Carter: Response to TMR4A and Created Heterozygosity

But short responses don’t seem to work with you guys. Watch–I’ll make a REAL simple answer:

Less recombination hotspots = reduced recombination.
More recombination hotspots and more functional PRDM9 genes = more recombination.

The activity of the PRDM9 gene is important enough to the point that if genetic erosion occurs at these sites, its essential function will be compromised. Over time, the function will become more and more compromised depending on how much mutation accumulation, inbreeding, etc, occurs.

Mutation destroys binding sites.

It is much easier to break/destroy something than to build it or create something novel. It makes far more sense that these sites were created in abundance and also created to do their job amazingly well, and over time, they breakdown, or simply get lost due to genetic diversity reducing instances.

I hope some of this was helpful to you. I do like you. I think you are far more up to date on the creation model than most people (as in you at least attempt to understand our position in order that you are not arguing against a strawman and I appreciate that). Shoot me an email, we can have some chats on this throughout streamyards if you’d like.

This is a great and testable hypothesis. Have you found the data that tests this hypothesis?

What alternate hypothesis have you considered?

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Well since PRDM9 controls activation of Mammalian recombination hotspots, it seems rather easy to test. We see more PRDM9 sites in Africans and more recombination hotspots. They also have more recombination (evolutionists interpret this as Africans being an older population). We can then look at non-Africans and see if they have a lower number of PRDM9 sites and fewer recombination hotspots as compared to Africans. It turns out they do. And it turns out they have experienced less shuffling. Why have Europeans had such degradation of PDRM9 sites–well I explain in great depth in my video tonight, as well as a very brief explanation in my comment above.





I have a detailed book on this with plenty of sources to keep somebody busy for the next million years…this book is IN text lol

I’ve answered these objections in text.

I also don’t do this for you guys, I do this for my audience. I do this for my brothers and sisters in Christ. It’s not a good use of my time to argue with people in blogs all day who won’t change their minds. If I see novel arguments, I bring it to my audience to show them how easily defended the biblical creation model is. This is where I spend most of my time–with those that care for the answers. Why do you think Dr. Jeanson or Dr. Carter don’t argue all day in blogs? It’s not good use of their time. And so I spend just the right amount of time in text as I need to. I will say, you guys give me job security for probably the next million years :slight_smile:

That doesn’t follow logically – not at all. There are far more recombination hotspots than crossovers per meiosis and no reason to think that their number has any effect on the probability that a crossover will occur.

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This doesn’t logically follow at all. Hotspots are regions of higher recombination rate, but the magnitude of recombination rate in each hotspot can also vary. It’s trivial to imagine a scenario where a population/species with more recombination hotspots has a lower average recombination rate per hotspot, resulting in an identical overall recombination rate compared to a population/species with a lower number of hotspots. That’s why I said in my original comment:

It’s true that Africans (notably West Africans) have more recombination hotspots in their genomes (see paper below), but I’ve yet to see any evidence that this results in a substantial increase in the overall genome recombination rate, rather than simply spreading out the same amount of recombination more evenly over the genome, as it were.

Nice hypothesis, do you have any data to support it? What makes the European allele of PRDM9 “more broken” than the African version? Can you point to which mutations degraded it, and show that they result in few recombination hotspots? You’re throwing out a lot of claims as though they’re facts, but very little data.

More genes? Like more copies of the gene? Citation please. They have a greater diversity of PRDM9 alleles, and notably a higher frequency of the C allele compared to European populations (~13% vs ~1%), but not “more genes”.

Citation please.

Demonstrate that this has happened then.

Demonstrate that the binding sites have been destroyed by mutations.

This doesn’t distinguish between the two hypotheses. You’re using the fact that Africans have experienced more genomic shuffling as evidence that they have faster recombination rates, but this is also explained by the hypothesis that they’re an older population. You need to demonstrate that they have faster recombination rates, then you might be able to apply that to make inferences about timescales. That’s where you’re out of luck, because studies don’t show a substantial increase in overall recombination rate, more like a <10% increase in Africans relative to Europeans (as I pointed out before, again).

Talking big picture, African populations have ~47,000 recombination hotspots, while Europeans have ~43,000, and around 41,000 of these are shared between both populations (Manu et al). Combine this with the overall recombination rate data I mentioned earlier. Can you demonstrate that these relatively small differences account for all the observed differences between European and African linkage disequilibrium? I think not.

You’re forced to stick to this idea that recombination rates and distributions were substantially different just a few thousand years ago and that if only we knew those rates and distributions, all the data would neatly fall in line with YECism. Good luck with that.

A book (using the term generously), especially one that isn’t free, isn’t a discussion. A discussion on a forum like this is a discussion.

That’s the thing - by avoiding discussions like this the vast majority of the time, you fail to firmly grasp the arguments and data in question, and end up delivering a lot of faulty interpretations and incorrect data to your audience, and they can’t tell the difference. They lap it all up regardless. This topic is a perfect example. I haven’t watched your video yet, but if you made the claims you did here in that video, in your best confident and dismissive tone of voice, then I’ve no doubt that many members of your audience came away from the video believing exactly what you intended - that the YEC model is easy to defend. In constrast, when you actually engage in a discussion about the specific details, as you have here, if becomes clear that you don’t actually have the data to back up your confident assertions.

To a certain extent, sure. But there’s a big difference between arguing with random people in obscure forums and engaging with scientists with technical criticisms. The specific medium is largely irrelevant. A conversation where 3 detailed replies are made back and forth in the space of a day can be more useful in furthering the discourse than weeks spent writing independent blog posts to indirectly reply to criticisms.

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If you predicted my responses, why didn’t you preemptively counter them in your comments? It’s clear you’re only interested in dragging out arguments you can turn into YouTube content, rather than having an actual useful conversation.
Don’t get me wrong, I kind of understand it. YouTube is your full time job and you’re terrible at producing original content, so you have to milk these arguments as much as possible, but you could be a little less brazen about it.

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Sure sounds like you’re straight up saying you’re not even pretending to be interested in a productive discourse, and it also sounds like you’re at the very least implying that the same is true for Jeanson, Carter, etc. That’s consistent with their work, but I don’t recall anyone every saying so so brazenly. My impression from, for example, Jeanson, is that he’s very much interested in at least being able to claim he’s involved in a serious, scientific discussion.

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Aww, wasted such a good opportunity to use that old Carl Sagan meme. :smile:

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I admire your forbearance. I couldn’t tolerate more than a few seconds. About as bad as chalk screeching on a blackboard.

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What I’ve come to realize is that what SFT does is straight up evangelism, not scientific discourse. His chosen method is to use science-y words, but what he and his guests are doing is preaching, not discussing science.

As evidence of this, compare the transcripts of videos on the same topic, in particular before-and-after videos when someone else has responded. See if the “rebuttal” to whatever critique is materially different from the original claim. (It won’t be.)

It’s recitation of a mantra similar to how one might recite the Nicene Creed during a Catholic mass. But instead of affirming one’s belief in one holy catholic and apostolic church, it’s affirmation that the genome is mostly functional, that mutation rates prove a recent creation for Homo sapiens, etc.

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I have never interacted with someone who is employed by AIG, CMI, ICR, or The Discovery Institute, where that isn’t true. It’s not about science, it’s all apologetics. And it’s not even evangelism in the sense of being constructed to convince those who do not believe. It’s merely and only designed to give comfort to those who already believe, by telling them in technical and science-sounding ways(usually by putting on an authoritative act, couched in fake humility and courtesy) that the science supports their cherished beliefs.

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Don’t forget people are much more likely to donate money to your organization when you tell them what they want to hear.

With respect to the great apes, at least AiG has committed to them all being the same “kind.” There is a new display at the Creation Museum that makes this quite clear: image

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Their diagram shows 9 species of great apes before The Flood, 8 of which went extinct at Flood time. Then it shows well known hominids like Ardipithecus and Australopithicus coming into existence well after The Flood. But they also tell us all fossil remains of Ardipithecus and Australopithicus were buried by sediments during The Flood. None of it makes a lick of sense of course.

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There seems to be one genus of great ape (one with a very large current population) missing from that diagram. I wonder why.

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I thought flood sediments were cretaceous? So that puts Ardi after the flood. So their diagram seems to be consistent with other things I’ve read from them. So I’m curious where you read that

Oh boy, you really would need a new thread to discuss the absolute mess and infighting on what is/isn’t flood rock in the YEC communities…

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AIG and ICR both say all sedimentary deposits are from the Flood. The only question in their mind is what was the pre-Flood base rock. Some say the K-Pg boundary is the Flood/preFlood line, others say the Flood laid everything down to the Vishnu schist in the bottom of the GC. It depends on which YEC you ask. There’s no rhyme nor reason to any of their claims.

Could you cite something for those claims? Your first sentence contradicts the remainder, and I have never seen a creationist claim that the flood began at the K/Pg boundary, though I have seen many claims that it ended there. A more important point is that creationists can’t agree on where in the sedimentary record the flood either starts or ends.