiometric dating, a completely isolated physics based sort of just equation that we use to measure radiometric or radioactive decay confirms this, they corroborate one another. And not only that, but paleontological evidence can also be corroborated with other methods like ice cores or dendocrinology or natural nuclear reactors like the Okla reactor. Then, of course, there's morphology, adivisms, vestigial structures, deep homology. Here are some nice pictures. We sometimes we see horses, you know, display these these additional toes that they used to have when you hit this and the like vestigial pelvises, which I know some people say have a function in copulation. But not so. Ask any of the whales that require a third party to mate. We see deep homology in the form of the Pax 6i gene, you know, rector pili with our hair standing on end. And of course, our wisdom teeth. None of these makes sense. And when we're sort of taking this idea of a designer into our mind, and I know that genetic entropy is going to be brought up. And that's the reason why we have these sort of degenerate traits, but I'm ready to have a conversation about that. So my question for standing is sort of threefold. Well, I think there might be more than three. But where and more specifically, why do you draw the lines between the kinds and what separates the humankind from the ape kind? You can do this genetically or otherwise. I don't care. Another one is how can limited ancestry account for the gradient of forms that bridge the kinds in the fossil record? So here we have an Amphisionid and we have a wolf and we have a grizzly bear. Now, morphologically, it essentially looks like you took 50% of the traits from the Amphisionid and then sort of parceled them out into these these two very closely related animals that we have today. And lastly, why do we see adivisms and vestiges in nearly every animal? And why do these vestiges seem to indicate and suggest that they're from our genetically derived ancestors? Why do they match evolutionary theory? What's the deal with a whale having a pelvis? And then also us finding similarly, sorry, similarly structured organisms living in the same location with the embolute drum, which is an inner ear structure, unique exclusively exclusively to the cetaceans and through geologic time. So so these are sort of my questions for the conversation. And that's it. Thank you very much, Erica. So now we will switch back over to or I should say, we'll switch into open discussion sections. So I will close your shares. Thank you. Gosh, OK, thank you. Very sassy. I appreciate that. Next, we will go with the open discussion section. So very exciting, folks, and the floor is yours. Thanks for being here again. Yeah, all right. So we're going to start. You get to pick because we've that's how we did it last time. Sure. Awesome. Well, I appreciate your opening. Thanks for the visuals. Definitely lots of good questions, lots of good topics. Since you started off with ancestry anyways and where we can draw the line and kind of how there's a perfect gradient, a perfect nested hierarchy of life, I guess you can put it. My question to you then would be regarding certain taxonomically restricted genes that we can look to to separate ancestry, right? So if we're going to look at limited ancestry, for example, if we look at orphan genes and orphan genes, they lack similar counterparts in other organisms. As in like there's no evidence for common ancestry with, say, humans and chimps because of these taxonomically restricted genes that are specific to humans and then also very specific to, say, chimpanzees or like the cat family. Well, sure, of course, there would be because the divergence time between humans and chimpanzees, well, the divergent time would be approximately 13 ish million years ago with with the speciation time being six to seven give or take. So that's plenty of time for you to get emergence. That's a sort of genetic novelty. That's why we have ERVs that are also unique to humans. But you can point to those and the exception does not make the rule. You can't point to the exception and say, oh, look, they're, you know, individual ERVs or orphan genes, et cetera. I don't know nearly as much about orphan genes as I do about ERVs. But then I will simply turn and point to the 99.9 percent of ERVs that we share that are identical and in identical locations. So are you suggesting just to kind of turn that into a question? Are you suggesting to me that there have been separate genetic events regarding sort of these ancestral viruses for every single primate lineage and then also humans? Who I'm assuming you wouldn't accept our primates? So good questions. I definitely want to talk about the endogenous retroviruses. But going back to the orphan genes first as a counter to that, the orphan genes, for example, they're fully functional gene sequences. And what they do is they code for both a functional messenger RNA and a protein. OK, these orphan genes, though, Erica, they don't fit the hypothetical fairy tale of evolutionary theory. And our prediction based on ancestry and proving limited ancestry would be function. OK, so if these orphan genes, which according to our model are needed for the uniqueness that's associated with each created kind as, say, described in the book of Genesis, which obviously we look to as a starting point. The fact that this amazing category of genes are taxonomically restricted and extremely functional and unique to each type of organism would suggest a limited ancestry for the main fact that they are fully functional. I mean, how did these come about in separate ancestries? According to the according to the evolutionary theory, I want to I want to just make an analogy real quick just for the audience. It's like looking at three different books and then finding specific words that have important meanings in the different books that aren't found in all three books, right? There's no evidence for any type of ancestry. That's why they call it orphan genes, right? There's no actual evidence for the ancestral genes leading to these genes. So, I mean, how would those pop up in an evolutionary theory? Well, I'm asking, though, why why are you so? Yes, it thinks can be taxonomically restricted. I mean, obviously, there are, as I said previously, there are sort of unique ERVs to humans. There's also unique breakages like that are just in the primate order. There's a breakage that does the same thing, the Gullo breakage that also exists in guinea pigs, but it's very different. It's in a different location and it lacks some of the sort of regulators that that ours has. So, I guess I'm kind of wondering why it is that you're suggesting that in any shape, form or fashion that these orphan genes cannot emerge after splits, after divergence points. Well, I mean, it can be suggested that they do pop up. Like I believe that the evolutionist explanation is de novo gene synthesis that they popped up through the non-coding regions of our genome. But the question is, is there any empirical observational data for that occurring? And the fact that they've popped up to be extremely functional in the genome seems to be more ad hoc, post-hoc reasoning. But if I'm arguing for limited ancestry and these types of taxonomically restricted genes that are extremely important in the genome, or what are expected to be found, and this is exactly what is found. Right, but what you're doing here is would suggest limited ancestry. It's exactly what we expect to find. Go ahead. Right, but you've got I think I think a clear distinction has to be made. So when we when we're looking at data in general and we're trying to support a hypothesis or see if the data does support a particular hypothesis, it can, obviously, as we know in the nature of science, data can support multiple hypotheses. But the sort of the issue with this is you're suggesting orphan genes again, I don't, you know, that's kind of why I wanted to make it more about biology in general, because I'm not a geneticist. But I know about it. Yeah, but I know enough about genetics to know that these kinds of these these kinds of sort of emergent genes, ERVs, et cetera, things like that, they don't preclude evolutionary theory in any way. You're arguing that it supports limited ancestry. And again, I don't know enough about it. It may support limited ancestry, but it also doesn't preclude evolutionary theory and universal common ancestry. And in light of pretty much, in my opinion, everything else that that sort of I brought up in my presentation that I'm sure will touch on later, which not only does this support universal common ancestry, but it also precludes limited common ancestry. You see what I'm saying? Because there can be data that's like, yeah, it fits both frames. Like, I know Jensen likes to do that with nested hierarchies, which I disagree. But the fact of the matter is then he turns and I'm sure we'll do the same thing and covers other subjects that he believes supports a limited ancestry by precluding universal ancestry. Right. You get what I'm saying, sorry. Right. Yeah. And if we look to homology, right, engineers build in a homologous type pattern, or we can look at DNA level nested hierarchies, we can look at nested hierarchies on a on an amino acid level, right? I know Dr. Herman Mays likes to look at neutral variation, for example. But when there are competing hypotheses, we need to look at lines of evidence that can differentiate between the two. Now, I disagree. Absolutely. Right. But I disagree with your point in that orphan genes can be explained through fish to fishermen evolution because because of the important functional roles that have been discovered in them. They are taxonomically restricted. And I've yet to hear an explanation from you as to how these orphan genes can pop up, can be specific to lineages. For example, humans, to the great ape family, to the cat family, to the dog family, how are these popping up and having very important functional roles? I mean, that doesn't just happen. We also don't see that empirically in the lab. That's the thing. There has to be some type of explanation in order to have that competing hypotheses. But I don't see no explanation for these. So that's why they call them orphan genes. That's it. You know, we're in specific taxons and that's it. Sure. But you're suggesting that the existence of and I know that you mentioned that sort of the the conventional science side that would say, OK, well, you know, it's kind of this novo emergence. But that does happen. I mean, I know you're frequently a fan of using ERVs that play roles in embryologic development because they've sort of been retrofitted. That's that's like a huge tenant of evolution, the adivisms, right? Like this idea of taking, you know, something that used to do something else and, you know, or not out of it, I'm sorry, in some cases of vestiges and and using it for something new. I mean, because you're right, most ERVs, though, have zero function, but some of them do. And they did pop up, right? At least according to real real real quick before you because I understand that you want to move on to the endogenous retroviruses just to kind of end the part on orphan genes. We can do that. I don't want to beat a dead horse. Let's move on to endogenous retroviruses and retro transposons, for example. It's just it's my it's my I would just disagree that orphan genes aren't a line of evidence that can differentiate between the two hypotheses, right? Universal common ancestry and limited ancestry. We can just agree to disagree and look to the de novo gene synthesis. We definitely see empirical data, whether it's in the lab or some type of technical paper that can actually show a non-coding region of our genome suddenly pop up as a protein coding gene. So I kind of know where this is where this is going. So I am going to openly in front of everyone make sure that this is clear. I don't know very much. In fact, I know very little about orphan genes. What I do know quite a bit about or a decent amount about is endogenous retroviruses and the reason why I'm making a connection is because it sounds like conceptually there are quite a few similarities. So I'm not I'm not saying that that I know enough about orphan genes to say this is certainly the case. I probably need to look into it, you know, but I don't particularly find presenting a piece of evidence that knowing absolutely nothing about it except for the blurb that you've given me here could go either way in light of everything else that we're getting ready to discuss convincing as a gotcha, you know what I mean? Because it sounds it sounds very similar to any lines. Yeah, it sounds very similar to the gotchas that creationists use with ERVs. That's why I keep making the comparison, not because I'm trying to dodge away. Oh, I don't want anybody to know. I don't know very much about orphan genes. I don't. I'm not a geneticist, you know, but that's the way the cookie crumbles sometimes. So I, you know, I'm just saying I didn't, I don't find that convincing. I mean, if there are, you know, geneticists out there who are saying, yes, de novo orphan genes can happen, then the fact that we have de novo ERVs, you know, emerging from, from ancient viruses and the thing, such things like this. And of course, new information through, through various mutations, I don't see a problem. It's completely in line with other conventional arguments that we're going to talk about. Right. If I could just jump in real quick, because I definitely want to, I definitely want to jump into the ERVs and the, and the retro transpozons. And I'll give an answer to that. Just on the orphan genes and in the, it's not necessarily just a gotcha type, type argument. I will go on, on record that, you know, the evolutionist community, they are somewhat baffled. And that is why they look to de novo gene synthesis. But to me, that's more of a circular argument because the evolutionists know that orphan genes exist. Therefore, they need to hypothesize why do they exist? So they resort to de novo gene synthesis. Well, why do they resort to de novo gene synthesis? Well, because orphan genes exist. So I'm just saying it's more of a circular based argument. Now, when it comes to the co-option in the functions found in endogenous retroviruses, I agree that these endogenous retroviruses are the retro transposons, for example, Erica, they are shared among humans, among some of the apes, of course, you can find nests and hierarchies in the placement and positions of the ERV. So I agree with that. But the question I think we need to ask ourselves, Erica, is what are these endogenous retroviruses? What are these retro transposons? Are they actually the leftover remnants of viral infections in our DNA? Like you're suggesting, right? Or are they, say, created units of DNA function? Because for years, Erica, it has been assumed that they were the former, right? The leftover remnants of viral infections. And that is because, like you iterated in your opening, they bear strong similarities to actual viruses. And this predicts that these sequences are non-functional. And I know you look to co-option as an answer to the function, but this is a testable prediction based on the design model. And we are beginning to accumulate data. So what we do know at this point in time, Erica, is the trajectory of experimental results and the trajectory points to increasing and surprising levels of function. So to me, it looks as if these are not remnants of viral infections, but actual functional DNA units. Now, what's the role in, you know, ancestry and in speciation? But this specific prediction, it does differ from creation and evolution expectations. Go ahead, take as much time as you need. Sure. So I'm going to kind of respond to that in twofold. One, I'm not kidding here. We do know of a lot of endogenous retroviruses. We're not completely in the dark about this. And I know of, like, a handful that actually do something. And so I'm kind of wondering where you're coming with this with this sort of concept of, oh, well, the trajectory is, we're going to find out that they have more function. And I think I know where you're going with it. And I think it has to do with the ENCODE project, because I've heard you speak sort of before on ENCODE. And for those of you out there who don't know, ENCODE was a sort of group that did quite a bit of genetic work on discovering the functionality of the human genome. And they came out with this quite large number. 80 percent they came out to say the human genome was functional. Now, their definition of fun, that sounds impressive until you actually read the work. I don't want to interrupt. I feel like I feel like ENCODE in general is I just feel like ENCODE at this point is is a is kind of a rabbit shell because we're specifically on the endogenous retrovirus. Sure. But you'll see you'll see you'll see the point I'm going to make. It's it's it's relevant because I actually watched your discussion with Chris, your series of discussions with CRISPR earlier today. And you mentioned several times this concept of, oh, well, the trajectory seems like we're going to find a lot of functions. But so I thought to myself, OK, well, time to look into that. Let's let's see, because I know CRISPR was was saying no, absolutely not. The vast majority of people in the field are saying similar to ERVs. No, it's not looking like we're going to find more function, because every time they investigate, they find a function for something new. It makes up a smaller and smaller and smaller portion of the genome. And there was a paper that came out in 2017 very recently that put an upper cap of and very unlikely upper cap of 25 percent of functionality with a likely range of 10 to 12 percent. So that's the most recent literature on that. And it doesn't follow the trajectory that you were mentioning. So I don't think that you can say because you find functions in one ERV or you find a little bit of function in say an intron or whatever, you can't just say the trajectory seems like we're going to find more and more. And then you eventually we find out all the ERVs are functional or all of the human genome is functional. That's all I had to say. That was the connection. Oh, awesome. And I appreciate that that response and those points as well. And I did enjoy my discussions with with CRISPR and would definitely recommend anybody watch them. But you say that like just one endogenous retrovirus, for example, was found to be functional. Oh, that's hyperbolic. I'm sure it's more than one, but OK, OK, no problem, no problem. Even in the ERVs, though, it's it's not just low levels of function. And that's the problem that the evolutionist faces, because the ERVs, they actually have crucial functions, Erica. For one, they help regulate genes. So they're not just functional in the embryo. They help regulate genes and even determine cell types. So I know that you're claiming that they were co-opted, but I would just say that that's mere uninformative gloss because I would have to see empirical evidence, whether it's in the lab or some type of technical paper that actually shows us a non-functional endogenous retrovirus going from non-functional to extremely functional in determining cell types or regulating genes. Before I continue, actually, would you be able to present something like that? Hold on. What I want to what I want to talk about is is your request there. You're saying, OK, well, I want to see. I'm not saying you have to present it right now, but does something like that exist where it has been observed empirically that a non-functional endogenous retrovirus went from non-functional to a functional DNA element important in the embryo, important in regulating genes, important in determining cell types? I mean, could you present that to us? I mean, I would I would say you've already done so because we have what I mentioned earlier, right, is that we have seven. And what you agree to is that we have, you know, so many non-functional ERVs, you know, you can't hardly list them out on a piece of paper. And then we proceed to talk about a functional ERV. So I think sort of the burden of proof is on you to find function for them if the vast majority is non-functional and you're making the claim that functions do exist for all or at least the vast majority. The burden of proof is on you to show that they have function not on me to see because we have point A and point B. Well, real quick, real quick. This would be like. Well, I don't want to because you brought up some things about end code. I was kind of just clarifying with you and I want to kind of touch on everything because it's not just one or two ERVs that are that are being found. I mean, there is accumulating paper after paper. I mean, I've got papers here from 2019 that are now showing these ERVs. They frequently act to distribute regulatory information and thus confer genes with new patterns of expression and function. The training I don't doubt it. I don't doubt that there are tons of ERVs that have functions. The problem is I checked today, the vast majority of ERVs are functionless. And so functionally, have they functionally tested the vast majority of endogenous retroviruses, though? Because remember, remember, no, real quick, real quick. Evolutionists assume, and you admitted it earlier, that the vast majority of our genome is based on genomic fossils, evolutionary leftovers, but far from being junk DNA, the pervasive retro-transposons or the endogenous retroviruses, for example, that populate our genome. They have a powerful capacity to influence genes and even chromatin. I mean, the functions are endless. I can go on and on. Even the pseudo-genome. We're finding, I'm saying that your argument about co-option and suddenly the burden of proof is on me is more of a circular argument just like with the orphan genes and de novo gene synthesis. So you're seeing that these endogenous retroviruses are playing very important functional roles in our genetics. So instead of actually giving us and providing us empirical evidence for the co-option of these endogenous retroviruses, you're just assuming that they've been co-opted because it doesn't fit the evolutionary theory, but it hasn't actually been demonstrated. And I'm saying that the trajectory of discovery does favor genome-wide functionality because every single month more and more papers come out suggesting more and more function. No, you're OK. First, I'm going to make a quick analogy. If I come out and I say horses are the most important mode of travel, that's just what they are. And you say, well, no, that can't be so. And I say, yeah, look at the Amish. They can't get around without horses. And then you say, well, no, because mostly people get around in cars. And then I say, no, it's really, really important in this one particular case that the Amish use horses. You are you getting what I'm saying? These functional ERVs have indeed been co-opted and the way that we know that they've been co-opted, other than the fact that they look very much like ancient viruses, just in structure when we look at them genetically, is the fact that the vast majority don't do anything. And when you say things like, well, the trajectory looks like that's a very vague statement because the fact of the matter is your talk with CRISPR was what, at least a year ago. And I checked today and they kept it right where he said they were going to cap it. He said upper limit, I think he might actually might have said 20 percent. So he was a little off. He said upper limit, no more than 20 percent. Right. 2017 upper limit, 25 percent. And just and in real quick, I'll pull something up for you. I'm actually happy that you've at least admitted to that because I even debated a biologist. I think it was two weeks ago and I've debated like T jump, for example. And every time I ask that question, right, you know, how much of our genome, both non-coding DNA and protein coding DNA, do you believe the evidence suggests is functional? And you just said it there, just like CRISPR said, it can't be any more than 20 percent, 25 percent. But the thing is that's because any more than that makes that type of fish to fisherman evolution impossible. Simply based on location, accumulation. Well, I've got a paper here that suggests that the genome has to be under 20 percent functional. Let's say evolution could not. Well, actually, actually real quick before we go on too many rabbit shells, because I still want to touch on end code because a few things that you said, I disagree with. Are you disagreeing with the fact that we do see massive amounts of literature nearly every single month that gives us unexpected functions of RNA? And then as you answer that too, how much of our genetics of our genome do you believe we've functionally tested according to the gold standard of genome testing? Go ahead, so first we can swap papers in a moment because I definitely I straight up sat down today. I sat my butt down on Google Scholar and I combed for all literature that I could find that was recent on functional DNA and the most cited paper, the most seemingly sort of groundbreaking biggie that came out came out this this paper in 2017. Now, of course, we're always discovering new things about genetics. And of course, some of those things are new functions. But again, this conversation you had with CRISPR was at least a year ago and we have discovered we haven't passed the cap. We haven't even gotten close to passing the cap that he said. These these guys are saying and I'm going to read this to you instead of sharing my screen just because it's annoying for everybody. I know and it causes a delay. Well, real quick before you do that, can you just answer the question as to how much of our genome has been functionally tested because that's important in this discussion because I'm going to respond. I'm going to respond to that with the same sort of rhetoric or rhetoric back and forth that you that you and CRISPR had. So humans are mammals. And that's why we use mice and not for testing in things like that are drugs and sort of pharmaceuticals. And that's why they are pharmaceuticals tend to work. So we're well, because we share so much in common. We have done extensive knockout tests on mice. We can knock out so much of their genome and they will be just fine. They reproduce, they have babies, their babies are just fine. So that's because that section that we're knocking out is non-functional. It doesn't harm them to knock it out. So and I'm because I know this end code conversation is going to go down the oh, well, maybe the non-coding or the non-functional quote unquote DNA is actually for development that debunks it right there. The fact that these mice with enormous portions of their their non-functional DNA knocked out can go and reproduce just fine. They might have a couple of like weird little morphologies, but other than that, they're famous. Well, before you go on for too long in the with the mice, the problem is as many non-coding RNA genes, even pseudo genes, for example, much of the non-coding regions of our genome, they're only expressed under certain conditions and much of the genome is likely involved, for example, and used between conception and birth. And the fact that many of these non-coding sections of our genome are only expressed under certain conditions, you'd need almost unlimited sensitivity in these genetic knockout tests being done on mice to conclude with any type of certainty that those genes being knocked out really are non-functional because of these genes are being turned on and off, let's say after the developmental stage or just based on environmental conditions during the life of the mice, especially because these mice, the genes are being knocked out in the laboratory. Therefore, many different environmental conditions that are outside of the laboratory that a certain gene that isn't expressed and it's being knocked out. Well, you're not going to be able to know that it's functional or non-functional. And in the answer to your question based on genetic knockout tests, especially with humans, because it's unethical, it's less than one percent of the genome that's actually been functionally tested according to the gold standard of science. So I even asked that question to CRISPR and he went on looking for a paper to show how many of these experiments were performed based on these genes that are only expressed under certain conditions. And he never came back with the specifics on that. So you'd have to show that. I don't believe that those types of knockout experiments on mice have been. To be fair, in that conversation, while he was looking, you were like, you can just get into me later. So there is always the possibility, as I frequently do, that he just forgot to send them to you. Now, I have obviously. And that's fine. Yeah. And that's and that's fine. But I feel like you kind of obfuscated the point there. Because again, for everybody who's who's watching, right, these knockout tests have been done on adult mice or rather the impacts are on adults. They reproduce. They pass those knocked out genes to their offspring who develop just fine and then reproduce themselves after living, living their their merry mice life. So the point is, is that if you're suggesting that there is some that there is no plausible way that I can see to suggest that genes that have been knocked out, even though we've done an enormous portions, are secretly doing some kind of function when nothing bad happens when you turn them off. Well, no, no, I'm not saying that. Already broken. I'm not saying I'm not. Well, just to be sure that Erica's finished here, because we had you talk for a long time, and I want to just be sure that Erica gets plenty. Also, you got it. Well, I'm not saying that it's I'm not using a pseudoscientific argument suggesting that many non-coding RNA genes are only expressed under certain conditions. I mean, this is actually a fact. And my main point regarding that is we have only begun to discover just how functional, for one, the human genome is and how functional the mice genome is. And I'm saying it's mind boggling how many experiments. And I'm not saying it's impossible, but these number of experiments have not yet been done. And that's a fact. That's because knockouts have happened. And then mice still. But the amount of experiments that would be required to conclude is my point with any level of confidence that a particular set of DNA sequences has absolutely no function is mind boggling. Yeah, but the amount of the amount of experiments that you would have to do to conclude anything without beyond a shadow of a doubt is astronomical. The point is that the fact that you can knock out enormous portions of a mouse and then the mouse can reproduce and then its offspring can also reproduce because nothing of merit has been lost is parsimonious only with evolutionary theory, which is that's what I'm saying. To use your word from earlier, the trajectory indicates that enormous portions of the genome can indeed be knocked out because they don't do anything. So and I want to segue this in because I didn't say that they don't do anything. I'm saying a lot of those regions in the nonco, because the noncoding DNA, it functions much like a computer. It's involved in regulatory functions. It's involved in embryonic development. It's even involved in the stagings of proteins for. But they can't regulate if they're off. But I'm saying that they can't do anything. No, but if these specific genes and we have to look at which ones, what types of developmental windows, which types of environmental conditions, because if they if these experiments are being done strictly in the lab on these mice, will these noncoding RNA genes, for example, even some of the pseudo genes, yeah, you're going to knock that out. You're going to snip it out and it might not have some overall effect on genotype or phenotype, but that's because it's just not expressed. Yeah, but we're not talking about. If you consider that and then you consider if you look at comprehensive knockout experiments for humans, for example, it's unethical, obviously at this point, we functionally tested genetics wise under one percent of the genome when you consider noncoding DNA and encoding protein coding DNA. But the thing is, and the question I asked you earlier regarding the RNA, we we do see massive amounts of literature that gives us unexpected functions of of RNA, for example, look at are you familiar with protein moonlighting because in the past, right in the past, one of the ideas, you can just pick up a textbook from 40, 50 years ago, one gene, one function for protein one function. Yes, I'm with you. Continue. Exactly. Now, if we're looking at the protein multifunctionality or we were looking at, say, on an amino acid level, these redundant codons, and I'm sure you've heard me say this before, those were always assumed to be absolutely neutral. Now we know they don't just tolerate error in the cell. These redundant elements, they're used to slow and speed the process. So the level of information compression into every single letter boggles the mind. It's it's actually incredible and even I'm sure I'm sure that is indeed the case, but that's not the problem that I have with with your statement that and in this conversation and in previous ones that the majority of the genome is functional. The fact of the matter is if you knock it out, it doesn't work. It doesn't do anything. If it doesn't do anything before you knock it out, there's no harm, no foul, right? So the fact of the matter is if they do something important, anything, regulation, whatever, it doesn't matter. If they have a job that's even minute, if you knock it out, that job doesn't get done. How much of the genome has been knocked out, though, on a percentage wise? Oh, I could not give you a number on that. I could. I could. And I could be corrected on this. But the last time I checked, it is less than 30 percent. So based on the fact that these tests are being done in the lab, based on the fact that less than 30 percent of the mice genome has been knocked out and the fact that, as I've said, well, three or four times, many non-coding RNA genes are only expressed under certain conditions. Less than one percent of the mice genome, the human genome mammals in general, has been tested for genome functionality. And all you have to look at, like I talked about earlier, you just have to look at the history of genetics. Like you said, back in the forties, one gene, one protein, one function. I've said that multiple times. You can see how many things have been changed. So, yeah, I agree that the results from the ENCODE project, Erica, I do agree that based on their suggestion that at least 80 percent of the genome is functional biochemically, right? Because it's showing that the non-coding DNA is transcribed into RNA. Those are preliminary. I agree with that. But I'm saying the trajectory is clear based on genome testing, based on the history of genetics, that the trajectory does suggest most non-coding DNA in the human genome is functional. At least it serves in a regulatory capacity. I mean, do you actually stand by a genome of only 20 percent max functionality? Here's the thing standing. I go by current literature. And what I try to do when I don't know something about a topic is I check the most recent literature. I see how many times it's been cited and I see who is on the paper and investigate their background, because that's, you know, it's, you know, it's just like what they teach you. It's appropriate sourcing. And I'm going to read you this excerpt. It's quite short from this 2017 paper, which was New Limits to Functional Portion of Human Genome, reported an evolutionary biologist at the University of Houston has published new calculations that indicate no more than 25 percent of the human genome is functional. This is a stark contrast to the suggestions made by the scientist with the ENCODE project that as much as 80 percent of the genome was indeed functional, they took a deceptively simple approach, basically, to sort of sussing this out by looking at deleterious mutation rates and replacement fertility rate, which is quite odd and I wouldn't have thought to do it, but I'm also not a genesis and not kind of that's not really my world. But this is the quote that I think is important. This is from the paper. It's a grar et al. If you if you want to look it up. I've got that in front of me. Or I can send it to you, yeah, too. I have it in front of me. Oh, good, good, good. OK, for 80 percent of the human genome to be functional, each couple in the world would have to have would have to be get an average of 15 children and all but two would have to die or fail to reproduce. He wrote, if we use the upper bound for the deleterious mutation rate, which is at two times ten, eight mutations per nucleotide per generation, then the number of children that each couple would have to maintain a constant population size would exceed the number of stars in the visible universe by an order or by tens, ten orders, rather, of magnitude. So this is the most recent literature. Not only does it say, yeah, probably no more than 25 percent, they're saying it's impossible. So that is evidence that precludes. It's just using math, deleterious mutations and reproductive, reproductive rates, replacement rates and things like that. And it directly precludes what you just said about trajectory, because like you said, these papers come out every day and every time the new DNA that they find that's functional in the new portion of the genome gets smaller and smaller and smaller, they might say, oh, wow, we found out that point one five percent of this given portion is functional, add it to the list. You know, but it's sort of exponential. There's not that much more to kind of sort of complete what we know at least about the proportion of what is and what is and functional, I encourage you to read the paper because I'm not a genetics person, but I found it quite easy to understand and the math is pretty straightforward. Right. So I appreciate that response. So in that paper, what Gore says, he says that human evolution would be very problematic if the genome was ten percent functional, but would be completely impossible if 25 percent or more was functional. So what he's demonstrating here is what results from an evolutionary mindset, because he knows, based on the possible functionality of the genome, if we look at mutations, if we look at what's what's inherited mutation accumulation in general, it would make that type of ape to man evolution impossible because of the fact that if you have a genome that is say 50 percent functional, 60 percent functional, well, that means these so-called neutral mutations that supposedly build up with no real effect on phenotype and genotype would actually be more so nearly neutral. That means there's a heavy bias is what you're saying. I'm saying there's a heavy bias and you can even see that with the ENCODE researchers themselves. You can see that they did their research without that evolutionary bias. And evolutionists like the author here in this paper, they would have to fight the results of ENCODE. They would have to fight any type of trajectory that suggests the genome is any more than 20 or 25 percent functional based on the accumulation of mutations. Because, for example, Komora's theory of neutral mutations, right? Neutral mutations build up. Those neutral mutations are used over time by organisms to change, to adapt to modify. But Komora, Komora, come on. Komora was taken greatly out of context. I looked into that as well with with genes and or Tomkins. I can't remember which one, but I want to make a very short. Well, but a real quick before you do go under that and take as much time as you need. The point that I'm making here is obviously I disagree with the with the you know, with the idea or with the with the belief that the genome is 20 percent functional or 25 percent non functional or functional max, because and even if I were to just say concede that or just choose to agree to disagree, even if though, 90 percent of the genome is perfectly neutral junk DNA, say only 10 percent of it is functional, that's still a huge problem. Because based on what we know about the human mutation rate, right? We accumulate 100 new mutations per person, per generation. That means, Erica, if I were to just agree with what you're saying, about 10 harmful mutations are still arising in every person, every generation. That means even the most fit individuals are still more mutant than their parents. And so even with intense selection, if we're looking at natural selection here against the less fit, it cannot stop mutation accumulation. But like that paper suggests, the more functional the genome is, the more of a problem genetic degeneration becomes. OK, take as much time as you need. Yes. So here's the thing and I'm going to use this to segue into genetic entropy because I feel like that's kind of where you're, you know, pulling a little bit, which is fine because I got my notes right here because I don't know enough about just off the top of my head with give at least numbers. But I want to make a quick comment about bias. Now, in social sciences, anything that require really not really that many, great many areas of science that require an interpretation of the data. Bias can be problematic. Here's where bias can't be problematic with math. When you're just doing equations based off of either known rates or variable rates or whatever, as long as you've got your error bars, they are going to cover your bias. That's that's what they're there for to say, OK, well, it's give or take, right? So you can say, yeah, he's biased to evolution. So is the vast majority of science. And I would agree with you because I am also biased towards evolutionary theory. But it doesn't matter because all he did was use math to get his point across. He he plugged in equations. You can say I disagree with it, but that's the same thing as being like I disagree with whatever the Pythagorean theorem or something like that. Just like an equation. Now, if you went in and you discovered, I guess that's a bad example. If I showed you an equation and you were like, I disagree with it. Now, if you go in there and you find an actual problem with it, that's another story. But as far as bias goes, it's not problematic when you're dealing with mathematics or physics or things like that. Or at least it's far less of a problem because there's less room for interpretation. Now, as far as genetic entropy goes, it's not real genetic entropy or at least the conventional science term is error catastrophe, and it doesn't happen for for several reasons. If if you've got sure, go ahead and give me I want to make sure that I'm kind of addressing the proper point so I don't go on a big spiel and then we're talking about something different when you talk about genetic entropy or you talking about the accumulation of near-neutral mutations that causes degeneration. I would say if you look at genetic entropy or genetic degeneration, for example, it is the fact that natural selection cannot stop the accumulation of most harmful mutations. The problem is, is that the human mutation rate, for example, it is widely accepted to be 100 new mutations per person per generation. Now, even if I were to agree to disagree on your point or assertion that, you know, max functionality of the genome is, say, 20 percent, 25 percent, even though I want to make one last point about the function of the genome anyways, I would say that it's it is a fact that ENCODE, which you were referring to earlier, it does. It does at least show that most of the human genome is functional, but also functional on many layers. We literally have layer upon layer upon layer of programming, Erica, within the genome and no computer program has ever been seen to arise by trial and error by chance. But genetic entropy would suggest that these mutations that evolutionists are saying drive the evolutionary process are either nearly neutral, which are slightly deleterious to the genetics or detrimental. And that's the problem is what type of selection is going to be able to filter out all those bad mutations, whether nearly neutral or just detrimental. Go ahead. So the thing about ENCODE, again, just to give my, I guess, final point on it, for those of you who are watching, one, the definition of functionality is incredibly loose. And if you watch standing's conversation with CRISPR, who is has has sort of hands in many different fields. He knows quite a few people or he's a cancer guy himself, but he knows quite a few people working in various areas of bioinformatics and things like that. And his conclusion was that he could maybe find two people out of the dozens upon dozens upon dozens that he works with who would agree that the definition of functionality was was even remotely appropriate, because their definition of functionality covers everything. And the reason is because that's how you sell a project. I've been trying to sell my project for grants because I'm doing the master's program right now for for for several weeks and you have to make it sound good or else you don't get the funding. So I'm not saying that like it's anecdotal. That's how it is. That's just academia. And just for the record, I'm not disagreeing with the definition that Encode used and the definition that that CRISPR says that they use, right? Encode defined function is specific biochemical activity. And that's why I agree with you that the result suggesting that over 80 percent of the genome is actively transcribed in RNA is preliminary. That's why we've made a prediction as creationists that based on further genetic testing, NACO test, for example, testing mice under various types of environmental conditions with these non-coding RNA genes can be expressed in various ways is functional. That's our future prediction. And I think, of course, and my answer to that would be Encode has already been busted by this 2017 paper. And I think there was another one in 2016, maybe, but I picked the most recent one because that good practice, I suppose. You know how many, I think this is an important question before you move on. Do you know how many cell types Encode tested? Oh, no, I don't. Well, here's the problem, here's the problem. So based on what Encode discovered regarding the function of our DNA, I understand that they defined it as, you know, specific biochemical activity. We have more than one thousand and I'm sure you already know this. We have more than one thousand cell types. So I'm saying, and I'm saying this to you in the audience and to James, the moderator, I'm saying that more function is going to be discovered in the future, because if you're testing only 200 cell types and we have over a thousand cell types in our genetics, I think it's just based on an evolutionary bias to say that max functionality of our genome is 20 or 25 percent. And I know that the reason why he concluded that in the paper is based on mutation accumulation, because if it's any more than that, mutation accumulation makes eight to man evolution impossible. That's a fact. The thing, the problem, though, is that I don't I don't know, excuse me, I'm not sure for certain where you're getting your mutation rates from, I have a hunch that it's geneson's rates and or the or at least the people that geneson sort of pulled from. And if I'm correct on that, which I don't know that I am. Are you saying 100? Are you saying the hundred new mutations per person, per generation? I mean, you could find out which whichever mitochondrial rate, mutation rate and nuclear mutation rate that he uses to make the case and replacing Darwin. Am I correct on that or no? No, well, right now, I mean, if you want to get into replacing Darwin and the created heterozygosis hypothesis and mitochondrial DNA, mutation rates and stuff, I mean, that's a totally different topic than that. All I'm asking is if is it the same mutation rate that geneson uses that you're using to say it over 25 percent or not over 25 percent, but the dealer, deleterious mutation buildup would make it to man evolution impossible. No, no, that's just secular literature. I mean, the mutation rate is generally known to be 60 to 100 new mutations per person, per generation. I believe on trio studies. Yeah, I can. I was I was mostly just curious because there are potentially infinite problems with the way that geneson did his method, his methodology and we can go into that, but that's a totally different topic. Yeah, that's why I was I was just checking it's up to you. We can talk about genetic entropy or we can talk about the L.M.N. Papal groups, whatever you want to talk about. I'm good to talk about it. I just my closing thoughts are I think that you got to look to the current literature and I think that it was handily proven exclusively with math that there is a 25 percent cap. We are coming out. Hold on one second. We are coming to the closing of the open discussion pretty quick here. So we let's see. We had a standing start. And so we if you want to do one quick rebuttal, hold on one second. Discussion wise, it's been about 50 minutes. Well, can we bump it to 60 minutes so we can touch on just a couple more things here? It's up to you. I know it's getting late for Erica. I don't have a preference. It's up to you guys. I can stay up 10 minutes later. I think what we can do is if we want to how about we do this instead of an extra 10 or 15 minutes, if we want to just stay for truth, we can give you another round to kind of make your points and then we'll give Erica one more round to make her points. And each of each of those being just a few minutes. Um, that OK. Um, should we do a couple more minutes of back and forth? And then because that kind of sounds like it would be like almost like a concluding statement, if we're just going to go a few minutes uninterrupted. I mean, whatever you guys say the best. Yeah, so that's right. You had heard right. So we'll just have it be like a few minutes kind of making your points and then we'll give a chance to make her a few points. And then we'll wrap it up. OK, who wants to who wants to start then their few minutes? Final points, as I just said, given that you were about to start, like you can now start and then. OK, so I think since what we were kind of heading into there is is genetic entropy, you can answer the question as to, you know, what type of selection is going to be able to filter out all the bad mutations? Because the major issue is the is the fact that selection, it can amplify the best beneficial mutations and it can get rid of the worst detrimental mutations, but it's pretty well powerless to the nearly neutral mutations, those are invisible to to natural selection. You could think of it this way, Erica, I mean, we've got a genome of what? Three billion letters, three billion are passed on for mom, three billion passed on from from dad. But if you take a one letter, say, change one letter randomly, are you going to have a huge fitness effect? No, it's going to have a tiny fitness effect. It's it's kind of like rust on a car. You can't see each rust event, but it's continuous and destructive. Or like a single spelling mistake in a book the size of an encyclopedia, right, make one single spelling mistake. It's not going to have a huge overall effect, but the accumulation of them over time, yeah, that's going to destroy the message and the and in the book. But why can't natural selection filter out all the bad mutations? Erica, there's two reasons here that you'll have to address. There are too many bad mutations continuously pouring into the population. And most bad mutations are too subtle, as I talked about earlier, to be selectively removed. And we see genetic entropy in real time, Alzheimer's disease, dementia, autism clearly has a genetic component to it, asthma, autoimmune diseases, cancers, what is it, one in three now, immunological disorders, diseases. I mean, there is a pandemic. It's pretty well entropic degeneration on on all levels and the 100 mutations per person, per generation is a fact. And, you know, you're going to have to address how that accumulation of mutations is going to be rid of in our genetics, because I mean, that's what we see. We see genes are going down and not up. And if fish to fisherman is true, I mean, you're going to have to explain the major problem, which is a net gain versus a net loss of information. So I mean, if you want to kind of address those points and give me your thoughts on genetic entropy and what your best argument is against genetic entropy, that would be a good way to proceed. OK, so genetic entropy does not happen. The ecological term again is error catastrophe. And the reason why it doesn't happen, even though ecologists who have no affiliation with creation and evolution, anything along those lines have tried to induce error catastrophe and have failed time and time again. They've done it with E. coli, they've done it with phages. It doesn't work. And the reason they do it with those is because they accumulate mutations way faster than sort of macroscopic life so they can see if deleterious mutations are going to build up in a rather short amount of time. And here's the reason why they don't. Near neutral mutations that if they're near neutral and sort of beneficial, then they're going to be slightly selected for selection isn't an all or nothing thing, right? Let's say you have a near neutral mutation that is sort of a negative, right? It might not kill you, but it might decrease your fitness, because if it's if it is a negative trait, right? If it is a bad mutation, by definition, it's decreasing your fitness. So you're going to reproduce less than your peers and whatever offspring that you do manage to produce will reproduce less than their peers. And they will continue to pass on that that sort of slightly bad mutation until eventually it is eradicated from the population by one reason or another. It might simply be misreproductive opportunity. So if it is even remotely bad, selection acts against it. That's just how it is. If it's neutral and when I say neutral, I mean truly neutral, they can accumulate all they want. Nothing is going to happen. There's nothing to select against. That's the definition of something that is neutral. There is no good or bad kind of impact to it. Now, what you might have in sort of your best case scenario is if an entire group of organisms all get bad mutations at the same time. And as they build up upon one another, they sort of have I think it's the static sort of impact on where they build up and it makes them subsequently worse when they combine with one another. But the problem with that is the definition of genetic entropy and of error catastrophe means that it has to accumulate across generations. Regardless of whether it's at the static or not, the negative mutation will hit the second and negative mutations or negative selection, selection against sort of this this trait will happen. The second fitness is reduced one way or another. That's happening in one generation. So there is no plausible way to suggest that error, catastrophe or genetic entropy can occur because it is the accumulation of bad mutations across generations that eventually harm fitness. We don't see that ecologists have tried understanding error catastrophe because cancers and things like that aren't error catastrophe. They're similar in ways, but again, it's not cross-generational. So understanding it would be quite helpful for fighting those diseases, but they can't do it because it's not a phenomenon that occurs. Sanford, I believe claims that happened with H1N1, but I read that paper. Not only is it a bad paper that actually makes several mistakes, but it swaps its definition of error catastrophe around whenever convenient. So essentially, my answer to your question is there is no such thing as genetic entropy. We don't see it naturally. We don't see it in a lab, even though we've tried. At least the definition that creationists give. So it's not a problem because it's not real. Got you. Thank you very much. And, Stanley, for truth, I know that you probably have another round in the barrel. But just for the sake of it, we can always do the tiebreaker debate. We can do an end game debate. We should call on that from now on, like the trilogy end debate where we have like the final of three. So we definitely can do that. But I do just want to make sure that Erica gets to sleep on a decent, hopefully a decent time. Sweet, it's no problem. The conversation flew by. It was a lot of fun. It's also because I'm tired. Now, next up, Steve is Dean. Thanks for your super chat. He says, Stanley, for truth, cannot be stopped. He's a beast, Spongebob. You have a fan out there. That is far too sweet of Steven to say. I obviously paid him to say that before the debate. If you could read a couple more super chats, I'm running upstairs for literally 30 seconds, James. Deal. Steven Steen, that sicko also says. James is the new Adam sent from God to fix us soy boys, flawed genes and restart the human race without flaw or weak jaws. I've heard you are an alpha Chad. I've heard that from from other people. That's hilarious. An alpha Chad. I had never heard that before, but I like that. We'll call Steven alpha Chad for no one. Let's see. Bent Hovind. No relation, it says in the name says Erica. Says Erica and Dapper Dino should debate standing for truth and Kent Hovind at the same time. I'd be down for that. That would be epic. We do be fun. We actually, oh, I forgot to mention, so we do actually it's coming up quick. We do have as you see in the bottom right, Kent Hovind will be returning. We had a we got off on the wrong foot one day and I will take responsibility for it. And long story short, we for a while, it looks like we weren't going to have Kent Hovind on anymore, but Mark Drisdale convinced him. So you see Mark in the picture there. He on the left side, he looks kind of like an action hero star. The bald head and the goatee. He has convinced Hovind to come back on. So that will be a good one. But you don't want to get you don't want to get on Kent's bad side. He'll ban you from dinosaur adventure. That's true. So it's also Genesis and cosmology. A discussion will be going on this coming Monday with Skydive Phil, popular YouTuber, really, really pleasant guy, and also Dr. Jeff Zwerink. So that's going to be a really fun one. That's one that we've had planned on two different dates because I was just, I don't know what was wrong with me. It's the first time I had ever wondered like, oh, my gosh, is there? I mean, like really wondered. Is there something wrong with me? Like I really thought so they contacted me. They called me. They're like, James, it's not today. And I was like, oh, no, you're right. So long story short, glad you're back standing for truth. I could hear you really wondered that once. I wonder that every day. Yeah, well, that's thank you. I appreciate that. And standing for truth, I think I could hear you cackling in the back. You must be back. I'm back, my friend. Got you. Thanks so much. So I wanted to take myself known. You betcha. Let's see. Michael Dresden with his normal trollish super chat says, I'll save you all. The time evolution is a myth. You can respond to that, Erica, or you can not dignify it and ignore it. I can't respond wrong. Gotcha. It's short and pithy. I like it. Speed of sound of gravity. Who says, by the way, he said that he or she said standing for truth. You are afraid to debate them. So they said standing for truth. Buck, buck, buck, buck, buck, buck, buck, buck, buck, buck, buck, buck, buck. You know, you know, speed of sound sends his regards standing. He says he wants a rematch. So, okay. So and that's funny. Erica mentions that. So I've had two debates with speed of sound. So definitely over two hours, maybe two and a half hours of dialogue. We debated the same topic that Erica and I just debated and a topic specific to chromosome two fusion. So I recommend anybody go look at those debates. I suspect he only wants another debate because of something called damage control. You know, he knows he lost, but you know what, Mike, maybe, maybe one day I'm going after the big dogs now, though. That's what they call me. That's right. Jay Shai, thanks for your super chat. Said, what if there were people outside the garden whom evolved then made it with Adam's descendants still making Adam and Eve our genealogical ancestor? Cain hints to other people who might kill him. So. Standing for truth. Well, I would say that we don't even need to go that far because the Bible tells us we came from just two people, Adam and Eve, of course. And if you just look at my opening, I went over the fact that we've got these pieces of DNA, for example, the Y chromosome DNA, you know, the Y chromosome we only get from our fathers. And it's passed on, unbroken from from father to son. And every once in a while, a mistake happens. And every time this happens, a new branch in the family tree is formed. So all we have to do is look at all the branches in the world, James. They go back to a single person, not to a chimpanzee. OK, and that's what this debate was, limited ancestry versus universal common ancestry. But to a man who lived just a few thousand years ago, and the same thing goes with mitochondria leaves. So we can just believe the Bible. And when we start with the Bible, as it's just plainly understood, we can make accurate predictions and retrodictions. Gotcha. Thank you very much. James, if I can make a recommendation for some reading for that individual, they should check out John Walton's series because he actually subscribes precisely to that with the question asker was talking about. Sort of like a theistic evolution type thing. I've read some of his work. He's just he's an academic. He seriously knows what he's talking about. I'd give it a look. It's pretty interesting stuff. Gotcha. Thanks so much. And next up, stupid whore energy as she likes to call herself. Very sick. She says. I haven't heard from her in a while. That's right. She says, new genes can arise from non-coding sequences. That's why orphans are not a problem. Right. So it's just as I iterated earlier, it's called de novo gene synthesis. And I don't want to beat a dead horse, but just go back and watch the discussion. It is a circular based argument. It's never been observed that these non-functional, non-coding DNA regions are suddenly co-opted to have an important functional role, but orphan genes in general, they are taxonomically restricted. They are functional and they do suggest, along with many other lines of evidence, that limited ancestry is true, because there's so many lines of evidence that the evolutionists have a major problem explaining other than weak rescue devices, in my opinion. Gotcha. Very sad. Go ahead. As a question sort of for standing, what do you make of all the astrological phenomena that we draw ties to, despite never having actually laid eyes on them in person, like black hole physics or supernova or novae, I guess, neutron stars, things like that. We just get data, we just get readings, and we formulate entire hypotheses about them that then are confirmed by other data that we receive. So you don't have to be a direct observer of something to know that it happened. You can see the aftermath and get the same idea. That's where a lot of science goes. I agree. I mean, you can have all types of hypotheses. Those hypotheses have to have supporting evidence. The evidence has to be demonstrable. It has to be empirical. So some of the things you just mentioned are demonstrable and the inferences that are made are based on really tight, scientific based evidence. But when it comes to like the Y-chromosome dissimilarity between chimps and humans, we didn't talk about that. And I researched that this time and I was ready for that. We didn't get to talk about it. Well, remember round three endgame, Avengers style. Listen, eventually I want an age of the earth conversation, OK, I want to or we can talk about anthropology again. I don't like being out of my element. I enjoyed the human evolution debate and now we did one on this topic. So yeah, maybe the next one can be age of the earth related or looking forward to it, put it that way. Very juicy. Mike Billers, thanks for your super chat. They asked Ken Stanley for truth, reexplain Erica's explanation for orphan genes and maybe stop using it in the future since it's explained. Well, I know the answer to orphan genes that is given because it is a major problem to evolutionist theory is de novo gene synthesis. I can't remember if that's the argument that Erica used, she, I guess, looked to endogenous retroviruses, for example, and the functions that are now been found in these so-called ancient viral elements have been co-opted. It just comes down to the fact that are these anything more than just stories, rescue devices? So I understand the I understand the arguments put forth by the evolutionists. I just don't see them as being very convincing. Gotcha. Thanks very much. Moving quickly, Josiah Hansen, thanks for your super chat. Ask Erica, protect your hand when giving such a spanking. Very nice. Gotcha. Excellent. Let's see. Next up, thanks for your super chat from Florida man. Edo, hypno toad evangelist. Appreciate it. Bless. Blatant blessings on you. Gotcha. Thank you very much. Let's see. They're asking you one second. They asked, why can't creation answer the phylogeny challenge? I'm guessing that question is for me. I would say that the that the phylogeny challenge is is fallacious because it all comes down to, you know, where can we draw the line regarding ancestry? Where can we where does that phylogeny break down? But the thing is that entire argument misunderstands biology and genetics because and theology because they seem to imagine that God created humans and then all of other by all of other, you know, biological life and that there's absolutely no similarity between humans and any other species out there. So based on the biblical model, there's really no reason for us to believe that that's true, as in, you know, there should be no type of hierarchy in the biological world. As in, you know, there's no reason to believe that we shouldn't be more similar to, say, apes than to another species, say a whale, right? So we, too, predict nested hierarchies in biology, whether it's on an anatomical level, physiological, morphological nested hierarchies. So that's why I always say we need to look to differentiating kinds of evidence to show which explanation, limited ancestry or universal ancestry is true. And that's where we can get into function. We can get into why chromosome, mitochondrial DNA, predictions. This is how we're going to truly answer the question of ancestry. So a long story short, the phylogeny challenges its fallacious and it's based on a misunderstanding of science and theology. Hey, James, can I answer this one, too? But just from my side, I think the best the best question that I've the question that I have for creationists on this one, of course, has to do with primates because I love primates and I am a primate. But frequently, creationists lump all the apes into an ape kind. And my question kind of runs along those lines because frequently, a kind is described as things that bring forth things, organisms that can bring forth with one another. But chimpanzees obviously can't reproduce with gorillas or orangs or well, they can with bonobos, but they're actually very recent divergence. And there's been slightly disturbing, but a bit of sort of theoretical research looking into how reproductively compatible humans would be with chimpanzees. And it's more than it is with gorillas. And it's not actually been considered to be impossible as terrible as that sounds. It's it's simply a ring around the egg, the zona pollucida that sort of gate checks any spermatosomes or sperm in general that try to come in. So reproductive isolation is kind of a bad way of drawing the line, which is why I always ask why and how we draw it. And that's why I don't think they can answer the challenge, because there is no way to draw a line. Genetics is is a gradient and it runs through all living things. And that's why paternity tests work. And that's why, you know, genobic comparisons work. Well, if I can make just just one quick point, if you just think about it, Erica, OK, according to our model, I'm just going to throw some, you know, kinds out there, say humans, pigs, rats, ducks and dogs, they're all land-dwelling. OK, even though they are separate kinds, according to our model, since they are all land-dwelling and share many similarities with each other, they can share similar nested hierarchies or designs. So where are we going to draw the line between those separate kinds? If they already share certain levels of nested hierarchies, morphologically speaking, genetically speaking, physiologically speaking. So that's the thing. That's a fancy way of saying you can't draw the line. That's a fancy way of obfuscating that the line can't be drawn. And if your model is correct, then the line should be able to be drawn because it is, I mean, of all the things in Genesis that are like Genesis one that are like super clear, there's quite a bit of emphasis on the kinds that's repeated over and over and over again. You would think it would be quite obvious. Well, even though we predict nested hierarchies, evolutionists, when they say that there's this perfect nested hierarchy, there's this perfect phylogenetic tree of life, that's not actually true because any time there's an inconsistency, Erica, and say a lack of uniqueness in that phylogenetic tree, as you know, it's usually explained way by what, convergent evolution. So that's a rescue device. There's also something called independent lineage sorting. If you look at different genes and say humans or apes or gorillas or orangutans, depending on the gene you're looking can create a totally different type of phylogenetic tree. So even though you're implying that there's this perfect nested hierarchy of life, that's not true. There's many, many types of inconsistencies I can point to. Yeah, but the thing is, is the the inconsistencies are while present, they're present in every branch of science, from medicine to astronomy to, of course, evolutionary biology. That's the nature of the beast. The question is how strong and how parsimonious are the lineages that we do have these straight through lines? And the answer is incredibly. Obviously, I know Prim, it's the best. It's that's it's undeniable from my position. I mean, but that's just me. You have to say the truth, I'm sorry, but just to get through more questions, we have to like jump through number three. Yes. Dapper, Dino, thanks for your question. Asking to both, are you familiar with the observed de novo emergence in Drosophilia or sacramyces? Yeah, so the fruit flies, for example. Read that paper for why it's done in the lab. It's also inferred. And what they've done in the lab is they've forced these orphan genes out of the genetics of these fruit flies. So he's trying to say that this is an example of de novo gene synthesis. When all it is is an example of a loss of orphan genes, which can be which can happen, obviously. So I want to see an example in real time, not in the lab of de novo gene synthesis and not just an example of an orphan gene being lost. I mean, that's how would you even do that, though? How would you see the emergence of a de novo orphan gene not in the lab? Like you're not going to like, I don't know, maybe you follow like a like a colony of Drosophila around with a net and you catch him every couple minutes. And then you do do some genomic sequencing to find out. I mean, I don't know how you would even go about doing that. It's an impossible experiment. So are you admitting that it's never been seen? No, it has in the lab, but you would just ask for it outside of the lab. So you can't do it. It hasn't been seen in the lab. I just told you that all that was seen was the loss of orphan genes. That's not the gain of orphan genes, Erica. Hold on. Hold that thought. I'm not sure. I let me pull up this paper. James, pull up the next question, if you would please. Yes. Next up, thanks for your super chat. Pax Americana asking, staying for truth, even early church fathers, such as St. Augustine knew that Genesis wasn't a literal account of creation. Why you see isn't even theologically sound? Yeah, technically, if you look at what the plain reading of the Bible is, if you look at church fathers, quote, unquote, throughout history, the majority of them did believe that the geology of the earth was explained by Noah's flood, Ponscum to people evolution was not heard of. But the most important thing is we can just look at a plain reading of scripture and we can see that God created Adam and Eve and we can also make predictions and retro-addictions in the science tells us we come from a white chromosome, Adam, a mitochondrial Eve, the human species overall has low genetic diversity, which points directly to Adam and Eve. That's why the evolutionists had to resort to the out of Africa population bottleneck theory. I mean, Erica and I discussed that thoroughly in our previous debate, but a plain reading of Genesis clearly is consistent with empirical scientific data. So looking to the Toba catastrophe, if you would standing, that's one of the primary explanations for the bottleneck that there's quite a bit of evidence for. Right. And I did. And it looks like there's no major consensus on whether or not this Toba volcanic eruption is resulted in the population bottlenecks. There is, I believe, some sides in science that believe there's some inconsistencies with that theory, while others hold to it. So I mean, that would just might be a discussion for another debate. Yeah, I think I think that it's best explained with a combination of that and founder effect from populations leading Africa. But that's just me. Just to move through as fast as possible. Jay Shy, thanks for your super chat. They said, Francis Collins, a Christian, mapped out the human genome in this convinced of universal common descent. Why didn't this lead him to your conclusion? I think that it's he's asking Stanley for truth that. So he looked at actually, can you repeat that real quick? They said, Francis Collins, a Christian, mapped out the human genome and and is convinced of universal common descent. Why didn't this lead him to your conclusion? Standing for truth. Good question. So Francis Collins, I definitely recommend his book, The Language of God, the major arguments he looks to, for example, you'll see him speak of ancient repetitive elements, the non-functionality of our genome, shared genetic mistakes, for example. But he's had to actually go back on a lot of that because he's one of the scientists who has admitted that encode has revealed that much more of the genome is is functional, that the genome has many more functional DNA elements than previously thought. And even Richard Dawkins has had to go back on that. I mean, he's the one who quoted and I don't have it right in front of me that over 90 percent of our genome may as well not even be there, implying that most of it is useless. Yeah, Richard Dawkins, just go knock out that 90 percent of the genome. So it's just based on an evolutionary bias. But yeah, Francis Collins, I'd recommend reading his book and all his best evidence for universal common ancestry has been completely overturned, just like the junk DNA paradigm has been overturned. Got you. That 2017 paper disagrees with you, though, standing. That one doesn't quite agree that 90 percent couldn't be knocked out if we're dealing with the 10 to 12 range, which is pretty, pretty typical. I'm sending you a paper standing. I think this is the one that was being discussed. Go ahead, James. Sorry. Gotcha. And then let's see. Kevin Trembly, our friendly moderator, if you can do any favor and only we usually only time people out or delete their messages if they are using hate speech. So even if they're I mean, if they're abusive, like, please ask them why they're being abusive towards somebody, but in other words, they try to discourage them. But we usually try to only delete or ban people if they're engaging in hate speech. Next up, Mr. Archaeopteryx, standing for truth, an amoeba genome is 100 times bigger than a human's, does an amoeba need 100 times more information? Or is most of it nonfunctional? Well, amoebas looking at an amoeba genome is a lot more different than, say, testing the genetics of mammals, humans, specifically, which is where we're making the direct predictions. But organisms like amoebas, yeah, they are subject to whole genome duplications. Also redundancy, you know, and in a lot of these organisms that do have two or three or four times the amount of genetic content than, say, a human may just need more redundancy for environmental conditions. So I mean, epigenetics, environment all play a factor in in our assessment of the genomes of all forms of life. So, yeah, amoebas, you know, they are subject to whole genome duplication. So some of it could certainly be nonfunctional. Hey, James, real fast. For those of you who also want the paper that I just sent standing, it covers the orphan genes quite well. There's some excellent sources within it covering orphan gene emergence, which I believe I didn't get a chance to read the entire thing, but it's sort of alluding to the fact that this has been observed in the lab, not positive. Don't quote me on that. Side note, it was I also had the chance to briefly look, hold on, pause, I'm pulling it up, look at my email. And I had a message from CallMeEmo who brings up an excellent point that I wanted to post to standing very briefly. I think it's if that's OK with you, James, it's very short. Yes, yes, I've seen his argument and we've we've well, I'll ask you the question because it's quite short. He he brings up the an excellent point that I didn't even think of. But so am I debating Emo now, too? Well, I saw I saw where I was. I mean, some arguments against what you said. OK, go ahead. Yeah, what's I listen, I just think it's a good point. It's not my point. So that's by far enough. But I did think it was quite good. He brings up the fact that orphan genes, if even within kinds, vary wildly from species to species, which would support de novo origin far more than sort of a taxonomically restrained limited ancestry. Well, he assumes that those orphan genes are found within kind. So, for example, you can find orphan genes that are taxonomically restricted to humans, gorillas and chimps. But he's assuming that gorillas and chimps are of the same created kind. That might just indicate that they are three separate created kinds. And the paper that you posted on the fruit flies, for example, we have an article in our book, Rahm Adam, myself debunking that. What they did technically was they forced adult males to reproduce with infant male females to get rid of their orphan genes. So it's unrealistic in nature and therefore irrelevant to the entire argument. Like I said earlier, I hate to say it, but if you think that that's unrealistic in nature, I've got some bad news for you. There is a lot of weird sort of sexual crossings across adult juveniles in various instars with arthropods. Arthropods are extra weird. But but yeah, it kind of busts up the point that you made previously, though, that that because they're taxonomically restrained, they are the ones to dictate what a kind is or isn't. And I'm saying it's I'm saying it's it's a line of evidence that can dictate what's created and what's not. And that can actually dictate to us that humans, chimpanzees and gorillas are all of separate created kinds. But the thing is orphan genes are very specific. For example, we have noticed that all taxonomic restrictive orphan genes and say felines or the dog family correlate perfectly with what I'm saying. So right here, we've identified a feline kind. A dog kind, a human kind, a chimp kind and a gorilla kind. I mean, yeah, that's that you got unrealistic. You're going to tell me that chimps, gorillas and orangutans are separate kinds, but that every feel it and every dog is within the same kind. That's wild, dude. That is like out of this world. The orangs and orangs and gorillas, really gorillas and chimps diverged incredibly recently, even in a blue shirt. Yeah, we do have to be really short and pithy here. Yeah, you can you can you can finish up staying. Sorry, I keep inciting things, James. I'm I like interaction during the Q&A. It's fun. It's fun. OK, got you. Thanks so much. Next up, appreciate your question. Speed of sound of gravity asks Sandy for truth. What H3K4 ME1 in Tompkins graph graphs indicate? Histone methylation signatures. It's indicative of active gene promoters in transcription. He's trying to stop me, but I would recommend going to watch my debate. He's really good in genetics, so I've enjoyed my debates with him. But I got to be honest. He didn't do quite well against me on chromosome two. We discussed it for an hour. It was a good debate. He's even admitted in one of his hangouts with some evolutionists that he was blindsided by some of my arguments. So, you know, kudos for him to trying, you know, in trying to stop me there. But sorry, Speed of Sound, you failed, man. Next up, appreciate your feistiness. Appreciate your question from Terry James, who says if creationism, quote unquote, predicted nested hierarchies with disproving nested hierarchies, falsified creationism, or would you take this as evidence against evolution? Well, like I said, there are inconsistencies with the phylogenetic tree of life. That's why they need to look to convergent evolution, for example. I mean, you can see evolutionists invoking convergent evolution, which shows that this so-called phylogenetic tree of life is not as it doesn't flow as well as they say it does, because you can even look at an example that at the top of my head, let's say whales, dolphins and bats, for example. OK, they're the only mammals that have echolocation systems. And maybe Eric has an answer to this, I'm not sure. But on the basis of gross anatomy, the whales and dolphins, OK, they're classified closer to the cow and other ruminants than to the bats. But on the basis of their echolocation systems, they should belong with bats. Now, it gets even worse for them because molecular analysis of the protein Preston puts whales and dolphins squarely. Seventy percent of women stated that anyone in the audience who doesn't know Preston is a sound sensitive protein and it's essential for hearing in general. So it's just one of the mechanisms, hearing mechanisms of the echolocation system. So this plus other lines of evidence I can go into is strong evidence that the phylogenetic tree does not represent objective reality and should. Yeah, it should falsify universal common descent. But we do protect some levels of nested hierarchies. So that's my answer. Thank you very much. Senator Ferriero-Cirabia, thanks for your question. And they asked, Erica, how does a random evolution process create symbiotic associations? How does nature, quote unquote, select anything to work with another being in ecosystems? That's a that is a fantastic question. And I think that that is is quite intuitive because you would think that that would be somewhat of a complicated process. But symbiosis has been happening from an evolutionary standpoint from the very beginning. I mean, we have the endosymbiot or endosymbiot theory or hypothesis rather, which is that quite a large a large cells for phage another smaller cell. And that's how you get the mitochondria. But the truth is that it's close, loose associations that then have such a fitness benefit for these two organisms being in close proximity to one another that it actually becomes more beneficial for them to stick together than to stay apart. We've seen this recently in certain species of primate use, for instance, verbit monkeys, they can actually rely on the predator calls of starlings. Now, that has been a recent adaption in many locations. Now, of course, it's location specific because, you know, symbiosis does take a long time, but that fitness benefit of being able to utilize a starling call to know whether a predator is around because they have a better vantage point has has popped up somewhat, you know, in the distant past, and it's actually led to some really interesting conservation methods where they teach verbit monkeys how to respond to starling calls and they actually spend more of their time, you know, kind of making their sleeping quarters near starling nests because of it. So that's that's basal basal symbiosis. But that's how it happens. It happens with loose associations that through time become cemented. And that's what I got to say about that. Gotcha. Thanks so much. Appreciate it. And we do have another question from stupid whore energy who asks, actually, she says, actually, slightly deleterious mutations are responsible for neutral constructive evolution. I think that's for you standing for truth. Right. I'm glad she brought that up. I mean, that's exactly what I was iterating earlier in the debate. You know, they assume these neutral mutations build up in the in the genome and they're almost used as a reservoir for change in adaptation and in forward evolution. So that's based on an assumption. What we now know about the genome and as Erica and I discussed during the during the debate, most random changes contradictory to the evolutionists are going to be deleterious. But even if, like I said, Erica, even if the 90 percent of the genome is perfectly neutral junk DNA as stupid whore energy is insinuating here, that means, and Erica didn't answer this problem and I don't think anybody can, that means 10 harmful mutations are still arising in every person, every generation. So even the most fit individuals are still more mutant than their parents. And you can have any kind of selection all you want. And it's only going to amplify the best and get rid of the most detrimental. But we are going to degenerate. Gotcha. Thank you very much. Just to keep moving, Mathew J Disco says standing for truth. Where does the simp gene come from? The simp gene, if it's if it's a like many genes, for example, if we look at allele frequencies, whether it's rare or common ones, they can arise, say, close babble, depending on their frequency in the... I'd have to know exactly what that simp gene does. Got you. I'd have to have clarification. Do you know what that gene does, Erica? New to me. Again, to reiterate, genetics is not my field. I can speak with a decent amount of authority with primates and with human evolution, genetics. That's why I had notes. I would say that the majority of our genome is created heterozygosmine. But there are some alleles that have... There are some mutations, for example, blue eyes. That's based on a mutation, according to our model, post babble, post flood. But we can determine that based on allele frequencies around the planet. So I'd have to know exactly what that does if it's a mutation or if it's created. It's one of the two. Gotcha. Appreciate it. Next up, appreciate your super chat from Jay Shai, who says standing for truth forgets we have recombination. Yep, recombination occurs. But recombination is no help to forward evolution. I mean, recombination and gene conversion, for example, those are a couple of mechanisms that we look to in our created heterozygosmine hypothesis. That's actually going to create diversity quickly, especially if the DNA differences are built in from the start. It's kind of like shuffling a deck of cards. I mean, you're going to have diversity in every single generation. That's why two people can technically have millions of children and every single children are going to be different. No two children are going to be absolutely identical. And that's because they're heterozygous. And like I said, in my opening, that would be optimal design. Yeah, that's all I have to say about that one. Got you. Next up, thanks so much. Sidgifrogous Arabia, who asks Erica, is genome degeneration real? If no, what evidence can you give going against it? If yes, what evidence can you give that deterioration of ape DNA doesn't follow the same degeneration before evolving somehow? So the problem with the problem with this concept of degeneration is that it depends entirely on what on what this individual is talking about. This is a reference to degeneration, at least in the form of genetic entropy. The answer is selection always selects if it's not neutral. Even if it's partially bad or partially good, selection still occurs. It just might not occur as quickly as far as variations in how selection works and other kind of genetic concepts like mutation and things like that. Mutation is not constant. It's it's not constant in a single species through its lineage and it's not constant further throughout and into other species lineages either. Chimps have a 30 percent higher mutation rate than we do. And orangs and gorillas actually have a 40 to 50 percent faster mutation rate than us. So accumulations of any kind of mutation are going to vary depending on the species and depending on how far back they diverged. Now, again, I'm not 100 percent sure what what they're asking with regard to genetic degeneration, but if it has anything to do with genetic entropy, there is no way natural selection doesn't select. That's it's not an entity. It's just literally response stimulus with the environment. There's no people like to say that evolutionists use natural selection as like a god, but that has nothing to that there's no it doesn't follow. It's a non sequitur or natural selection is simply how an organism interacts with its environment on a genotypic and a phenotypic level and the changes that occur based on sort of a combination of chance and fitness. Gotcha, actually, if I can say so, no, no, no, no, no, less than five words, less than five. Okay, less than five words, go. The problem is oh, that's three natural selection acts on phenotype and not genotype. And I'll just leave it on that. Tioga, thanks for your question or a super chat. They said, I stan, Erica, my biology queen, all in capital letters. My God, you've made it worth staying up this late. That is a lovely compliment. Very nice. Subtracted. Thanks for your super chat as well. They say, hey, standing for truth. If Adam and Eve didn't know they were naked, how was Adam aware that Eve came from his rib? Genesis 223, you need to be naked to see your ribs. I'm going to have to think about that one. Obviously a theological based question. But how did Adam not know that Eve came from his rib? Wasn't God, didn't God put Adam into sleep when he took his rib? Maybe you don't even out of it. I don't know. I'd have to think about that one a bit. Gotcha. Jay shy. Thanks for your super chat. They said X and Y Adam were separated between 30,000 years. Right. So I was hoping, well, I figured we would get into the discussion on mitochondrial Eve and Y chromosome Adam. But based on observed mutation rates, the empirical method, trio studies, for example, we can use pedigree based studies. Adam and Eve only lived just 6,000 years ago, but evolutionists have to counter that by using unobserved and unrealistic mutation rates. So they don't use the empirical method when it comes to mutation rates. So yeah, realistically, you can look at the studies and look at how those dates are derived and they're really, really heavily based on evolutionary assumptions. Gotcha. Thanks so much. Almost there. Let's see. Situatorist Robby, thanks for your super chat. They said, standing for truth, is a platypus a kind of mammal or bird? Or bird? Yes. Because of the bill, I guess. I would say platypus defies evolution. I mean, what did the platypus evolve from? It looks to me like the platypus is of its own separately created kind. I know there's, I'm not sure if there's a universal consensus as to the history and the ancestry of the platypus, but yeah, definitely not a bird kind. Gotcha. Appreciate it. Next up, appreciate your super chat from stupid whore energy strikes again. She says two transposable elements in humans and chimps at the same genomic locus means the original insertion was in the ancestor because there are tens of thousands of possibilities for a TE to insert itself within large genomes. Right. So these, these TEs, which as he iterated stands for transposable elements, but they are an important source of highly, highly regulated. They're biochemically active. They are non-coding elements, but they are important in transcription factor binding sites and in non-coding RNA. So they are, they are pervasive in the genome, but they're also functional. So based on their position and location, that's predicted based on our nested hierarchical expectation based on similarities and dissimilarities. But the fact that they're functional DNA elements, just like the endogenous retroviruses, the ALUs, that's exactly what we've predicted all along. Gotcha. Appreciate it. Next up. Stupid or energy. Thanks for your super chat. She said neither Dawkins nor Collins have commented on encoding or encode. Yeah, encode project. Yeah. Gotcha. Well, they have both of them that have commented on it. You what? I didn't hear that. I've got quotes from both Collins and Dawkins that have commented on it. Actually, you've referred to the CRISPR debates I've had many times. I've quoted Collins many times on encode and junk DNA in general, and CRISPR had had no objection to it. I mean, I'm not sure where. I don't remember. I can't comment on it. I don't know. Got it. Actually, I've got a quote from Richard Dawkins here. He had a book in 2009. What he said was it is a remarkable fact that the greater part of the genome might as well not be there for all the difference it makes. Then after encode in a debate with, I believe it was Jonathan Sacks is his name. He said regarding encode, he said, I know there are some creationists who have jumped on it because they think it is awkward for Darwinism. Quite the contrary, of course, it is exactly what a Darwinist would hope for to find usefulness in a living world. So you see that he's kind of embraced the encode result. So I mean, there's a there's a couple quotes right there for you. I don't know that that's embracing it. That's embracing the work that they've done and and perhaps being open to the idea that there's more functionality than previously thought, which you're right, there is. But the question is how much and you got it. I'm telling you, current literature, you got to stick with it. Gotcha. We appreciate it. Next up, folks, thanks so much for all of your questions. It's been a true joy. We are going to wrap up just to let Erica get some sleep as she is in London. And so let's see if I remember right, huh? You're the you're more tired than I am. Yeah, that's really true. I am impressed. Go ahead. We're going to get to our debate, Erica. Now, this is child's play. I stay up the site. Listen, I'm I've been writing with the same project proposal for months. I have to stay up later. I get nothing done. Gotcha. Something called coffee. Erica says you're a beta if you're tired already. So thanks so much. Yeah, you're a virgin data and I don't what is it? Virgin beta cuck is that the phrase? Very glad. Thanks so much. You're the first person that's ever said that on our channel. We appreciate it. Oh, good. I'm really glad to hear that. That's my claim to fish. A lot of triggered people out there right now. I appreciate that. That is good work, Erica, and to trigger. That's what I'm here. That's right. I like that. That's why we have you actually quick question. I just caught a glance in the chat. And somebody was saying that I need to address. Erica's L. M. N. Did you bring up? I don't think we discussed that in the. Yeah, so I mean, there were. I think I brought it up and I was like, let's maybe discuss it. And but then I don't think we actually we can do that for a third debate, but it wouldn't be fair for me to jump to that question because there were a lot of other questions before that question and it technically, I don't know if it was originally put in the form of a question, but we so I can't jump ahead of that one, otherwise it'd be kind of cheating everybody else who was in line first. Actually, from what I recall is during the discussion, we were not going to talk about it. Standing for truth. I appreciate it. However, we are not going to. I don't want to just ignore all the questions that came in before that. So there's just so many much. If you'd like, there's always a possibility for a third debate and like I said, I don't want to for all the people that asked the question before Jeremy at war, I don't want to just ignore there. So thanks so much folks for being here. It's been a true pleasure. Erica, what were you going to say? I think I could. I didn't mean to cut you off. I was happy to cut standing for truth off. But no, I was saying that you were master James standing go easy on James. He's exhausted standing for true. That's my old arch nemesis. But by the way, do want to mention folks very excited as if you didn't know already, I maybe mentioned it before, but in case you hadn't seen, we are pumped for the fact that not too far away. Actually, we do have a sweet event that we're excited about. If you enjoy standing for truth for some reason, we are pumped about the fact that we are going to have none other than standing for truth's father. He is going to be on shortly and that is actually none other than Kent Hovind or daddy standing calls him. So that's you'll see that on the bottom right. That would be the end game of their trilogy of debate. James, I could have gone my whole life without hearing that standing refers to Kent's daddy. Yes, James, you made that up. Okay, maybe made that up. He doesn't really, but, uh, but I might start telling people he does. So it's been fun folks. The both of our speakers are linked in the description though. So I want you to know folks, if you've enjoyed listening to them, I forgot to mention this up front. If you've enjoyed and you're like, I want to hear more, well, you can, I put their links conveniently down below in the description. They're waiting for you right now. Actually, just notice standing seriously. This is a coincidence. I actually, I haven't put yours in there yet, but I'm putting it in there right now. So do want to let you know folks, if you have, we do want to be open to topics. So feel free. If you happen to have any topics, please let us know as we do want to have more topics, new topics, new formats like tag team, triple threat, other things like it's, it does help us a lot. If people let us know like, Hey, I like this or I don't like this. So feel free to give us that feedback. And now standing for truth is officially he officially has his link down in the description. And so again, thanks. Those links of both Erica and standing are down in the description. If you've enjoyed and want to hear more of them and thanks for being here, everybody. Thanks so much for your questions. And most of all, we really appreciate standing for truth and Erica being here saying up late and debating for us. We appreciate you guys being here. Always a pleasure, James. Always a blast, James. You know that I'm looking forward to the next, the next debate. Always a true joy. So with that, keep sifting out the reasonable from the unreasonable everybody. We hope you take care and have a great night. We'll see you tomorrow with Tom jump and Benjamin Blake speed walk-ins debating the definition of atheism. So take care. We'll see you tomorrow.