Valerie: Questions about TMR4A

Games over a subject this important are stupid.

Here are the two papers he referenced:

In this paper we have used logic and numerical simulation to show that there are several Designed Diversity mechanisms that can reconcile a literal Adam and Eve with the allele frequency distribution now seen in the human population. These genetic mechanisms include: 1) designed diversity within Adam and Eve’s four sets of chromosomes followed by accelerated genetic drift associated with multiple population constrictions; 2) as above, combined with more powerful demographic forces such as selective sweeps, lineage extinctions, and differential subpopulation expansions; and 3) designed diversity within Adam and Eve’s originally created gametogonia. Together, these various genetic mechanisms seem to falsify the claim that there is “no way” that two people could give rise to the human allele distribution that we see today. The designed gametes model appears to be especially robust, and in our opinion is even elegant. It seems to be the best explanation for how Adam and Eve might have simultaneously given rise to our current human allele patterns and our current linkage patterns. Future research will examine the concept of “demographic stirring” and how it may accelerate genetic drift. Given the premise of a miraculously created Adam and Eve, the most coherent, powerful, and compelling explanation for most of the genetic diversity found within the human race is “designed diversity”. This is especially true when we consider the various forms of human beauty and the various forms of human gifts and talents. Human traits of this type cannot rationally be attribute> to Darwinian mutation/selection. In addition, designed diversity appears to have enabled rapid human adaptation after the flood.

The one human genetic compartment that has not received as much attention by all sides in the origins debate is the Y chromosome. For YE creationists, their expectations for Y chromosome differences today are easy to derive. Because males are XY and females XX, Adam would have been created XY, and Eve, XX. Therefore, a single Y chromosome would have been present at Creation. Consequently, unless God created Adam’s gametes with Y chromosome differences (Carter, Lee, and Sanford 2018; Sanford et al. 2018), all modern Y chromosome differences would be the result of mutations since mankind’s origin. Conversely, evolutionary expectations are also easy to derive. Because evolutionists explain all genetic differences ultimately by mutation, they also explain all Y chromosome differences by mutation. Thus, in theory, the Y chromosome differences and mutation rates could represent another direct test of the YEC and evolutionary timescales.

In this paper, we examine the pedigree-based mutation rates in high-coverage Y chromosome sequencing studies and explore the implications of these results for the Y chromosome molecular clock.

Our results demonstrate that a Y chromosome molecular clock exists, and that it specifies about 4,500 years in total for human paternal history (figs. 1, 3). Rather than being an anomaly, these results fall in line with the expectations derived from comparisons of low coverage and high coverage Y chromosome sequences (Poznik et al. 2016). Since high coverage sequencing is known to increase the tree tip length over the lengths derived from low coverage sequencing, and since father-son relationships among the living represent the most terminal aspect of any tree, our empirical results match precisely what previous results had predicted.

Conversely, our results also strongly challenge the evolutionary timescale (fig. 2). Rather than confirm a history for humanity that stretches back hundreds of thousands of years, these results reject this hypothesis. If men have been around for hundreds of thousands of years, they should have accumulated mutations 8- to 59-times the amount currently observed. Instead, we observe only a few thousand years’ worth of mutation accumulation.

Did you listen to the video @thoughtful? We covered the information in the first paper and also the second. Do you recall what the problems are with those two papers? Does either one reference TMR4A?

I listened to a good chunk of it. I don’t totally understand the allele paper since I need to learn more about genetics, except that your position is a straw man because there are other options to create the needed diversity to explain what we see today.

Regarding the y chromosome your position is again a straw man because you keep bringing up the whole genome, but again above I quoted the sections that explain the y chromosome is the only part of the genome not subject to different assumptions so it can be tested head to head. If you have problems with the sequencing, that y chromosome mutations are unable to be counted properly, then write that up in a paper responding to Jeanson.

However, the history he’s already explained using his tree makes sense to me and is comprehensive. I realized recently I think I had made a genetic drift argument from it without knowing what I was doing. Though I still need to study that more too to understand what I was doing. Haha. :slightly_smiling_face: I also identified various parts of the tree that were likely belated to Genesis 10 nations on my own based on that. Also based on the Nimrod research I did I could see some migration after the tower of Babel but a lot more after Nimrod became a dictator because people flee dictators. It accelerated migration away from the ME.

We discussed those other mechanisms in video. Which other ones have you found?

How can you reject something you transparently admit and display you have no understanding of? Proverbs 4:7.


See the Allele Frequencies above. I have to study more to understand their argument.

I reject common ancestry because it denies the plain meaning of the Bible whenever it references Adam, creation, and the flood. I reject it because it undermines creation norms of a good creation without death and disease as well as marriage and Adam’s headship at the beginning of creation. I reject it because it makes God the author of evil.

Well, I and others addressed that directly. And that data is not a mechanism. It is an observation. They did not address TMR4A. So why do you say falsely that I used a strawman?


I don’t believe you are addressing the arguments but I’ll give up that point until I understand their arguments better.

You did not respond to my point about y-chromosome. Prove from Jeanson’s paper he needed to and did not adjust for any coverage problems even though he addresses 4 studies.

Also do you think God creating disease and death is more biblical than them being the result of the fall? Please address how this doesn’t make God responsible for evil.

Please address how Jesus’ miracles of power over creation, healing the sick, and raising the dead as evidence of his power as the Word who created are compatible with your view of creation.

So you disagree merely because you do not trust me…

Why would I try to prove a claim I’ve never made?

That’s a factor yes. But the argument from the paper is obviously different from the one you were making. I don’t have to know much of anything to see that.

Should I pull up the time stamp on the video?

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@thoughtful, I’m very willing to engage directly with Carter, Sanford or Jeanson. They understand their arguments and mine. I do not think it is productive to work this out, by proxy, with you. I’d really love to hear from them directly where they think I mischaracterized them.


I responded to this thread because I thought the dare given to @sft was silly. Then I responded because you asked me about the problems with the paper.

I have never been asked to be a proxy by anyone, nor am I being a proxy here. I am giving my own impression of the videos and what you and SFT referenced.

The subject of genetics is of interest and concern to me as it relates to my brothers and sisters in Christ and their understanding of the Bible, the whole church and it’s view of origins, and how it is relevant to the health of the billions of people on the planet. :disappointed_relieved:

I’m praying those same concerns are highest in your mind regarding this issue too, so that you consider it your own responsibility to make sure you’re not mischaracterizing their arguments. Only you can answer for what you do with your life. Based on what Sanford said in his interview with Tour when he mentioned you, I’d be surprised if you didn’t have his contact information or couldn’t get it from a friend, and that he wouldn’t love to talk to you about his paper linked above or anything else on the issue.

You talk about coverage in the video at 35-37 minutes. You refer to low coverage as 10 or 20 times and say to do it well it should be 100 or maybe 1000 fold. Then you again refer to genome studies when Jeanson is looking at 4 on y-chromosome only.

I’m copying what I think are the relevant parts from Jeanson’s paper.

With respect to sequence coverage, the authors reported in the main text of the paper that “the Dutch father-son pairs were blood samples sequenced at >80× coverage” (page 463), but did not give specific information on the Estonian pairs. However, they stated that “sequencing of the whole genome was performed at Complete Genomics (Mountain View, California) at standard (>40×) coverage for blood- and high coverage (>80×) for saliva-based DNA samples” (page 463). We conservatively adopted 40× as the sequence coverage value for the Estonian samples.

The reported sequence coverage for Maretty et al. (2017) was 78× (page 87). Divided by 2, this would translate to a 39×. Skov et al. (2017) reported 40× coverage for the Y chromosomes in the dataset. We adopted the latter for our analyses.

Your inability/unwillingness to stop copying and simply summarize is a strong indication that you don’t understand it.


So, to summarize: you don’t understand it but you know @swamidass is wrong and you say it’s spinach and to hell with it, so there. Did I leave anything out?


first, what do you mean by “it”? I was referring to the first article I linked from Sanford and others. I put it up late last night and skimmed it and my brain was quite dead, and I didn’t think I had the ability to understand it much. That was a mistake as I read part of it in the last few hours, and I’m getting the main argument. I have to read the whole thing. But yes, that paper did not reflect the #2 option that Swamidass and his interviewer were presenting as Sanford&Co view IMO.

that paper did not reflect the #2 option that Swamidass and his interviewer were presenting as Sanford&Co view IMO.

Did we watch the same video? Or am I just confuse? Because here’s what I got from their interview:

Model 1: Strawman “Clone” model. Obviously not identical clones, but if God is gonna modify sex chromosomes, you may as well assume he’s gonna modify others to make diversification easier.

Model 2: Created Heterozygosity, aka Jeanson and (I think) Carter

Model 3: The optional fallback of Carter and Sanford. As in, if future work shows Model 2 doesn’t work, designed diversity in gametes might solve the problem.

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I presume the model also includes A&E having hundreds of children so that gametic diversity isn’t lost.

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I just checked - #3 was extra time (not a YEC model).

#4 was their biology was unlike anything we see now. @swamidass said no one was going there and it was argued by the presenter this was “magic.” But supernatural creation is “magic” :joy:

Sanford&Co paper does seem to argue: Heterozygosity + Designed Diversity, or as you said, possibly designed diversity in gametes (which wasn’t #3). So I don’t think the video presented any option as YEC do.

This was just one paragraph that indicated that to me. I have to finish reading the whole thing and look up terms I don’t understand:

The Designed Diversity Model requires an expanded vocabulary.
Traditionally it has been assumed that genetic variation only comes
from mutations, giving rise to mutational variants (“mutational
alleles”). However, given a miraculous creation, there could be
a very different class of created variants (“designed alleles”).
Mutational alleles and designed alleles would be different in several
important respects. Mutational alleles need time to accumulate,
while designed alleles can exist from the beginning. Mutational
alleles are essentially random typographical errors in the genome
and so are typically harmful, while designed alleles would logically
be created to be beneficial. While mutational alleles always arise
in a population as a single isolated copy, designed alleles would
logically be created at higher frequencies.

That is Model number 2.

I’ve explained how TMR4A rules out this model in a YEC timeline. As far as I know, they have not published anything on TMR4A.

Yes I’m presenting it as ruled out, which is not how YECs are presenting it.

But your TMR4A is based on mutational alleles, correct? Did you miss the paragraph where I quoted the reference to designed alleles? So it’s more like #4 than #2 if I’m understanding this correctly.

TMR4A is a measurement, not a model.

Just like Sanford and Carter, Model 2 allows for new alleles to be added by mutations. But there were also designed alleles from Adam and Eve.