everybody today we are debating creationist genetics and we are starting epic debate where at modern-day debate we host debates on science politics and religion and this one should be a very interesting one in particular this is a backlash debate what we mean by that is that Dr. Dan and Sal have engaged on similar topics within this ballpark before that's linked in the description if you love this topic and want to hear that in case you haven't already and so this is kind of in continuing battle on these topics and so it should be a lot of fun want to let you know though if it's your first time here consider hitting that subscribe button as we have many more debates coming up we are very excited about for example tomorrow it will be is the god of the Hebrew people immoral or evil that should be an interesting one and then Friday we will be will be back for a feminism debate feminism on trial as we have two female speakers that will be hashing it out that should be a lot of fun and also want to let you know if they happen to have any questions today feel free to fire it into the old live chat and if you take it with at modern-day debate it makes it easier for me to get every single question into that list for the Q&A super chat is also an option in which case you can make not only a question but a comment for the Q&A and it'll also push your question or comment to the top of the list and with that want to let you know we are very excited I will in just a moment so what I'll do is hand it over to Erica for the actual moderating I'll be keeping an eye on the live chat and also kind of collecting questions for her and I to alternate asking the speakers during the Q&A but I am excited to introduce Erica and then she will be giving Dr. Dan and Sal a chance to introduce themselves I want to first say thanks so much to our speakers and our comod all three of you thank you very much Dr. Dan Sal and Erica just for being here tonight it's gonna be a great time man nothing is more fun and coming on modern-day-to-date and like nerding out about science stuff I can't think of a place I would rather be with these two based and of course epic speakers to to chat about genetics I I'm very psyched and I hope everyone out there is psyched as well moderation it's a I've moderated before but not to the degree that we'll be doing today so I'm excited and I'm ready to go so Sal is gonna introduce himself first so once I once I forgive me for just one thing that I I would just have to be I have to say we are so excited about this Erica we I know that you you maybe don't like to be in the spotlight but we are so excited for you Erica's I don't think you've been on since the last time that you've been on this unique and special thing happened in your life we're very excited so I don't know you guys have heard so I have to say this folks we are so excited we are celebrating with you so I mean Erica I can I'll let you say it yourself because it's your special thing we're so excited for you James has put me on the spot but I did I am I'm very excited and happy to announce to the MDD fam as the youngsters say these days that I got engaged so there is indeed someone out there who in real life actually likes just like listening to me talk about like monkeys and stuff like that so it's great I'm very happy I you know I one of these days I'll drag him into the frame so everyone will have to feast their eyes on on the person that is on the guy that's gonna be my spouse so I've got good news Erica we may actually a lot of people don't know this we have at modern day debate we have our own journalists and it turns out that they were actually on your trip and they happen to well they happen to see this special event and so we as a way of celebrating with you Erica we we have to show that the audience this is really important so folks oh my god you may be surprised I have to show everybody has to see this so give me one moment as we switch over so this this is apparently what our journalists had found this is the extremely exciting engagement event we it's a small world I guess we were surprised I don't is that is this legal I don't but this is definitely not James but oh my god you have to say so congrats to both of you it's oh my god I could 2020 I mean anything I I get I can't believe you guys found out I mean was it was did you guys find out that the honeymoon was planned for dinosaur adventure land is that how this came to light that's exactly that's exactly what it was this is we just never knew it's it's crazy Erica but we're happy for you we are always there for you this is special I uh can I show is it okay if I show the real picture is that I mean okay well I guess yeah sorry no no I think that would be fine yeah you can you can uh let's let's like light doxin show I lightly yes it's I will I folks this isn't the real picture let me show you the real picture this is no it's no more jokes this one I will show you the actual picture it because it's such a great picture so let me just pull it up this is the real picture so and well Erica trust me that it's the the real picture I hadn't pulled it into zoom but I I just am we're so excited for you Erica so very exciting and really special I'm sure he's a terrific guy so we're just really excited for you and so with that oh my god oh I'm probably as red as my shirt good god we will be kicking it over now to Erica our moderator as she will be as I had said she will take the reins now and so thanks so much Erica and the floor is all yours oh well I'll do my best but I think I just had a pulmonary embolism just then so I'll do I'll work through it and do my best moderate all right let's let's get this show on the road I'm ready to I'm ready to talk some science and I'm beat red as it is so Sal go ahead to introduce yourselves to everyone everyone is uh let us know who you are give us a refresher oh thank you James Erica Dan thanks to our viewers I hope we can put some of you into nerd heaven tonight in this debate I'm Salvador Cordova and I'll be representing the Christian creations perspective I'm a former scientist and engineer in the aerospace and defense industry but presently do research and news reporting in the area of molecular biophysics I work directly for world famous applied geneticist and retired Cornell research professor John C Sandford whose work I'll be discussing tonight I also do computational and research work remotely for various labs and professors around the country some of my work focuses on the beta-lactamase nylonase family of enzymes and the post-translational modifications of the topo isomerase family of enzymes in cancer research I have five science degrees including an ms in physics from Johns Hopkins University and an ms equivalent in biology from both my professional work in addition to classes I've taken at the f a s graduate school at the national institutes of health where I had the privilege to study under the staff of top evolutionary biologists and bioinformaticians I used to believe in evolution I no longer do I self identify as a Christian creationist okay awesome all right Dan your turn everybody thank you for watching and especially thank you for the returning audience thank you for coming back for round two thank you again James for hosting and Sal for uh and Erica for joining us here so my name is Dan Stern-Cardinelle I'm an evolutionary biologist I have a phd in molecular genetics and microbiology and my graduate research was on viral evolution mutation accumulation and fitness effects so this topic genetic entropy is is right in my wheelhouse with with what I like to talk about so I'm thrilled to get going all right so with that I think we're going to launch into our openings now Sal's going to start off for us we've got 10 minute openers um and and I'm going to oof I'm going to crack down on that don't go one second over 10 minutes or you know you know how I am um so all right Sal let just whenever you start I'll start the timer and I know you've got a timer on that in too so uh we'll just hold each other accountable this is part two of a debate about genetic entropy and creneaceous creationist genetics some follow-up references to this debate are available at the website www evidenceandreasons.org even though the website is still built being built out the website does have further material about the issues laid out in this debate and more material will be added periodically to recap a bit the primary focus of tonight's debate is about the hypothesis of genetic entropy and secondarily about creationism the genetic entropy hypothesis was put forward by retired Cornell research professor John Sanford who is also presently my employer the primary claim of Dr. Sanford's book is that the human genome is slowly deteriorating with each generation Dr. Sanford was a Cornell research professor during much of his 45 year career as an applied geneticist the sizable fraction of all genetically engineered organisms were created through his inventions which helped feed starving billions his inventions are in the collection of the Smithsonian National Museum of American History Dr. Sanford was an atheist but at age 39 became a Christian and by age 49 had become a Christian creationist his knowledge of applied genetics contributed to his present belief in creationism and his rejection of evolutionary theory professor Sanford is among a growing number of scholars who are creationists but who attain prestigious scientific credentials for example professor of molecular biology change tan is an ivy league phd and postdoc from harvard and i'm going to be working with her so i'm excited about that rob statler is an accomplished biomedical engineer and scientist who whose medical devices have been implanted in millions of patients pictured here are a couple of first rate books by the individuals just mentioned in 2017 emeritus professor of mathematics bill basiner along with john sanford published in the journal of mathematical biology a corrected version of fisher's fundamental theorem of natural selection the theorem they proved is stated right there at the bottom this is a fragment of the proof of that theorem their article on the theorem set a record for the number of downloads of any article in the journal of mathematical biology's history this is all the more amazing giving given that it was these two creationists who set this record by publishing a mathematical correction to a long-standing theorem in evolutionary biology this theorem is part of a larger body of literature by dr sanford and colleagues that has advanced the genetic entropy hypothesis and other criticisms of evolutionary biology in peer reviewed scientific literature their article resulted in bill basiner becoming keynote speaker at this international biology conference in 2018 and also later that same year dr sanford getting invited to speak at the national institutes of health but independent of dr sanford's work consider some of the statements by top evolutionary biologists about genetic deterioration in humans michael lynch probably one of the most respected evolutionary biologists had this to say it remains difficult to escape the conclusion that numerous physical and psychological attributes are likely to slowly deteriorate in technologically advanced societies the incidences of a variety of afflictions including autism male infertility asthma immune system disorders diabetes etc already exhibit increases exceeding the expected rate this observational work may substantially underestimate the mutational vulnerability of the world's most complex organ the human brain because human brain function is governed by the expression of thousands of genes the germline mutation rate to psychological disorders may be unusually high at least 30 percent of individuals with autism spectrum disorders appear to acquire such behaviors by de novo mutation it has been suggested that there has been a slow decline in intelligence in the united states and the united kingdom over the past century my translation of this is we're getting sicker and dumber so how can darwinian evolution how can darwinism fail to arrest this problem i'm going to illustrate it suppose 20 of a population acquires new mutations slight birth defects in each generation now let's suppose we have perfect selection and it eliminates 20 of the population that are mutants and i'll illustrate that by invoking the terminator and he's going to say hasta la vista baby and he's going to eliminate one of the mutants and sayonara muchacho and he's going to eliminate the other mutant and what remains are the uh the survivors are free of mutations and they are uh become parents of the next generation so that's one scenario what if we have a scenario where all the offspring have new mutations they have some slight birth defect that their parents didn't have a defect that may not be noticeable uh outwardly but it is a slight defect in their genome so how what will happen in this scenario well we certainly can't uh perfect selection would wipe out everyone and that wouldn't be good either so what is the recourse the recourse is we have imperfect selection where we just take out maybe the worst but the remaining still have some slight defects the species survives but each generation is dumber and sicker so this is a problem this is not a creationist theory this is something that is recognized in evolutionary biology as illustrated by this observation by dan grower in 2016 he said the genome of each human newborn carries 56 to 103 point mutations that are not that are not found in either of the two parental genomes if 80 percent of the genome is functional as trumpeted by encode project consortium 2012 then 45 to 82 deleterious mutations arise per generation and he observed the consequence of this and his talk in 2013 three problems if the human genome is indeed devoid of junk DNA as implied by the encode project then a long undirected evolutionary process cannot explain the human genome if on the other hand organisms are designed then all dna or as much as possible is expected to exhibit function if encode is right then evolution is wrong and we'll talk a little bit more in this debate about the encode project consortium it was so far a 500 million dollar project by the national institutes of health so let me illustrate the problem again assuming we have let's say I'll just pick the number since he mentioned 82 mutations that's supposed it's 80 mutations there's some parameters here we could talk about that shows why this little simplification is valid but suppose a generation zero we have this parent free of birth defects and that parent has a child with 60 mutations and has even more children but on average all the children have about 80 mutations so even if we had perfect selection and wiped out well the parent passes away and perfect selection comes along and wipes out the worst but even the best of the worst of the defective children survives and has mutations and becomes apparent to the next generation so we will repeat this process and it should be evident that as Dan grower said if we have a mutation rate of 80 per individual per generation there'll be genetic deterioration and all i'm doing is illustrating this so parent dies and we have elimination of the worst but still even under survival of the fittest the genome keeps deteriorating and i'm just going to keep repeating this and you could see the number is increasing this is something Dan grower observed I know I have a minute and a half and i'm almost done so fast forward to million generations we'll have a million mutate 60 million mutations at that point and this one solution to this problem was proposed by Susumu Ono this was understood by many population geneticists that we cannot tolerate too many mutations so they said one solution to this is to invoke junk DNA and he said there seems to be a strict upper limit for the number of gene loci which can we can afford to keep in our genome consequently only a fraction of our DNA appears to be appears to function as genes and i'm going to skip a little bit it then follows that the moment we acquire 10 to the 15 loci the overall deleterious mutation rate per genome becomes 1.0 which appears to represent an unbearably heavy genetic load and so that's an archaic version of what Dan grower was saying Dan grower had it more up to date and i'll close my opening with this why was the junk DNA hypothesis postulated and my answer is the idea of large amounts of functional DNA is incompatible with evolutionary theory and i think that sets the lines of the debate for this evening and i'll yield the floor to my distinguished colleague uh professor dan stern cardinal thank you all right okay thank you sal i i really liked those little uh nuclear explosion animations i'm always a big fan of uh animations being incorporated into things um so dan you're muted right now so you want to unmute yourself first so we can hear that's how i do thank you there you go all right so dan when you start talking i'll hit the clock all right just want to check two minutes if that's all right just want to check um you should be able to see the powerpoint slide yes yes we did wonderful all right here we go so um thank you everybody for coming back for round two um i'm going to start with a little bit of background information but i want to recommend that if you haven't watched round one go back and watch the intros our opening arguments from round one they were longer and they're going to be a little bit more detailed so just strongly recommend to do that before crashing right into this because i'm kind of we're kind of both building off of round one so we're talking about genetic entropy here as sal said this was the idea proposed by dr john sanford in his 2005 book and the idea here is that within a population mutations accumulate over generations as a result fitness declines and this will ultimately lead to extinction now the relevant topic here the relevant underlying idea is evolutionary fitness and evolutionary fitness is reproductive success basically how many viable offspring do you have offspring who they themselves will reproduce the central claim that mutations cause reproductive output to inevitably decline over generations and this will ultimately lead to extinction there are other ways to talk about fitness besides an evolutionary context you could talk about things like function or structure of different things you could talk about that kind of a macro scale or at a genetic scale talk about information in the genome or something like health or intelligence but all of those things are upstream of reproduction at the end of the day the question is long-term viability is a population going to be able to survive or is it going to go extinct that's the question that sanford tries to address and his answer is inevitable extinction the idea with his argument is that he is trying to refute evolutionary theory as a broader idea but if you have to redefine fitness into something different in order to do that then that shows how weak the argument is you can refute an idea by redefining the terms into something that suits your liking better you have to engage with the idea as it exists so from part one cells argument which we heard right here is that fitness it shouldn't be about reproduction it should be about something else health of the organism engineered features of the organism intelligence health structural precision at the cellular or genetic level and defined that way most mutations are harmful and the genome is too constrained and this is what sal was just saying the genome is too constrained to be able to tolerate very many mutations therefore the genome is degenerating over generations and that is the concept of genetic entropy so there are a couple of problems with this idea first is that that is not john sanford's argument in genetic entropy he talks very specifically about mutations and the genome itself not about other aspects of an organism's well-being that also changing the terms does not address the problems with sanford's argument the shortcomings that i'm going to discuss in a minute apply equally to sal's version of the argument so here are the specific components of sanford's hypothesis first is that virtually all mutations are harmful these fitness effects are constant the accumulation of these mutations is approximately linear the rate of accumulation and the relative frequency of harmful mutations does not change generation over generation and this accumulation over generations is inevitable selection can't slow the accumulation nor remove mutations once they have occurred i raised a number of specific objections to these ideas last time that were not directly addressed so i want to reiterate them briefly here in the hopes that we can address them in around two so the first objection is that fitness effects are not fixed and beneficial mutations unquestionably exist so for example in humans lactase persistence that is a beneficial mutation there are no downsides to that mutation contrary to what creationists claim there are no loss of no loss of regulatory mechanisms or anything associated with that mutation that's just straight up beneficial but there are also mutations whose effects are context specific so the mutation that causes sickle cell disease is very harmful in people who are homozygous for that trait who have two of the mutations but if you're heterozygous if you only have one you don't have the disease but you're uh you're resistant to malaria so if you live in a malaria endemic area that trait will actually be selected for the being a heterozygote in influenza we can look at mutations that can for resistance to tamiflu and there can be a cost to those but you can have secondary mutations that recover the fitness costs and then an elephants i love this one an elephants the toskles trait is very bad because they use their tusks to do things like root around for food but in a context where humans are constantly hunting elephants for their tusks being tuskless is actually really helpful so context matters and beneficial mutations exist the second problem is that the fitness effects reach equilibrium sanford claims that over time as mutations accumulate the fraction of deleterious mutations stays at approximately 100 but that's just mathematically not possible as every as a harmful mutation occurs is replaced by the potential reverse mutation in the universe of potential future mutations so over time as harmful mutations accumulate you approach an equilibrium where the frequency of helpful and harmful is approximately equal and that's not bio that's not anything specific to genetics that's just basic math the third problem is that selection occurs according to sanford everybody deteriorates approximately equally equally enough that selection can't distinguish between them so mutations accumulate even when you hit a threshold of viability even after that point mutations continue to accumulate but in reality populations have variation so as some individuals cross that threshold of viability other individuals stay just below it and you have selection against the enviable genotypes so what you end up with is a population that hovers right on that knife's edge of of viability and that's called mutation selection balance so for those reasons sanford's reasoning is completely wrong so my goals for part two of this debate are one provides sound opportunity to respond to those specific shortcomings in sanford's argument a second establish the correct definition for fitness and show that cells new definition doesn't solve the problems created for the creationist argument that the first uh the the correct definition causes third examine the supposed limits of evolution things like a viable mutation load the percentage of the genome that could potentially be functional and if we have time for things like generating and maintaining information or traits in the face of constant mutations and then finally if we have time i'd love to talk about specific supposed examples of genetic entry but we'll see how the discussion goes and see if we get there so i want to end this uh opening argument with some specific questions for sal that i hope we can answer as we go forward uh one do you disagree with any of the three objections i raised last time and just for get it here two on fitness do you disagree that the outcome of genetic entropy ultimately is genomic deterioration and eventually extinction three what if any are the limits and thresholds of evolutionary processes in terms of like mutation load and percent of the genome that could be functional and still be viable over the long term and in particular what are the evidence for these limits and then finally can you identify any specific instances of genetic entropy so a couple related topics that i hope we get to you mentioned the 2018 basiner and sandford paper on fisher i'd love to talk about that i don't know if we'll get to the the idea of information in genetics and biology but we'll see if we get there on epistasis may come up uh in code i'm sure we're going to talk about in code although i really think that's kind of a distraction because as we'll see i don't think there's good evidence that there is a limit to uh viability dependent upon what fraction of the genome is functional and then finally um we possibly if we get there talk about environmental change the idea that well it's it's not that organisms are just getting bad on their own it's that they're getting kind of specific to their environment they're becoming specialists rather than graduates and that if things change things go downhill uh that has its own problems for genetic entropy because that's not the argument that sandford makes so we can get to that if we have time and with that i'll turn the floor back over um and it's back sell thank you one thing i just want to quick jump in and mention because i forgot to mention at the start i have put all of the links of the speakers in the description folks so that way if you're listening and you're like i like that you can hear plenty more including erica her link is down there as well so all three of our guests today are in the description want to let you know that also one really quick thing just as a i have to mention i've been moving lately so i'm like super behind on email so i seriously hope nobody takes offense to that i try to answer every email unless it's attacking me ferociously i usually ignore those but i try to answer everyone and so sorry if anybody's waiting on messages i i really do try to get back to everybody and so with that thanks so much and back to erica who will keep us rolling along all right that was exactly nine minutes by my count so i was i was getting ready to to say one minute warning at nine minutes and then you finished up and it was perfect i didn't have to say anything to either of you you guys nailed it um okay so i believe we're gonna start with sal and for those of you out there in the ether wondering kind of how things are gonna go today um both of them have both of our speakers have kind of discussed slightly what they want to talk about um broadly speaking and topic wise so we're going to kind of let them take the lead on on what we're speaking about and they'll have about 20 ish minutes per topic of give or take um so that we make sure we don't stay on a topic for too long which uh you know these guys are pros they know what they're doing they were they were like these are the topics we're discussing and we're gonna get through all of them dang it so i'm going to toss it over to sal and uh and let him kick us off uh dan is it okay uh i'm gonna uh give a presentation for about 10 minutes and then we can fill out okay great that's great yeah i'll just i'll start a timer kind of in the background and let you guys know when we're like at 15 minutes and then more when we're at 20 if that's cool with you that's cool uh hopefully you could see my slide yeah we got it is junk dna really junk and this was a slide from um by professor dan from our first debate debate and he gets a listing of things uh his idea of how much is functional uh in some sense and certainly and what's not and i think that really defines the debate tonight and that's what we're i'm gonna have to i the next 10 minutes is going to be nerd heaven for some of you because this is just going to be pure technical stuff um so as i mentioned as i alluded to the junk dna hypothesis came out this is kind of an archaic form there's a more modern form uh and i read that by dan grower it regards functionality so i'm going to talk about functionality tonight and i'm going to try to do just in this first 10 minutes is just to do a setup i'm not going to actually respond to all of this here because that's going to take 20 minutes i'm going to break this up into two 10 minute segments so if encode is right then evolution is wrong and uh that really if the supposed uh junk dna is mostly function functional then evolution is wrong i'm going to actually argue in addition to that evolution is wrong even if only 11 percent is functional and that is the figure that professor dan provided and the reason for that is this table that can be derived from population genetics it uses the same math that professor grower used to criticize encode so professor grower said if encodes right every female has to give birth to 10 of the further 10 to the 35th children and um another geneticist said well you know maybe uh maybe the mutation rates only three per kid but the females still need to have 40.2 kids if we use dan um professor dan's figures from the debate on uh this past june that would still be 119,748 children per per female the math works out by the way that the percent functionality is about equal to the number of harm harmful mutations per individual per generation i should highlight that even slight changes in percentage even one or two three four percent whatever would be tremendous increases in the number of children that each female has to bear so even a three percent increase from the figure of 11 mutations to 11 percent per individual per um generation would result in a um an increase of 20 fold so again this is this is really uh i'm trying to lay out with the the lines of disagreement are so intuitively why did people suspect that uh even though ono said that uh most of our genomes drunk why were there suspicions that came about it wasn't a creationist conspiracy from a 2009 paper by uh director of the NIH uh Francis Collins uh his research resulted in something i'm going to quote from another paper but it resulted the the explanation the the consequence of this is what is emerging from these GWAS GWAS is genome-wide association studies however is that 90 percent of disease associated SNPs that single nucleotide polymorphisms we can call them mutations that's close enough are located in non-coding regions of the genome so uh that's not absolute proof that the non-coding or junk regions are functional but it gave rise to a lot of suspicions so let me continue with that uh by the way i have six hours of lectures on these topics at this website uh evidence and reasons.org i've talked about Mulder's limit Fisher's theorem and protein probabilities so some of this is actually discussed in detail this is uh Waddington he coined the term epigenetics and a lot of encode deals with epigenetics the idea is that DNA is not just a blueprint for proteins DNA is a scaffold for machines so here's some pictures of scaffolds DNA is a scaffold for machines DNA is also designated parking spaces and addresses with names and motifs for machines and this is the topic of the encode 40 nucleome project DNA is also part of a DNA chromatin computer so DNA is part of a computational complex and i mentioned chromatin this is a conceptual diagram of chromatin chromatin is made a DNA here and in eukaryotic cells the DNA winds around things called histones and these are histones and the histone with a DNA is what we call a nucleosome and nucleosomes make chromatin there are modifications on the DNA that can happen these methyl modifications on the DNA and i'll picture that here and we can call these one form of epigenetic modification it's a chemical modification on the DNA and this is an illustration of what will happen to these methyl modifications in a mouse embryo so three hours after fertilization these lit up DNA blobs here this is the paternal DNA from the daddy the daddy mouse and the mommy mouse here after uh after six hours it's lit up a little more but then after eight hours the methylation marks go away on the paternal DNA so this is some sort of DNA computation going on you can actually visualize it so this is a great experiment we're able to visualize the changes in this chromatin computer so there's a little reboot here that's kind of cute so why am i pointing this out this DNA then even in non-coding regions can be used as part of a computational complex and that's uh that'll lead into why a lot of this junk DNA isn't junk so again i'm going to focus on these nucleosomes and these histones these histones have little tails these tails are actually memory tails they can be written to with bits and these are all the uh ways that it can be written to that's the little histone tail they can also be read so there's readers and writers on this memory of the histone and by the way see that wire there that blue wire that's DNA so DNA is part of this computational complex of readers writers and erasers and that's not a creationist term that's the term in biological literature for what's going on in this DNA chromatin computer and in the stem cells handbook they actually use the word so uh read only memory and random access memory so the traditional view of DNA is the read only memory that codes for proteins that makes uh proteins it's the blueprint for proteins but then this epigenetic layer of the modifications i showed they used the word epigenetic memory so that's the chromatin computation i'm going to show uh one thing i'll say is we call this chromatin structure here because it looks like beads on a string and i'm going to show a little picture of that with an electron micrograph we have these nucleosome core particles this is the chromatin the wiry type stuff is the DNA that connects it i call it god made random access memory and it's just kind of cute it resembles man made random access memory way back in the 70s for magnetic core memory and even the abacus in ancient times so there is uh again i'm saying this is a chromatin computation i have two minutes left these are some of the uh chemical details last time i talked about the hot air modification so this is a uh karyotype of a human from chromosome 12 emerges a link RNA the link RNA goes to the it travels to chromosome two on the winds of brownian motion parks there like i said it parks dna can act like a parking lot when it's there at the hox cluster of chromosome two it recruits this polycomb repression complex and it modifies the histone when that histone is modified through this computation it changes uh when it's done in one case it will change the the quality of the skin so that's why the quality of the skin is different between the eyelids and the feet so that's a little bit about the chromatin computation and i have about uh dan if i could have two minutes and i'm just going to cut off uh i'm going to go over a little bit we could talk about this hopefully this is not controversial we have stem cells uh that uh come from the embryo the totipotent totipotent stem cells differentiate into all these kinds of stem these other cells cell types that make up our various tissues uh they go in organs and there's another picture of that i'm going to show the chromatin computation here uh this is a beautiful picture of it uh pictured here is the embryo of a nematode worm a worm of some sort and the the the little thing glowing here is a cell that is going to be the uh the parent uh to a cell lineage of the germline cells which are basically reproductive cells and i'm just going to zoom in a little bit you could see that as the color changes we're having a different uh the state of the chromatin computer is changing and so at some point you can actually see how it's gone from green to red these cells now are in different state they're going to end up being the gametes that go in the gonads so uh that's a little bit about the chromatin computation and uh that's all i had to say because i don't want to take up this segment but that is a little taste of where i'm going it's going to be in another segment and i'm going to discuss uh this is forms the basis why uh i don't think there is as much junk as the evolutionary biologist claim so dan thank you thank you all right um roger that there we go it's helpful that we've got the images i think it allows us to uh to really appreciate what what you guys are saying particularly when it goes into uh you know some of the more less lame and genetics i i don't know if i can speak for everyone but i definitely appreciate it so all right dan when you when you start talking i got i got a clock running so um so a bunch of things uh in response to that first um i agree that cells are complicated but complexity is not itself an argument against evolution evolution doesn't have a problem with complexity so in order to make an anti-evolution argument one needs to go the next step and show that it's actually incompatible in some way and there's a few there's a few stabs at that here but none of them work so first thing i just want to correct a couple small things so in the slide of mine that you showed um you you could it didn't say it explicitly on there but it or maybe it did i don't remember um but it had about 11 percent of the genome being functional and you said that works out to about 11 um harmful mutations per generation if you you get about 100 per generation the faulty assumption there is that every mutation in a functional region is going to be harmful in some way and i think we should be able to agree that that is simply not true so i provided the the example of of uh lactase persistence the ability to digest lactose throughout one's life that's obviously a beneficial mutation uh another example is that there are two alleles in Tibetan populations that facilitate living at very high altitude uh they they improve um oxygen saturation in the blood these are these are just like very obviously beneficial mutations and then there's there's just tons of variation that has no physiological effects uh there's just lots of variants and i i'm just gonna ask you directly Sal i mean can we agree that there are mutations in functional parts of the genome that are either beneficial or neutral like can we agree on that i'm not looking for that no that's that's a good question and it deserves an answer i think the best way to frame it is as you said that there there'll be mutations where there is no immediate physiological effect well is there i'm not going to let you off the hook on that though is there a long-term physiological harm to lactase persistence the answer is no there just isn't is there long-term physiological harm to being able to breathe efficiently at a higher altitude no we know what those alleles are we know what they do there's no harm to it there are alleles that are documented that just don't have a cause so that's the first thing is that we need to establish that just because a mutation occurs in a functional region that doesn't mean that it is harmful we know of beneficial and neutral mutations in those regions the second thing i'm going to pull up a slide here for this is that disease associated doesn't imply functional uh so i'm just going to pull up one of the slides here and uh this is a paper from just earlier in 2020 looking at the relationship between imprinting which you mentioned and which involves methylation and an immune response to retroviruses that invade our genome now a lot of the the activity that encode documents it was around things like methylation and this has to a lot of this actually takes place at herbs and dodgers retroviruses so like right here that's an herb well that activity doesn't imply that that thing is functional in the context of human physiology because the problems that could arise from that are that when those proteins are expressed those are viral proteins so if those get expressed they could actually hurt you because that's the virus trying to hijack yourselves to replicate itself so being a target for something like that and when it mutates and can no longer be a target for that because its its sequence has changed so our proteins are not able to recognize it as a target when that happens and it causes disease that's not an indication on its own that that region is functional and in the case of transposons and endogenous retroviruses which collectively are over half of our genome that reality being disease associated which is not in many cases but it is in some of them that's an argument against their being functional not for it because these are genomic parasites so if we can shut them down they can't do what they want to do one person find them want uh but if we for if they mutate and we can't shut them down there could be a disease phenotype associated with that so that's why that's not a good argument for functionality uh the other thing i want to get into though the main thing i want to respond to here is uh the idea that we can only tolerate so much in terms of the functional fraction of our genome so i want to just uh just give me a second here i'll find it here we go um this is the one if encode is right evolution is wrong i think dan grower was completely wrong when he said that and we have evidence of this now from a paper from just this past April mutational load and functional fraction of the human genome and what the authors did in this paper was a very cool model what they did is we examined whether and how analysis based on mutational load might set a limit on functional fraction so we now have people that are directly investigating this question of is there an upper limit to what we can tolerate given mutational load they they said uh we find that the functional fraction is not very likely to be limited substantially by mutational load and that any such limit if it exists depends strongly on selection coefficients of new deleterious mutations now is this relevant to genetic entropy it absolutely is because this includes this actually works the way sanford says and the way you've described in terms of every genome getting mutations every generation so what they said is that our approach is different uh because they compared mean fitness at mutation selection equilibrium with the fitness of an individual uh not with the fitness of an individual who has no deleterious mutations we show that such an individual is exceedingly unlikely to exist so they have everybody experiencing deleterious mutations in this model they just have it different for each individual in other words what i described earlier there's variation and therefore there's differences in fitness the cool thing about this model is it directly shows what we've seen experimentally so last time i described this paper springman at all 2010 this was a paper uh where the researchers mutagenized a population of viruses and what they showed is that you'd expect the the saturated with mutations population to go extinct instead most of it lost fitness but a few rare individuals ended up being very high fitness and the model in this paper mirrored those exact results where you end up having fitness peaks that are very high but they're very rare it's a low frequency genotype so how does this work this seems so counterintuitive it works because as you increase the functional fraction you get stronger selection so when you find those rare beneficial mutations even in the context of a background that has harmful mutations you're better able to take advantage of that and select for them so this is a table from the paper that just shows that s is the the strength of selection it's the selection differential for anyone watching it's just how strong is selection and then this is the functional fraction anywhere from two percent of the genome up to 100 percent of the genome and the bigger this number is the higher the maximum fitness of that population showing that as you make the genome more selectable you can actually do a better job finding those high fitness genotypes also the cool thing about this is it doesn't matter what your definition of fitness is it can be structural it can be about the 4d nucleom it doesn't matter it's just functional related to constraints on the dna sequence that's all that matters so the authors summarize calculations that report to establish a load should in our view be based on the distribution of actual fitnesses that are expected in a real population as we have shown the properties of this distribution depend not just on the number of de novo deleterious mutations but also on the selection coefficient against deleterious mutations in other words selection exists even if everybody in the population is experiencing harmful mutations and this is exactly that third thing that i brought up as a problem with dr sanford's model because sanford considers the mutations and how they accumulate but he ignores the selection and that's the problem that this paper addresses and that gets around the problem of well if the genome is x percent functional it's not viable over generations that's just simply not true when this is a model that shows it and it comports with empirical data that we've generated experimentally okay all right so sal would you would you like to take your next 10 minutes and respond to that or do you guys would would you rather have an open dialogue i think uh we agreed that dan can now put something on the table is that right tan uh did you want to put just so i will uh i will go to my next thing it's not so much like a point as just i want to just like settle questions so what i really want to talk about here are uh the the questions i felt like were left over from our our last round um so here i'm just going to put these questions up and we can go through them and this isn't going to be like a 10 minute thing this is just going to be back and forth because i just want to i want to see what you think of these questions so the way i think this should go is uh dan you'll take the lead for the next 20 minutes and you get to yeah okay yeah so what so the right so the way so the way i'm going to take this section is i just i want to i want to address these specific shortcomings with sanford's model and i want to see what you think of the underlying questions here because i i honestly don't know uh for some of these questions what your answer is to them and i want to establish those answers so um basically here are the prior questions um are fitness effects constant are there virtually zero selectable beneficial mutations um does the frequency of harmful mutations remain constant even as they accumulate and do populations experiencing random mutations have uniform fitness across everybody um there are right and wrong answers to these questions the correct answers um are that no fitness effects are not constant there's epistasis so if you have a mutation it has one effect if you have a mutation with another mutation it has a different effect that's what i showed earlier with the tamaflu example there's the heterozygote advantage that's the sickle cell example so it's harmful if you have two but it's not harmful if you have one and then there's environmental constraints things like our you know what predators present for example are there virtually zero selectable beneficial mutations no that's we should be able to agree that there are beneficial mutations that exist um at the viral level which i really like there's a tinsy protein in hiv called vpu and in hiv one group m this protein has a brand new function it keeps its old function it just does that perfectly um but it required a completely new function to address part of the human immune system that uh the ancestral vpu didn't have that's a beneficial mutation and again lactase persistence in the context of humans i mean that is a selectable beneficial mutation it's it's been selected for it's not a question of whether we can select for it it happened um does the frequency of harmful mutations remain constant even as they accumulate the answer to that is no because every time a mutation occurs that becomes impossible it can't occur again if it just occurred but the reverse mutation can occur and if the original mutation is harmful then the reverse mutation has to be helpful according to sanford's own logic so just the answer to that question is just no and then do populations experiencing random mutations have uniform fitness well mutations you can i don't particularly care for the word random um but i really like the word probabilistic mutations are probabilistic rather than deterministic so you don't know what mutations an individual is going to get so when you have mutations everyone gets hit with different mutations that leads to variations in fitness and even if everybody is suboptimal you can still have selection on members of that population so i guess my first thing is we should be able to agree on the end on these answers um so i guess my question is do you disagree with any of these answers oh yeah sorry yep sorry there you go we want to see all your faces oh well thank you um i disagree with the definition of fitness i disagree with the characterization of that these beneficials can lead to some sort of eculibrium it might be more helpful can can we go one question at a time i knew you have it on your screen yeah rather than asking me could we go point by point at that yeah so probably address that by the way that was a very good list and so thank you for bringing it up so uh the first one was just our fitness effects constant no okay great so we agree on that one are there well in an evolutionary definition and the problems with the evolutionary definition that was found out by luenton in 2003 i'm sure we talked about the evolutionary definition was it that's one reason he abandoned the idea of evolutionary definition of fitness because it was a disaster it can be characterized mathematically in any stable or same way he's not alone in that andrius wagner there are uh several other papers on this issue where the idea of evolutionary fitness is basically vacuous and that's why i i feel like we're going to be able to spend a whole 20 minutes on that okay i think so let's just for here i'm using the correct evolutionary definition so we can agree according to that definition that there are variable fitness effects for a particular mutation okay um also with that definition are there virtually zero selectable beneficial mutations with that definition no okay so far we agree this is not much of a debate right now um does the frequency remain constant so like as a mutate as deleterious mutations occur does the future frequency of deleterious mutations stay constant or does it change as they occur according to that definition no okay and then the last thing is will a population experiencing random mutations have uniform fitness i'm i'm not sure about that what was your answer i mean the correct answer is no because not everyone gets the same mutations at once so you're gonna have a variation i'll go with that yeah okay i mean oh goodness we're not fighting okay so we so we agree we agree as long as we define fitness correctly in the evolutionary definition well i have to i have to disagree i i think it's a terrible definition uh but i'll agree as far well we're going to be correct i'm just i have to say that that's a little bit of a leading definition so i just have to throw that caution and but i will i will i will agree that as far as it's if we use the evolutionary definition uh i'm not saying that it's correct i'm not gonna ascend to that but if we use that definition in that model then the we're in agreement as to the consequences so we know why we would disagree but within the context of it okay here's so okay so we agree as long as we're defining evolution correctly we agree that the answer to those questions is no and by correctly i mean the context of finding it very correctly evolutionary biology has a definition of fitness and as long as we use that i'm not gonna call it i'm sorry i'm just not gonna call it correct it's a disaster well i will say it's the accepted one it's the accepted definition in evolutionary biology that everybody uses not gonna get me to say it's correct i'll say it's the accepted definition and i'm sorry i'm not trying to be belligerent so okay okay so i want to just share one more quick slide here uh that's the one uh so here's the important thing with all that sanford's answer to all these questions is yes he's very explicit about this in the book genetic entropy his answer to those questions is yes and he's not playing fast and loose with the definition of fitness he's talking about reproductive output declining over generations and his answer to that question is yes to all those questions is yes um and he is wrong that was in his 2008 version yes that was in his 2008 version that's changed a little bit in this 2000 it's changed a little bit in his 2014 version and i'm happy to send you a copy of it would be i would love that that would be awesome but well i just want to be clear then so our do we agree that the argument as originally articulated by sanford and in the at least the first three editions because i have the third edition uh do we agree that the argument as articulated by sanford in up to the third edition at least is not does not work do we then agree on that and we have to use we're using now a different idea of fitness to make it work i'd have to think about that uh because he did retract one thing and so uh you can't ding him on that and that had to pertain uh in fact i will just for the the reader's sake let me see i actually i i looked i looked back his 2014 edition i i'm sorry i don't have it handy his 2014 edition did not say all mutations are deleterious he said almost all so that's i have the quote right here if you'll give me a second to pull it up from the 2008 edition and remember we're going by his arguments in you know whatever the genetic argument and he says uh i could even give you page yes the third edition hang on one second i will pull it up right here where he says uh that i forget the exact wording so i'll just not try to say it i'll just actually pull it up just give me a second uh sorry everybody watching as we're both trying to find a reference here real fast i just have to pull up a different set of slides uh so just give me one second here play the jeopardy music while we're waiting um here we go if you're bored in the comments go in here in the chat go okay here you go it can be this is page 16 of the third edition it can be very reasonably argued that random mutations are never good page 16 third edition so at least in that definite and the third edition he was making the argument that page 16 the 2014 edition it can be very reasonably argued that random mutations are almost universally bad so okay so sanford so sanford doesn't even you're robotting out a little dan dan oh sorry i said sanford doesn't agree with sanford anymore that's great we're making progress well i wouldn't characterize it like that i mean everyone will change his argument that's fine i mean he didn't agree with his own i think i mean i think that's a very uncharitable way to characterize it but if you want to say that that's fine but you can't represent uh the 2008 is his present view that's fair we that's fair he changed his view from his original argument we agree that his original argument doesn't work i'm not saying it doesn't work uh because it's not well the reason is is it's not if you have 99 of them that are deleterious and if we're talking about uh the functional sense uh the argument holds so it doesn't fail on that minor correction just like a lot of things with just a little bit of change in our parameters we could still have the same conclusion and uh it's actually gotten stronger over time so you're attempting to falsify it by just saying that he changed uh his wording from 100 percent to almost always but if 99 percent of your rotations are bad versus 100 so for every beneficial if you're having let's say one improvement to uh to one part of your body and the 99 other parts are going downhill that's not good so you can't say that his whole genetic entropy hypothesis has failed not to mention i'm going to cite even more people that are in agreement with them he's not in the minority geneticist there's no geneticist that i know of thinks and this is pertaining mostly to the human genome i know of no major geneticist that thinks that in functional terms we're improving and i gave a quote by michael lynch who's very respected and there are other people that are just right on board with michael lynch so trying to characterize this is solely john sanford's um theory is i don't think that's really fair because it would be nice to just say oh this is a creationist theory but i can name several geneticists michael lynch is one alexa kondrishov is another james crow is another ira walker and keatley have shown concerns that is a no michael ability to stop that is a misrepresentation of their findings and you should not cite that paper i'm happy to cite them that's not happy to cite them and you know they may not agree on the specific details but there's no it tells me i can you can you cite anyone that thinks our genome's improving no but that's any debate the debate isn't about whether we're improving the debate is whether we are well if we're not improving we're either going neutral or we're going bad the debate is about whether we are inevitably accumulating mutations on the way to extinction that's what no we don't have we don't have to go to extinction to have a deterioration you're framing it in terms of total extinction there can be genetic deterioration without extinction did that is that is of concern to all of us did sanford changed this line too uh when selection is unable to counter the loss of information due to mutation situation arises called error catastrophe if not rapidly corrected the situation leads to eventual death of the species extinction that's third edition page 41 did he change that also uh the numbering is a little bit different in this one i believe that's at the end of the chapter but i don't recall specifically so you said page 41 the reason this matters is actually probably leads into our next topic so i don't want to get into and this is this is a for the audience wondering why we're why we're hashing out over specific words here the reason this matters is that the next big thing we're going to talk about i think is going to be the definition of fitness and sanford is very clear about this that he's talking about he he states his argument in a couple of different terms depending on the chapter so he'll talk about information he'll talk about function but at the end of the day he's very clear that and that quote is an example of it that the end result of this is going to be extinction if you're talking about extinction you're ultimately talking about reproductive output are you making enough offspring that are viable to replace the previous generation so that's why this for the audience this may seem like a trivial point but this matters in terms of what the actual argument is because the argument is not that we're inevitably leading to extinction then like if sanford has changed his view on that then like great we agree humans aren't going extinct awesome that also means genetic entropy is not happening because the way sanford and i should note sanford coined the term and defined it in the book genetic entropy in the mystery of the genome so it is his term it's his concept if it no longer predicts the ultimate extinction of humans from genetic degeneration then it bears no resemblance to the original idea that sanford put forward that's the whole point of it it's as i said in part one it's an argument by contradiction right it's saying if this is true then evolutionary theory is false and then he spends the whole book arguing that it is true if he's now removing the extinction side of that it takes away the therefore evolution is false part of that argument so i'd be very surprised if you remove that part but i may be wrong let's find out no number page 45 it's page 45 in the updated version if eric it says here if not rapidly corrected the situation leads to the to the eventual death of the species in the final stages genomic deterioration leads to declining fertility which curtailes further selection okay the death of the species that's extinction so he has not changed that argument he removed the word extinction it sounded like but if he's talking about the death of the species the word for that is extinction right extinction yeah i'm in okay i'm not saying that but to say that uh i just have to clarify something genetic deterioration can happen before extinction that is how you know that we're headed toward it that is how we'll know i agree but then that goes back to the paper i just showed you showing that no it actually doesn't inevitably decline and that paper which is a model but the parameters by warren by warren you and right well the parameters one that was a paper by you and yeah yeah who uses the definition of fitness that is flawed i think that's going to be our next topic so let me just say this about this paper i'll give you the last word and then we can go into the definition of fitness but so the the that paper what that paper shows is that that paper actually uses parameters very similar to what sanford describes in that everybody is getting slammed with deleterious mutations in that model population it's not comparing optimal to whatever it's everybody is suboptimal in that model and yet they're still able to be sustainable because you have selection and the great thing about that model is that it actually matches experimental results that we've seen experiments in the lab with not just mutation accumulation but mutation saturation where population experiences every mutation that's the springman uh 2010 paper in that experiment you see results that almost exactly match what that model proposes so that i think that's it for the idea that whatever fraction of functionality if you have just mutations accumulating that necessarily leads to extinction you have theorists that certainly say that and sanford puts it in a creationist framework but here we have a model and data that match the model and the data are actually from before the model was published so it's not even like they're they're they're matching their experiments in the model they're working independently from each other and they reach the same conclusion so i'll give you the last word on this topic and then if you want we can hop over to fitness well thank you i'll try to go in the 20 minute those are very compelling objections i'll point out why i think the problem with evolutionary definition of definition of fitness is deeply flawed beneficial mutations can arise from loss of function this is known we call that reductive evolution michael bhe in the peer-reviewed journal uh bio um it was quarterly review biology says didn't even jerry coin thought it was a great article that most beneficial mutations are loss of function these adaptations are loss of function so neutral mutations so beneficial mutations in the evolutionary sense are considered loss of function can can be considered most of them are loss of function neutral mutations can be loss of function and deleterious mutations can be loss of function and that's why i said the fitness definition being used by evolutionary biologist is nonsense so you picked out examples like sickle cell anemia where the sickle cell allele is is a loss of function it will compromise the individual there is a book the survival of the sickest so or it says why we need disease because it is so apparent that we have all these diseases we have to characterize we have to equivocate we have to obfuscate uh that these losses of function are beneficial because the paucity of actual functional increases where we can get new organs and new capabilities uh such such as uh complex new capabilities like say a creature that didn't um have the capability to sense electric fields how does it acquire it requires so many simultaneous changes so the easiest change for evolution is to knock out something because there are many ways to break something very few ways to actually make something so that means most ways that um mutations work will be that you can break something easier than you can make it so what evolutionary biologists have done is to take all this breaking and claim that this is a beneficial mutation and look this is how things can evolve by reduction and there are papers that there are more and more papers to talk about reductive evolution reductive evolution is where we have beneficial mutations just trashing an organism and that's why i object to that definition and when you say correct definition of fitness it is not correct it's the evolutionary definition which makes it bad dang you guys are on it time wise that was exactly like 19 minutes and 55 seconds or something along those lines i'm i'm thrilled by this i've got to do nothing my job is easy i will come and hunt down chat though because uh we've got 313 people watching and only 80 likes so i'll hunt you down and ask you nicely like the video do it for james we all love james yeah um and with that i think we'll jump into the next topic what do you guys think which i'm guessing is going to be is it going to be fitness i hope it's fitness i don't know what's up it's going to be the topic that i choose uh if that's was that was my understanding yeah that's all right please i'll take the lead on this one um let me see i'm trying to is my shares is my screen shared yes we can see what you got all right so i'm showing a picture of god made ram i call it god made random access memory and i'm going to show a video here hope this works in a recent study we show that when the two meter long oh did i blow that i'm sorry got booted it's okay so i got screwed it you know let me let me try this again we're having a little technological problem i appreciate your forbearance here try this again i'm watching that like number climb up good job chat you're spared for now in a recent study we show that when the two meter long human genome folds inside the microscopic nucleus of a cell it forms 10 000 loops each of these loops connects two anchor points which are far apart along the chromosome but which loop back coming close together as the genome folds in our new study we find that loops formed by a process called extrusion let's take a look at how this operates on a segment of dna first an extrusion complex containing two subunits attaches to dna forming a small loop in the process next the two subunits slide along dna in opposite directions making the loop grow bigger and bigger the extrusion complex looks for a specific motif a dna word which causes a protein called ctcf to bind to the dna if a subunit encounters the ctcf motif that is pointing at it the subunit tends to stop if the ctcf motif is pointing the other direction the motif won't be recognized to the subunit the motif looks as though it is backwards this behavior leads to a result we call the convergent rule the pair of ctcf motifs at the ends of a loop must be pointing towards one another on the dna our simulations also show that when loops form by extrusion they lead naturally to the formation of what we call loop domains this means that if two pieces of the genome are inside the same loop they tend to bump into each other more often in this physical simulation you can see how the extrusion of two loops leads to the formation of two spatially segregated domains like the convergent rule the association between loops and domains was observed in our earlier study but at the time we did not understand why this was the case both findings and many others that you can read about in our paper can be explained by the extrusion mechanism in a recent study okay thank you for um thank you for letting me show that video we had some technical problems so we're talking about these extrusion loops this is how a lot of genome regulation is modeled now and this is the subject of the 4d nucleon project so i'm going to just model this is my drawing of that extrusion loop and this is going to relate to aspects of junk dna so that loop there has to have the ctcf binding motifs and that's the consensus motif right there now where does where did these binding motifs where are they often found by the way i do some work on the topoisomerase 2 enzyme they're find inside they're found in signs and ervs there's literature on that and so the gene might be only a small segment the coding part might only be a small segment in this loop but there's a lot of stuff where we have all these molecular machines that have to aggregate to be able to do regulation because that's how you have differentiation in cell types so the formation of these loops and where they are in the in the um in the nucleus affects cellular differentiation so there's something here with the sternberg collins paradox where it talks about how these transposons have to be positioned just right i don't have time to cover it but this is a depiction of the 4d nucleon here is the nucleus of the cell and here is the outer part of the nucleus and we have these things like we just talked about these um these loops that's what we have one part so the 4d nucleon says that a lot of gene regulation and a lot of the way things get transcribed etc has to be it's dependent on the physical location and structure physical location and structure now there there is gene regulation that co-regulation that happens in between chromosomes so we we might have this uh see like these intracromosomal reactions and i showed one with the hot air link RNA that's an example of intracromosomal reactions so what is this telling you if you're just cutting randomly these pieces of these loops here or if you're putting the ervs or transposons or whatever in the wrong place and they happen to have a ctcf binding motif you're going to be changing the compartmentalization all this it can't that's why when we have uh transp transposition mutations in people there's a lot of bad stuff that happens so it raises the question how did these um how did this 4d nucleon emerge to be able to regulate in such an elegant and powerful way it's not easy we can't build machines that sophisticated so uh here's an example with the fire link RNA link RNAs were considered junk at one time but this link RNA is able to help bring together chromosome 2 i'll show close up chromosome 2 chromosome 15 chromosome 17 and chromosome x it's going to bring so this was considered junk dna no longer it brings these chromosomes into proximity and they're able to co-regulate each other here's another example of dna that was thought to be junk this is uh that pink dot there is the exist link RNA it does dosage compensation on the x chromosome so that little pink thing is the x chromosome with the excess link RNA changing the chromatin state so i show these chromatin computers earlier so great tribute to the people who are able to make these visualizations there it is the excess link RNA exploits three-dimensional genome architecture to spread across the x chromosome if we think that most of the nucleus there and the dna is junk that does not agree with the idea that we have a this computational 4d nucleon regulation that can happen in three dimensions and regulate by the way these what they were showing is uh there and it's really hard to depict this well let me move to the next slide these associations change depending on cell type so we have at least 300 canonical cell types depending on how we count them but this has to change so that you have uh you know when you have a nerve cell you have versus a um a bone cell these interactions change and they depend on this what was called junk dna we're finding this out more what happens by the way if we disrupt some of this at the nuclear just a little bit at some of the dna uh the areas here well we have a condition called progeria premature aging the life expectancies around age 13 and this is from a biology textbook defects in a particular nuclear lamin are associated with certain types of progeria rare disorders that cause affected individuals to age prematurely children with progeria have wrinkled skin lose their teeth and hair and often develop severe cardiovascular disease by the time they reach their teens so what am i trying to prove here structure structure structure if this structure is just junk it's not going to work and even just a little bit of perturbation to that causes some bad things to happen we're finding that out that's why we're studying it that's why medical researchers think a lot of this is functional it's their job to find out what causes disease and they're being told by evolutionary biologists that this is junk and that data does not agree with that so let me go to some specific examples here uh some things that were considered junk like uh line transposons which are about 17 percent of the genome give or take we have the um line one this is uh from a bio archive and i'll show even more this is what they had to say by the way i'm sorry i had a little bit of a mishap there this is an example of a line one and it says dynamic expression this is this is like 2020 so some of the stuff you may be hearing about this being junk it may be an obsolete argument by now so from this paper uh dynamic expression and essential roles of line one in mammalian development line one is a transposon considered junk used to be line one is highly expressed during several stages of mouse and human development notably during the global reprogramming of dna methylation and histone modifications that take place during preamplant pre-implantation and germline development the study of one such context pre-implantation development has revealed essential functions for line one RNA and regulating both r RNA and two cell specific gene expression by promoting recruitment of key factors to chromatin line one expression also impacts global chromatin organization via direct or indirect mechanisms that remain to be elucidated in in separate studies line one expression and mobility has been linked to neurogenesis so that's one example now i'm going half minutes there sal just so just to let you know in the time i'm sorry i said you're at about nine and a half minutes there sal just to let you know in the time i pause it for talking okay i'm gonna uh dana i'd like to continue if that's all right with you because we're trying to i'm trying to answer your questions here about uh totally up to you guys i mean i'd like to get a word in because i have i have questions about what the argument is here because this is starting to sound the argument is you you posted that only 11 percent is functional i'm trying to contest that that you may be wrong you may be dead wrong i i what i said specifically is that we have strong evidence of functionality for 11 percent uh we also have a somewhere in the neighborhood of 10 percent that we're not sure about uh and i i think the best conclusion is that the actual functional fraction is in the neighborhood of 15 percent it might be as high as 20 but i'm not as convinced of that but i think 11 percent is what we can be really confident about right now and i think it's reasonable to say that maybe up to 15 so my argument is i'm just trying to show that all this stuff that has been saying that dr v's and transposons are junk that's an open question and i'm trying to show the reasons why and i think it's important people see this because i don't want uh evolutionary biologists to keep getting away with saying that aloo's and transposons other transposons and urv's are junk i'm trying to show the functionality i'll defer to dan here because he you guys agreed on the time for 10 minutes so if he's cool with you going over 10 that's totally up to you i'd like to get in if that's okay because i have i i i agree with some of what you're saying and then i think you take it several bridges too far well here can we stop the share um and if someone wants to finish with this 30 seconds and see what else he wants to get yeah by all means okay yeah we'll quit this year all right 30 seconds thank you yeah no problem so a yalla was saying that aloo's were junk and that has been falsified on many levels he can't categorically unequivocally say that uh it's an open question but there is a lot of evidence here it is uh just all these potential things a function not just potential but confirmed where there's association so i don't uh so this whole thing that evolutionary biologist came up with that saying the genomes junk that's an evolutionary biology thing that's not based on experiment this is based on experiment what i'm showing here so dan go ahead thank you for giving me a little bit extra dan oh no don't all up to you guys i'm just trying to i will stop sharing my screen thank you so um okay so the argument here is that the and i want to just reiterate just to make sure i get it the argument is that a lot of the genome is functional therefore it is very tightly constrained so if we have mutations because so much of it has some important function as it mutates stuff breaks and we degenerate is that a fair characterization it has the chance yes that's a fair characterization but also the other thing i'm trying to point out this is an example where evolutionary biologists got it wrong they're not dealing with the facts they're dealing with theory this is an example this is an example this one molecular biologist said this whole thing about junk DNA was the greatest mistake in the history of molecular biology so i'm highlighting this i'm trying to set things right because there's still a lot of this where you say you think 11 percent is functional no one knows the figure no one knows the figure but i'm trying to give reasons why it may be different but yes there are a lot of people that do think oh to be loose now we might have lost you so i was making a funny face and i don't think he's joking around i think he's mocking you dan but let's see we will wait for him back so i'll come back he always probably still talking it's like in the movie suburban commando when you could get frozen by the freeze gun it's just like that james it's just like you've ever seen that movie with hulk hogan okay i wouldn't miss i would never discuss a hulk hogan movie surely you know this about me by now it was pretty epic are you serious sorry i wish i now i feel like can i feel back when we do this here we go oh no it's going to be back he's gonna hop out i'll wait for sell i'm i'm glad it's not my wi-fi usually i'm the one that's having to like apologize for robotting out um don't worry oh wait we just got sell back i reconnected on another line okay sweet all right so i'm back so where was i uh about a minute ago we were biologists were wrong because more of the genome is not junk then they evolutionary biologists were wrong it wasn't the view of some molecular biologists and i was saying notwithstanding the fact that you cited uans and you're saying grower's grower's wrong there is another very respected population geneticist joe felsenstein that is you know drawing the line in the sand and saying it has to be junk you can see that in his uh textbook graduate level textbook version 2017 evolutionary theoretical genetics and just do a search in that book it's freely available online and just search and code you'll see his opinion so notwithstanding that you cited some papers that will say that fitness will increase under all this function that's not the universal view of evolutionary biologists on the whole that may actually be um i can't say it's you know whether what you cited is the minority viewer or not but they're you know felsenstein and michael lynch are pretty respected people i i hear your argument um first thing is that saying these smart guys agree with me is not an argument that's that's not how like being right or wrong works that's an argument from authority saying these well respected geneticists say this well that's fine but do you have data to back it up what i'm saying is we have new information we have new papers i've shown you so far tonight two papers from 2020 that back up my position so that's i think that's the first thing that he said the second thing is let's look at the overall genome because when these original estimates about junk dna which is not a term evolutionary biologists really any biologists use anymore when uh this term was invented we didn't know what was in the human genome it was actually as you showed it was before we sequenced the human genome we didn't actually know what the contents were now we know most of what the human genome is like i said there's maybe 10ish percent that's not well characterized but the rest of it we know really well and you showed that slide earlier uh that i actually showed last time that kind of broke down to broad categories now now the i want to say well hang on a second hang on a second you mentioned um a few specific things like you mentioned al use okay al use make up about 10 percent of the genome um is anybody proposing that every al you repeat is functional no not to my knowledge i know there are a few that have been identified as having some physiological role but nobody's saying anywhere near that full 10 percent is going to be functional as far as i can tell it's it's the ones that are functional are very much the exceptions is correct is that is that an appropriate impression based on what you your research into the topic it's no we don't know but 90 95 percent of adenosine to ionosine editing is done in a in the in million organisms is in the al use if we shut down the adar enzyme the creature dies or it has just brain seizures so um we don't know but the thing that i get pretty we don't know evolutionary biologists like oh no we'll say it's junk even before we even know what and that was back in what you know we're going to tell just speak first don't look at the facts they look at the fact second and only reluctantly begin to back down when the facts are just undeniable what you know that's that's what i was highlighting determination made what year was that that was what in the 1980s you showed it before i forget the year what was the year 1972 1972 before we had ever sequenced any genome at all even that tiny little phage 5174 right so now it's really i thoroughly know what's itself they come out and talk first make their theories like facts now i think it's actually come and run them over that's what happened that's why this is an embarrassment so i would have been better to just say we don't know we're looking then making these declarations of how the genome works just based on evolutionary theory and not on empirical evidence okay sal that is how science works we take our shot that is not how science works evolutionary theory is not science and if it turns out that's a good example then we correct it that is how science works and so let's look at what we know in 2020 instead of 1972 about the human genome and you showed the slide here i'll pull it up right here i'll pull up a little bit right here so the first thing i'd like you to have um erica it's okay i'd like to give dan the the last word he's been very courteous so i interrupted him a few times so no you guys are still going on time you guys have about five minutes left yes so this will yeah the last word i'd like to defer to you you've been very courteous and civil so thank you um this will not take the full five minutes this will be pretty quick i think absolutely so what i want to show you here is okay first actually well first let's look at this so this is a breakdown of the human genome right now um and i showed this last time i'm not going to go through everything but basically we know what it is right we know transposable elements mostly retro transposons we know endogenous retroviruses the remnants of viral infections there are about one percent pseudo genes are just broken um within all this stuff there is stuff that is functional so for example with an introns there are enhancers uh and that's actually uh the the reason for the lactase persistence it's an enhancer in an adjacent gene so the lactase gene that mutates to become more efficient uh it's within an intron of that adjacent gene so like the part that's introns that we're saying is non-functional we're saying it's stuff that we know is not something like that now if you dig into these numbers more you can get more specific so for example we have about 10 of the genome that's alu's nobody is saying that all 10 that full fraction is functional maybe it's maybe it's one tenth of it maybe it's half of it cells right when we say we don't really know what we do know is that it's not the full 10 percent nobody is making that claim and you can do that bit by bit through things that creation is claim or functional and say well here's an example that's functional therefore this whole class or implying that we should consider this whole class functional and that's wrong so uh another example of this is with endogenous retroviruses which are about eight percent of the genome it is absolutely true that some of the transcription start sites for endogenous retroviruses are now really important for human gene expression we've actually they wear those viruses land in the genome we've dealt with using their components as part of our own regulatory network um but that's very much the exception and you could find papers that show that um and Sal probably has a couple of them but for every herb that has a functional promoter uh there's dozens hundreds that are so degenerated that they don't have that um plus even if you were to look at the herb the promoter is a teensy little fraction of it if it's intact enough to have an an intact promoter you have to look at the rest of that endogenous retroviruses it's got three main genes gag pole and m those don't do anything for humans they're actually if they are expressed and there've been experiments on this in mammals if you you mess with an herb to allow the expression of those proteins they actually cause a disease so they're very much not functional to the extent that there would be part of that eight percent functional it's a minuscule part because promoters are tiny we're not talking one percent we're talking maybe one you know we're not talking one eighth of that like one percent we'd be talking like one percent of that one percent right it's a teensy tiny fraction so you can go through like yeah we like we have all these functions that we're finding in the genome one hundred percent i'm not going to disagree but along the way of finding all these functions we're finding a whole lot of stuff that we now know what it does and the answer is either nothing or it hurts you so that stuff cannot be considered functional and there's just one more little thing i want to show you here it's this figure which is from callus 2014 that shows uh this is probably hard to read for everybody but what this shows and this is kind of a follow on to encode is this shows genome biochemical activity broken down in a bunch of different ways so like for example the red circle is the fraction that is conservation and that's between eight and 15 percent of the genome is evolutionarily conserved that's a strong argument for functionality i think this little purple circle that's protein encoding that's like one and a half ish percent um this green oval is generates a phenotype so all that stuff cells talking about about like well this thing is associated with this disease yeah those things exist but it's not a big fraction of the genome there's just no way to put together all we know about the genome and all the different functions and constraints in the genome and get more than like 20 or maybe on the outside 25 percent functional it's very possible that in 10 years i will be completely wrong about that but based on what we know now in 2020 not 1972 not 2005 with the original encode paper or whatever 2004 whatever it was but right now in 2020 it's we know stuff and and it's it's not 80 functional it's not 50 functional it's maybe 20 functional and that's i think where we can i think that wraps up for that segment dan disappointing that was night or 20 minutes rather and two seconds so you two minutes over okay um sal that one was you right so we're back to me yep it's your segment is that right yep oh go ahead okay all right so the um and and just point of order uh for james i'm assuming uh this will be the last one and then um we'll probably go to questions is that right just based on the timing i think that would work best yes can everybody hear me yes sorry i cut out a little bit there but it sounded like is that probably probably another 20 minutes and then because i mean i can't speak for sal but i'd be happy to do another three rounds but we probably don't want to keep people here a little longer than i expected but if it was in the email it's my fault for missing it sorry okay it's my fault i'm fine uh dan maybe we i mean i'd like let's do one more let's do a real quick one let's do like say let's say 10 minutes because i don't have like presentation let's do like 10 minutes and then we'll call it good okay so uh final topic that we i really want to get into here is fitness because this is like the elephant in the room we have to figure out what the right definition of fitness is and the answer to that is the evolutionary definition of fitness is the right definition of fitness and i'm gonna talk about why so um we here we go let me just i'm gonna share this but this is i swear this is very short um this is not like a 10 minute thing okay so look we last time sal uh you said you're worried you said you i think it was the beginning of your rebuttal you said um you know you're worried about the future of humanity and a little while ago we went back through sanford and we agreed that according to sanford the ultimate outcome of genetic entropy is extinction so you can ignore the if no because we we agreed but if the answer is yes and we agree the ultimate outcome is extinction then we agree on the definition of fitness x y z something something something happens and then eventually reproductive output declines and extinction results that's what we're talking about here in the context of genetic entropy and in the context of a population being viable in other words a population not going extinct if you experience a mutation i want everyone to listen to this because it's counterintuitive but listen to this carefully if you experience a mutation that increases your reproductive output by a thousand percent okay you increase your reproductive output by a thousand percent but 90 percent infant mortality rate that's still an enormous increase in the viability of that population on net even if in terms of a health based or if or a physiology based definition of fitness a non-evolutionary definition of fitness that is a huge decline in fitness but in terms of the question of extinction that hypothetical example which by the way is is completely unrealistic it doesn't exist but that hypothetical example is an increase in fitness in that population with that new allele will be safer from extinction than it was before that mutation occurred the x y z in this formulation does not matter because everything one second whatever you hold on up with structural dam we weren't quite able to hear you uh if i think for me the last like five seconds oh so what the last five seconds sorry about that the last five seconds were that the x y z in that formulation doesn't matter whatever it is whether it's structural constraints in the nucleus or health of the organism as an adult all of that is going to be downstream of the genome downstream of the genome sequence and upstream of reproductive output and again i want to make this very clear this is all about reproductive output so you can talk about mutations or like sanford describes information loss the 4d nucleosome it's all about on one end you've got changes to the dna on the other end you've got changes to reproductive output and the question when it comes to will a population go extinct is will that reproductive output stay the same go up or go down that's the relevant question and this actually is what we've been talking about even though we're using different terms for because cell you have this thing you call the bonkers equation which is for everybody uh we didn't use the words tonight but it's uh the table that cell showed earlier where it's like if you had if you need um uh if you have x number of mutations or x percent of harmful mutations you need y number of offspring to be viable generation over generation if the problem that that equation describes is that each person must have so many offspring for the population to persist then we agree that the relevant question is reproductive output the problem isn't inherently that that population is less less smart or less fast or whatever the problem is that they're not having enough kids right and that is using whether you want to use it like you want to say the words or not that's using the evolutionary definition of fitness now the implications in terms of the actual discussion we're having here is that if you're insisting on a new definition creationists are acknowledging that they can't win in the terms of evolutionary biology using the correct evolutionary definition and it'll give you a specific example of this and this is where i'll leave this um and sally you can have the last word here the i'll leave this with a piece by paul price and robert carter um on creation.com uh that's cmi uh is the creation ministry's international um called fitness and reductive evolution and uh that's rob carter that's um dr rob carter that's dr sanford's co-author on that h1n1 paper that they claim to show genetic entropy and don't for about half dozen reasons um but in this in this piece arguing basically the same case that sally's making here they say in the conclusion only when we insist that the terms of the debate be fair and accurate will we have any chance to clearly communicate the truth of creation and the bankruptcy of darwinism to the world at large and that right there is saying the quiet part loud it's saying we can't win in the context of evolutionary theory so we need to redefine the terms of the debate to our liking and then we can compete but if you use those words it doesn't work so that's why we need to have the redefinition uh and i'm good so um sal if you want us to have the last word on that it's all yours no thank you got like five minutes if you want to use the rest of the time or banter or whatever you guys feel comfortable doing uh just go ahead whenever you're ready five minutes the notion of fitness in the common sense notion a submarine is fit to operate under sea a space shuttle is fit to operate in space an airplane is fit to operate in the air a car is fit to operate on the ground these are common sense notion of what it means to be fit and the question of how the complexity of life and it's able to do these wonderful things like an eye is able to see it's fit to see these are common sense notions these are not creationist notions these are our notions from our understanding of how machines and engineering works these are common sense notions of medical uh these are medical notions so it's really bad when we have a situation in alan or alluded to this where we have a uh blind crustacean like say chimeras minus and he made a very good critique against daniel denett uh it was a beautiful quote where he said selection is able to destroy design as much as it is able to build it though i would disagree that it can build it very well it can it can certainly destroy it so natural selection can destroy designs and he said natural selection does not trade in the currency of design so it's not i think very um honest uh i don't you know i i hate to use the word dishonest because i think this is just delusional dishonest means someone knows it's wrong and then they're gonna say the you know the wrong thing anyway so i i don't want to you know just make something um you know be very pejorative here but a lot of a lot of the definition of fitness ends up being just obfuscation so when we're talking like in some of these experiences we saw all these beneficial mutations coming in it could be just damage to the promoter region where the gene shut off there's so many ways to break a promoter there's so many ways to break a gene hundreds of ways you can you can throw these uh stop codons and have a protein truncation variant in thousands of locations of that of a big gene and if it causes the creature to reproduce more like say in the case of gamaris minus where it's in a cave and it's blind um it's counted as beneficial i think that's um you know that's fine as far as evolutionary definitions but they can't use what i'm just doing is i'm calling out you can't use the word beneficial in those cases where we've had loss of function and pretend this is proof of evolutionary theory that it can build complexity build integrated systems because you know what is the mechanisms that make common ancestry possible so it used to be believed that it was the product of natural selection and and mutation but uh there are a lot of people that accept common universal common ancestry that now have their doubts whether natural selection plus me kind of random mutation is adequate and these are some open questions and i'm just calling out the problem is if we're going to call reductive evolution an increase in fitness where uh gamaris minus loses eyes or when creatures loses the ability to fly then we can you know it's very easy to say hey look at all these beneficial mutations that are coming up but then it really doesn't answer the question of how uh complex organs and systems come up so this this is why i'm criticizing the idea of fitness i'm not it's not just the creationist who pointed this out richard luentin gave up on the idea uh and then there are other i have papers here by brady and then by grodwall and andrius wagner so this is a serious problem if you're if we're going to try to model if we're going to claim if people are going to claim the evolution of complexity through natural selection they better define it in terms of complexity in the engineering sense the other thing is another emerging discipline and i know i have about one minute another emerging discipline in biology is biophysics the biophysicists don't define um kind of this idea of functionality in terms of reproductive success they define it in terms of machines operating at the limits of physics when a machine operates at the limits of physics it is maximally fit um in some other discussions i showed the maximal fit in operation the optimality of an ion channel it has to have sub angstrom precision that just makes sense nuts and bolts have to fit together correctly that's a nice metaphor for the engineering notion of fit it the evolutionary biology definition uh is just not appropriate to the questions at hand so thank you very much these guys are pros you guys that was also just perfectly on time look at i i barely had to do anything um all right good job everyone i i had a ball listening to all that and uh and i'm sure everyone out there in the internet um at large did as well um but the fun's not over yet because we're gonna do uh some super chats and i'm gonna try to oh are we doing uh closings before or after questions oh james you know i sometimes i roast you in my head for forgetting about these things but then i forget them to yes you guys did have closings planned and i think we typically do them before we do the super chat so if you guys want to do closings um sal since you started us off would you prefer finishing first or would you like to go second i was i was expecting to do closings at the end if that'd be okay with dan yeah if that's okay with me yeah sounds good so we'll do the we'll do the super chat we'll we'll we'll bring in some money first okay so okay all right yeah we gotta we gotta line uh james's james's pockets here he's the uh the big business fat cat on this one right james making all the big bucks that's funny we are i have to make an announcement about the channel i am super excited and thankful as i just when i went in to check on the super chats we just broke 25 000 subscribers so i want to say thanks so much folks i am so thrilled the debaters are the people that i have to pass on the congrats and thanks to and just say we are excited about the future and so thanks to guys and gals like dr dan sal erica and others so really excited about that and i will kick it back to erica but i just saw that and i got excited so james people come here for your superb moderation i'm uh i'm the consolation prize everyone was hoping you were funny so i can start us off though with these super chats um so first of all from logical plausible probable uh live after show uh looking for link um and i believe that's on standing for truths channel if i remember seeing it in the side chat correctly so just pop into uh your youtube search bar and put uh standing for truth and you'll find their after show they're hosting one over there um from re-use in ski for five dollars oh sorry logical plausible probable so one second forgive me for interrupting but just wanted to mention that these are actually super chats i sent erica a document and i i think i didn't tell you this sorry about that erica these are super chats from the last debate that dr dan and sal had so we ran out of time catching up and what happened was when when we did run out of time i told people i said i'm gonna save your super chats if he's into super chat because we do want to read those we want to work hard to get those in and so these are actually from the there's only about maybe a handful of them that we didn't get to ask from the last one so if that's okay with you guys we want to and if it's if you're kind of like boy i haven't read that for a while that's totally okay to say that but we thought better late than never man james you made me look like a dingus or maybe i just didn't read your email all the way i saw super chat and then i just like i got over excited but though he is actually having an after show tonight anyway yeah that's what i was gonna say i was like okay well you know um but saved i guess um but from last time uh re-use in ski for five usd to both debaters uh do you think you or your opponent is more qualified argue this topic thank you to both of y'all for appearing sorry james i don't want to know what that apology was for james um i don't have an opinion but i think dan's very excellent professor he's very knowledgeable and he's definitely worth everyone has said he's been a worthy opponent of me so or i'd like to think i'm a worthy opponent of him so that's all i have to say on that yeah my my two cents is that it doesn't matter because qualifications are overrated it's about the arguments you're making um it doesn't matter who has what letters after their name cool yeah that's you know we screen interlocutors james and i screen the interlocutors to find the uh the diamonds in the rough like you guys so from uh dave gar last time for five usd uh for both please discuss uh apoptosis which for those of you out in the audience is controlled cell death in the context of genetic entropy micro level stuff here not at population level um i'm happy to take it or you can take it either way i mean i don't think i'm i don't think i'm qualified to uh i mean that's an excellent question and i'm sorry i can't give you your money's worth for for that one i also turned out the air conditioner so dan you got it i'll give you i'll give you a quick one here um and i apologize because i'm gonna take a micro level thing and turn it into a population thing i'm gonna set myself a timer here see if i can do this in one minute so the way i want everyone to think so apoptosis programmed cell death in the context of a multicellular organism you have cells that go through a a process of death in such a way that doesn't hurt the surrounding cells and this is the thing they decide to do it's not personifying them but you know what i mean and this is hard to explain evolutionarily but um i want you to think of the human body not as one entity but as a population of trillions of cells that are all genetically identical so if you haven't a leal that that makes it more likely to have offspring then that allele will in theory be passed on as long as uh it's it's present in in the appropriate cells in your body and they're all identical so an allele for apoptosis seems counterintuitive because that cell dies but if it helps the whole population do better which is to say reproduce then that allele is going to propagate and apoptosis will be selected for it's counterintuitive but it works really well all right sweet okay next up sal this one's for you from a cg freddo sarabia for 10 us dollars at sal does dna carry a template or information to create or does dna pick up the information along the way when and how did the information get there if not by evolutionary processes spoken maybe question mark or question mark i'm not sure i mean i guess these things spoken into being perhaps and then i may have i may have to ask you to read part of the question again but i'll answer the last part of the question how do i think information going to be i think a miracle did it there are two basic there are a couple models of creationism where a miracle we have like progressive creationism and then young life creationism young young earth creationism so he asked what i believe i believe that uh about six thousand five hundred years ago there was a miracle that created the first basically created all life forms so how does dna acquire it acquired most of the information at that first event can can we prove it um scientifically i think that is outside of science uh the reason i believe that the information came and i don't like to use the word information but the idea the information the configuration of dna uh that it came about by a miracle is the problem of a biogenesis which is separate from evolutionary theory is is very very substantial i'm more convinced of a miracle involved in the first life the reason that i think life popped up uh fully formed is the evolutionary transitions uh seem to be requiring miraculous changes particularly the change from prokaryotes to eukaryotes those that's just enormous and i know i mentioned changed hand earlier when she started teaching cellular biology she'd been an atheist she became a christian when she had to teach cellular biology and she was highlighting uh teaching the differences between prokaryotes and eukaryotes that made her creationist it was just too hard to believe this could happen so i don't know if she became a progressive creationist first but she's a young earth creationist like me now so what was the rest of the question i want to um what was the first part of the question yeah sure i actually think you kind of answered it says uh does dna carry a template or information a template or information to create or does dna pick up information along the way yeah it doesn't pick up that much information along the way i do think there is some adaptability in the dna there is some intelligence to the way it's constructed so that it can adapt to an environment and we have developmental plasticity that way but not very much so thank you for the question that was a good one gotcha all right and from stupid horror energy as she likes to be called for 10 us dollars if you find transposons in the same place in the genome it points to common descent because of all the places that they could have jumped to some of them get co-opted to perform some function some function so what so i believe that's there it's not directed to anyone in particular so i'm i'm just gonna let you guys both throw your two cents in if you would like i think that would be for sal because my answer to that is yes okay yeah i don't know if you wanted to comment or or what if it's i'm just i will i'll just briefly add that there's additional evidence for it um and it's that we can look at lineage specific mutations that occur once they're integrated so like for example you can look at insertions that are in humans and chimps that have mutations where humans chimps and gorillas share the same insertion but within that transpose on humans and chimps share mutations that gorillas don't have so there's actually another layer of evidence for common ancestry uh in that regard i think one way to to resolve this question and this is one reason i'm interested in young earth creations by the way i used to believe in evolution also in old earth the old universe we one way that we can um the question could be settled is we're able to establish that the costly record is young that'll i think that'll settle it so trying to just go after um you know in the absence of evidence we're just arguing in the vacuum pardon my interjection but we probably have to move quick as we are going on we're at two hours and about two hours flat so we to get through as many questions as possible we might have to go through as fast as possible in 30 seconds in terms of us reading them and then also i hate to ask but just because we've gone for a good amount of time maybe short and pithy responses those usual strong punches and jabs that you throw both dr dan and sal now they're they're they're they're there let's do it all right james i think you have the rest of the super chats i don't have them in the email gotcha okay well i'm gonna read through i'm gonna send irika that list as i caught me off guard and i will also say one thing i just noticed and subatomic and nano thanks for subscribing saw you pop on on the screen welcome to the community i think there might have been some others i missed but it's been flying fast and so we'll met basically the the basic idea no matter what walk of life you're from creationist evolutionists you name it we hope you feel welcome here and a quick reminder all of our guests are linked in the description so if you want to hear more from them you can by clicking on those links now i'm going to quick start reading and as i ask this first question and we hear it back we i basically will send that list of questions over to erica and then we will start taking turns reading back and forth but stupid horror energy strikes again she says sal should check a paper by laying at all science 2000 which provides structural evidence that the eight barrel proteins a widespread and complex fold aroused by a process of gene duplication and fusion i'm not familiar but thank you stupid horror energy for the reference i'll look into it thank you gotcha well i will ask the next one then just because i have that didn't give me enough time to send the thing to erica but you said pithy james stupid horror energy thanks thanks for your nice thank you objection says what do you think of the fact that the nucleosome touche is a good point what do you think of the fact that the nucleosome was lost in the dyno flagellata dyno flagellates phylum and that the origin of the 4d genome can be traced back to the prokaryotes according to the work by cremer at all that's uh my thoughts is that's based on circular reasoning that evolutionary theories correct to begin with so that may be all false thanks stupid horror energy well she strikes yet again she says this time does sal have evidence that al u elements shared by humans and chimps are part of the tiny minority that are within three utr of protein coding genes no gotcha next i have to give you credit sal you are nobody is more short and pithy in their responses well thanks stupid horror energy for your support of this channel i'm sorry i can't uh give you your money's worth tonight we i well i'm impressed by how pithy you are oh wait okay so i'm gonna send these to erica then do want to say very excited as we had a congrats come in and so this one is from who is that from let me just quick find this give me one second folks sorry i'm working on an old computer here it's okay james you couldn't do anything to uh to get on our bad side bless your heart okay next stupid horror energy strikes again says eric and kent congratulations really special very exciting for you erica next up i am going to type in erica's name and erica i have just sent that list of questions that we can alternate starting from the bottom we'll go from there converse contender huh i said i'm refreshing with baited breath over here you got it i also sent you the congratulations picture so and converse contender thanks for your super chances gosh i heard james was born on mount olympus not confirmed though thank you very much converse he's going to be moderating tomorrow and i gotta tell you folks tomorrow we are going to make a big announcement at the start of that debate so do uh tune in for that and speed of sound of gravity thanks for your quote said james i was on my way to bail my mom out of jail with this money but you're just too cool appreciate that speed of sound uh that next we'll kick it over to if you have the list erica godless recovery is next just to uh as we're working our way up yeah i'm with you yeah i think i think this one goes to uh everyone or maybe sal it says listening to creationists face palm emoji times three so they're coming at you sal no thank you for the super chat it was for two dollars i didn't mention that that's uh how much two dollars okay that's a dollar answer the sal approves he's oh okay you know all right but they but if i can humiliate myself or james i'll do it so there you go that's kind of you sal why don't you get from chat most people in chat would appreciate that bless your hearts and nathan foster thanks for your super chat said it's called evolution theory for a reason why is dr dan here arguing a theory which if it had evidence for it it would not be called a theory thank you for the question uh so this is a common misconception about science as a whole so in science a theory is an idea that has the highest level of empirical support it is a uh it's an idea that is robustly supported by multiple lines of evidence and it makes accurate predictions it explains observations so a theory in science is different from the word theory in everyday language where it's just shot in the dark a theory in science is as close as you can get to certain some other theories are things like germ theory theory of relativity those are all theories in the context of science you bet thank you very nice dan okay from uh dwayne burk for two pounds uh james and dan are twins that were separated at birth so we're he's hitting us with the with the juicy gossip we do and on the screen i uh tom jump dr dan and i are triplets as i always say tom and i are twins as well we do if you look at us hold on let me get in position wait there twins okay next now i have to pull this up and see what we're what we're i don't alec alec mckinsey thanks for subscribing we are pumped to have you as long as you're not a beta okay i just really want to say beta tonight next up erica the floor is yours but i think wait wait okay i have logical plausible probable next on my list is that next on your list or no negative i have nathan wait i have dwayne burk i think ps uh we're totally kidding alec mckinsey if you're a beta you're welcome here and uh all betas are welcome here all betas but wait so you have the list that i i just sent right yeah i've got david burk followed by lpp and then stupid horror energy twice foster again oh gosh no i'm so sorry i got us lost okay just want to finish this off here logical plausible probable thank you for your super chat set after show on standing for truth channel tonight open mic so that should be exciting on your brother standing for truth channel erica are you excited no i'm always excited to hear from standing standing and i are buds excellent okay from stupid horror energy as she loves to be called for ten dollars so i should check a paper one second so sorry we already i already read through all of hers oh we're good then okay well you read through nathan foster's other one as well no not we didn't actually read that one okay then from nathan foster for two pounds dwayne berksbeard helped sink the titanic very nice congrats dwayne next up thanks for your super chat and want to say appreciate all of your support talison oberlander you've been with us a long time said james you were supposed to screen my interlocutor very nice reference to darth dawkins i've tried to recruit darth dawkins to come back i said the people want you back darth no response but we'll we'll try for you and he doesn't want to hear you giggling like a schoolgirl that's true he got sick of it and there's only a few more super chats so i'm just gonna read you read him because i don't have it corporal annan thanks for yours said dan i love you you you you okay and jungle jargon dan's just as speechless as i am i jungle jargon thanks for your questions that asked dan how can you build an organ from mistakes so i will first and i'm gonna set a timer one minute um first i object to the classification of random mutations as mistakes because they are they are uh just random events but that doesn't hold a value judgment with it so i wouldn't call them mistakes they're unintentional but i don't think that implies a mistake um but the answer is that you don't build it all at once you have little pieces that do little things and we can see this developmentally for example in things like lungs where it starts to just a little fold in the digestive system and that's folded already for other reasons that we're not going to get into and you end up with an air filled sack and fish kind of gulp down air and that's called a swim bladder and if they can pull air from that a little bit that helps them get more oxygen into their tissues so that's useful just to give you an example and then uh developmentally it's really easy to tweak how these things form because genes that regulate developmental processes aren't saying like make a lung they're saying fold pinch off folding words fold outwards extend they they have very specific um kind of processes rather than structures that they they lead to so that's that's the answer next up thanks for your super chat from our dearest friend everyone in the chat's calling me a beta okay so Kevin Gilfoo stoked to see you again Kevin says really great debate tonight thanks to both debaters for coming on James i want to get yoked like you share your workout routine that's very funny i actually have to tell you Nathan Thompson nobody is more jacked than Nathan Thompson he has a tremendous physique he sends me pictures of it for real okay so with that i i don't know why but he keeps doing it so we hope you're well Nathan i saw you in the live chat if you're still here but i want to say folks i have gotten to know dr dan sal and Erica and i have to say they are really pleasant people folks so their links if you want to get to get to kind of know them more hear more of their stuff they're in the description and so you can click on those links subscribe get to have conversations with them build relationships highly encourage you to check out those as like i said getting to talk to them and hang out with them they are just very patient flexible and fun people so really uh want to encourage you to get to know them so thanks so much dr dan sal and Erica just for being you're hanging out with us tonight oh yeah well huge thanks to james for making this channel for us to come upon and also speak that's nice just small point of order uh do we have like two minutes to do closings because we're gonna we move those to after we can definitely do those just like i i mean honestly mine's like a minute we've run out of questions so now is the perfect time great uh sal do you want to go or should i start you're muted here sorry sorry you go ahead first and all right cool all right um so i'm gonna set myself a timer i'm we're gonna try for a minute here we're gonna see if i can do this all right so uh stop watch and mine's about five minutes or four minutes so so i'll be i'll be nice and quick here so basically uh recapping the evening we we actually agreed on a bunch of things including um uh questions that i really wanted to address which were looking at sanford's conditions that he laid out originally in his book on genetic entropy uh and we agreed that if you use the evolutionary definition of fitness then those that process doesn't work the way sanford describes then we got into whole stuff about how much the genome is functional and what is the appropriate definition of fitness i think the conclusion here is that the redefinition of fitness away from reproductive success does not actually solve the problem because at the end of the day we all agree that the the problem that genetic entropy proposes regardless of the mechanism the the ultimate problem is extinction and if we're concerned about extinction then it's ultimately all about reproductive output so by the end we actually ended up at a completely different argument uh that evolution is reductive that evolution can't build irreducible structures and all that stuff is debatable but that's not this debate this debate uh was all about sanford's idea of genetic entropy and because the conditions that he lays out as required for that process to occur because those conditions are just not true they're just not accurate then the idea of genetic entropy that there is inevitable genomic degeneration happening particularly in humans that idea is without merit thank you okay thank you very much dan let's pass it on over to sal okay my uh my closing is going to be a little longer um sincere thanks to everyone who made this evening possible and congratulations to erica on her on her engagement the author of genetic of the genetic entropy hypothesis john sanford was once an atheist then turned christian at age 39 and then creationist at age 49 like me he realized there's no salvation in the name of charles darwin in evolutionary theory with this in mind i'll close by reading the words uh john sanford wrote to close his book genetic entropy he wrote quote when i was young i accepted the fact that i was going to die and that all the other people i loved were going to die i accepted it but it robbed me of joy to say the least i was taught that there was still one hope that the world was getting better science was advancing culture was advancing even mankind was getting better through our efforts we could make the world a better place through evolution we could evolve into something better through progress we might eventually defeat death itself perhaps we might someday even reverse the degeneration of the universe my personal hope was that i might in some small way contribute to such progress i believe that this basic hope was shared to a large extent by my entire generation one of my reviewers told me that the message of the book is both terrifying and depressing he suggested that perhaps i'm a little like a sadistic steward on board the titanic gleefully spreading the news that the ship is sinking but that is not correct i hate the consequences of entropy degeneration i hate to see it in my own body in the thought in the failing health of loved ones or in the deformity of a newborn baby i find it all absolutely ghastly but also absolutely undeniable surely a real steward on the titanic would have a responsibility to let people know that the ship was sinking even if some people might hate him for it i feel i am in that position responsible people should be grateful to know the bad news so they can constructively respond to it if we had been putting all our hope in a sinking ship would it not be expedient to recognize this and abandon the false hope it is only in this light we can appreciate bad news only in the light of bad news can we really appreciate the good news that there is a lifeboat even as we cannot create life we cannot defeat death yet i assert there is one who did create life and who designed the genome i do not know how he did it but somehow he surely made the hardware and he surely must have written the original software he is called the author of life i believe the author of life has the power to defeat death and degeneration i believe this is the good news it is my personal belief that jesus is our hope i believe that apart from him there is no hope he gave us life in the first place so he can give us new life today he made heaven and earth in the first place so he can make a new heaven and a new earth in the future because he rose from the dead we can be raised from death even the death which is already enveloping us in these profound yet simple truths i believe there is a true hope i believe this hope is unshakable because i believe it is founded on the one who is eternal it is a hope that is has withstood the attacks of time and the corruption of religion it is a hope freely available to anyone who would receive it today i humbly put before you this alternative paradigm for your consideration jesus is our one true hope unquote and with those words by dr sanford i conclude my presentation today thank you thank you both and we had a few last minute super chats come in we're gonna quick read and then we will rock and roll so want to say thanks for your super chat nathan foster said dr dan please look up the definition of quote unquote theory in that you will come across the word supposition look that up and read it out loud i dare you do that thank you next stupid or energy thanks for your super chat said split between the moderators good job u w u is that some sort of slang james i believe that is pronounced who you serious yes we are so thankful that i'm deadly serious we're so glad to have erica who is a zoomer that's the right word right you know i really straddle that line between millennial and zoomer so i don't know i am oh that's right i however i'm a boomer which i am quite proud of so the joke's on you next i want to say thanks for your do we get okay we did we had we got all of them so want to say thanks so much there was one last t