Toni Torppa and Genetics

How do you think you are genetically different from your parents? Why are you unique compared to your parents, for you are not a clone of them. I can say that you have hundreds of thousands if not millions of new allele combinations that do not appear in your parents. Yet the information on these variants (new combinations) comes from your parent’s information, they are not mutations. Due to mutations, you may be different from your parents (60-175) in terms of base pair. So if even a single generation today can produce an incredible number of new allele combinations that make individuals unique, then what is the problem here now?

The problem is that you don’t understand the fact that high school level genetics shows that recombination processes can easily produce everything we see from heterozygous individuals, even if there was a bottleneck relatively recently. There were also so few mutations at the time of Noah that there were no genetic side effects from inbreeding, as they are today.

Geneticist Robert Carter writes in his article “The Non-Mythical Adam and Eve!
Refuting errors by Francis Collins and BioLogos "- https://creation.com/historical-adam-biologos

"Some alleles, however, have been added to the population through mutation. How much Genetic diversity is due to mutation? Given the 10 million common variations in the human genome, there are many more ‘private’ and very rare variants that occur in one or a few individuals in specific populations.These should be mutations that have occurred since the Flood and Babel.With an average (modern) generation time of 30 years, there have only been about 150, perhaps as many 200, generations in all of human History. Assuming a conservative modern estimate of 100 new mutations per person per generation, that gives us between 15 and 20 thousand mutations per person. This is a huge number when added up across the world population, and most of these should be unique. Yet, on the individual level, it might be expected that only a small fraction (less than 0.01%) of heterozygosity is due to mutation."

"How much created diversity might we assume? One way of estimating this is to look at the number of alleles shared among all world populations… Since most of the genetic diversity known today can be found among multiple world populations, most of the variation should have been here from the beginning. Is it possible for a single person to carry this much diversity? I ran an analysis of the HapMap data to measure the amount of heterozygosity within the HapMap individuals. Population-level differences were slight, with a global average of 4.33 ± 0.234 × 105 (±SD) heterozygous alleles per person. Thus, approximately 30% of all HapMap alleles are heterozygous within each person. If there are 10 million common variants, a single individual would be expected to carry upwards of three or four million heterozygous alleles! Because most people are phenotypically normal, there is no reduction in fitness associated with these high levels of heterozygosity. Why should there be if most of this variation was created by God and engineered into the original genome? I expect Adam had about 10 million or more heterozygous loci and that each of his children had half that much."

Just so you know who you’re condescending to: Stephen Schaffner | Broad Institute

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Oh, coffee. Why will you not stop shooting out of my nose and destroying my keyboards? Why must I buy keyboards in the Costco 24-pack?

I don’t know what glipsnort will say to your remarks, but I do find this about him online:

"Stephen Schaffner is a senior computational biologist in the Infectious Disease and Microbiome Program of the Broad Institute of MIT and Harvard, where he uses the tools of population genetics to study human genetics and infectious disease, including viral, malaria, and host genetics. Schaffner has developed techniques for detecting the effects of positive selection on genetic variation, carried out model-based studies of human demographic history, and developed tools for identifying recent common ancestry in malaria parasites. He often focuses on detecting cases of positive natural selection, where a given trait is beneficial for the organism and is therefore selected for in the population.

“Schaffner performs computer simulations of genetic variation and studies the history of human demographics. He also works to understand linkage disequilibrium, a term used in the field of population genetics to describe a combination of genetic markers that occurs more or less often than expected. These studies can aid the search for genetic markers linked to traits or disease.”

Now, I’m not sure what “high school genetics” is. If it’s some sort of James Dean-ish thing like “Rebel Without A Genome” or something else along those lines, perhaps glipsnort is horribly ignorant of it. But I do know that on those occasions when I don’t want to look like a fool, I seldom confront a noted legal scholar with remarks about how “high school business law” would tell him something he doesn’t understand. I suspect that my lack of depth in genetics would counsel similarly in that field, but maybe this is one of those “everything I needed to know about population genetics I learned in kindergarten” kinds of things.

So, I don’t know what they teach you in the high schools these days. But I do know that I hardly ever, in my high school days, opened the Biology textbook to page 7 and then personally overturned the entire dominant paradigm of biology. Perhaps I lacked talent.

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Have you guys built a model that you can present?

Let’s say we started with 10 individuals who were heterozygous for every gene, and all 20 alleles were different from each other. That would still only be 20 variants. If we start with 2 individuals, that number drops to 4 variants per gene. This is by far the most charitable model, with everyone being heterozygous and all having different alleles which isn’t something that we would expect to see in a normal group of people.

So what do we see in the human population? A lot more than 4 to 20 variants for each gene.

Say what??? There are only 20 to 30 thousand human genes, not three to four million. You only have two alleles per gene (i.e. our genome is diploid). You can only be heterozygous at a maximum of 20 to 30 thousand genes, and if we are 30% heterozygous on average then that number is closer to 5 to 10 thousand. There seems to be a fundamental misunderstanding of what alleles and heterozygosity are.

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This isn’t true if alleles are being defined as segregating SNPs, in which case there would be two alleles for every bi-allelic SNP (by definition). Given that many genes will have multiple SNPs, you will end up with many more than two alleles per gene.

From what I can see, we need to define the differences between alleles and SNPs so all of this is a bit clearer.

I also suspect the rarity of SNPs is of importance. My popgen-fu is a bit weak, but what the main argument seems to be pointing to is the molecular clock. How much time does it take for a new SNP to become common enough to be detected in small numbers from a survey of 10,000 or 100,000 people? If we start with a population of 10 people, shouldn’t the vast majority of those variants be common in the descendant population?

Given the context, I think it’s pretty clear that “allele” is referring to various kinds of sequence variants, which can occur at multiple positions within any given gene.

As @glipsnort noted above, most of the variation present in human genomes exists at low frequency. Of course, there are also are many variants that common within and among populations.

Here are a few recent papers that go into some detail on this topic and may help answer some of your questions:

A global reference for human genetic variation
An integrated map of structural variation in 2,504 human genomes
Insights into human genetic variation and population history from 929 diverse genomes

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You should definitely read the book Replacing Darwin https://answersingenesis.org/store/product/replacing-darwin/ It teaches really well what is meant today in genetics by the genomic position of alleles. Somehow ironically, on the page from which this introductory post was moved here, the professors despised Jeanson’s book, which teaches these basics of genetics really clearly. So it comes to my mind whether it is now intentional that students not to learn certain things - so that evolution can be better justified? When you understand how recombination processes can produce diversity, then the whole idea of evolution (mutation + selection) becomes even more insane.

That’s a statement that makes no logical sense. The fact that recombination can produce new combinations does not in any way constitute an argument against, or in any way undermine the reality of mutations occurring in addition to recombination, and selection acting on the variation that results from both of those processes.

Drat! Now you have cost me a keyboard as well. (It was done in by diet root beer and not coffee—but same idea.) There should be a reader warning on this thread.

Being a bi-allelic SNP was what got my uncle out of the draft in WWII. (When they simplified the classification system, he got relabeled as 4F.)


POSTSCRIPT: Perhaps I’m remembering that wrong. The original classification may have been bi-allelic SOB. (I don’t know about “segregating SNPs”, but the military definitely segregated a lot of SOBs. They called it the stockade/brig.)

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I find that when I get members of the Scottish National Party to say “bi-allelic,” it sounds so doggoned much better than when I say it. Unfortunately, due to the SOB that is COVID, my trip to Orkney (where they sound like Vikings who learned their English from Scotsmen, if you can imagine that) has been postponed. The islanders have made it clear that if you defy their current attempts to deter tourism, they have all seen The Wicker Man and will not hesitate to take appropriate action.

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First off, no amount of recombination between existing alleles will make the human genome look like the chimp genome. Recombination can’t explain the divergence between species.

Second, where do new mutations in the human genome go? Do they just disappear?

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First, coffee in the keyboard. Now, every projector bulb in the building is burned out, as though an immense energetic projection had overwhelmed them all at once. Not a good day.

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Another nice recent paper:

Population Structure, Stratification, and Introgression of Human Structural Variation

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Probably not many here will remember one of Sean Connery’s early roles in Darby O’Gill and the Little People. (1959) Disney’s sequel was supposed to be set in Scotland and contain a scene where Connery was to sing and dance the traditional Scottish jig “I’m Just a Bi-Allelic SOB from Orkney.”

Yes. That one knocked out my Wi-Fi for a few minutes. Buffer overload I think. I had to clean it out manually with a factory reset. And the varistors in my surge suppressor gave up their lives for that one.

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I’m afraid I don’t remember that one, either. But I do remember “I’m just an Orkney from Muskorkney.”

Yeah, solid state just does not do this all that well. I would recommend a huge Variac, but the problem is that you need reaction times in the milliseconds to be able to reach over and crank the voltage down. I haven’t reacted that quickly to anything since my radio-shutting-off days in the 1970s. Oh, those Bee Gees!

Now that I think of it, though, a great big gap-type lightning arrestor like we used to use on antennas might do the trick. It’d take the really big pulses down to a level where those varistors might be able to survive the stuff that still got through.

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The problem is this. Take each genetic variant by itself – never mind combinations with other alleles, so we can ignore recombination. Suppose there are only two alleles for a variant. Count how many copies there are of each allele in the population; that gives you the allele frequency for that site. If the frequency is 10% – 10% of genomes have 1 allele, 90% have the other – how did it get to that frequency? A new mutation occurs as a single copy of the new allele. In a mutation that occurs today, that means the new allele has a frequency off 0.000000007%. In a population of size 10,000, the initial frequency is 0.005%.

How does one of these new variants get to moderately high frequency? They can get there by a process of random change in frequency from generation to generation (‘genetic drift’) but that takes a long time – and there are a lot of low and moderate frequency variants in the human population (and even more in other species). You can’t get there from a single couple in a few thousand years.

Don’t try to teach your grandmother to suck eggs.

Geneticist Robert Carter is ignoring the site frequency spectrum, which is what I was talking about above. It doesn’t matter how much heterozygosity you put into the first couple – you’re never going to get a site frequency spectrum out that is heavily weighted toward low frequency alleles, since all alleles start out with a frequency of at least 25%. Anyone writing about population genetics (which is the subject here) and ignoring the site frequency spectrum should himself be ignored.

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Do you understand what geneticist Robert Carter means in these sentences by variant?

  • “Since most of the genetic diversity known today can be found among multiple world populations, most of the variation should have been here from the beginning.”

  • “If there are 10 million common variants, a single individual would be expected to carry upwards of three or four million heterozygous alleles!” Historical Adam biologos - creation.com

Can you tell me because I want to know if you understand what Carter means by that. A proper understanding of this issue is crucial for the dialogye.

He means that alleles that are shared between populations have generally been around since before the populations split from one another. Since for him the populations split shortly after the creation of humans, those variants must have been in the created couple.

Because humans have two copies of their genome, they have places where one copy has one allele and the other copy has the other allele; these are heterozygous sites. If all of the common alleles had a frequency of 50%, each person would have about 5 million heterozygous sites in their genome. (In reality, each human’s heterozygosity has roughly equal contributions from each slice of frequency, e.g. the same number of heterozygous sites are contributed by 50% alleles as by 1% alleles.)

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