OK, let’s look over the evidence (and please correct me if I miss important evidence or list some evidence incorrectly.)
1. The allele in question has only been found in 33 people in the world, despite a lot of scientific attention.
As I've said, it COULD be a mutation, but this simply has not been unequivocally proved. What's "a lot of scientific attention?" Since this is a very rare allele you have to be awfully thorough and even then how could you know you didn't just overlook it?
2. All 33 are direct descendants of a person who lived in the 18th century (call him Apo).
Yes. And how many of his descendants who don't have this allele are known? My own grandfather has at least 100 living descendants now. The 18th century is 100 years before his time, so the number of descendants could be a LOT larger than 33.
What do you know about Apo's descendants, their parents, their grandparents, their greatgrandparents. There are many branches of a family tree after 250 years or so. How do you know you didn't miss some who had the allele in Apo's sibling's lines?
3. The allele is different from an allele generally present in the human population by a single amino acid change.
Yes, an easy target for a mutation; but that means that the good allele is just as easy a target as the bad allele, which is why it could very well have been the other way around and the bad allele is a mutation that happened WAY back there in the human race, from which only a few lines of the good allele escaped.
4. Both hetero and homozygous individuals appear to be healthy, and no disadvantage to the allele can be found.
OK I'll have to read the article carefully. Is it known for sure that there are some who are homozygous for this trait?
5. Mendelian genetics and general probability apply.
I would hope so.
6. The allele is dominant.
So I've heard.
Now, which explains these better?
Test #1 - why are all 33 descended from Apo, and none found in, say, Chicago?
I'm not sure you haven't overlooked some in Chicago. Maybe in the last generation. Or in Iceland, or in Tierra del Fuego. Or even in Italy for that matter. How can you be absolutely sure?
If it was a mutation in Apo, then no one but his descendants should have it. That checks.
Yes.
If it was present in Adam (required by Faith), then somehow, despite being harmless, it must have been selected against to go from a frequency of at least 0.25 %, to a present day frequency of 33 in 6E9.
More likely killed by a mutation, or mutations in several individuals over time. Since there is nothing about it to select for it or against it, I would suppose it could have been lost to the majority of human posterity through a severe population reduction at some point, that severely reduced its frequency simply at random.
The odds of a human having it are approximated by 33/6E9, and so the odds of all of them being in the same town of 1000 people is
(the odds of a person being in that town vs the rest of the world)^(number of people with the allele)= (1000/6E9)^33
= 2E-224 = 0.000(200 zeros)2
Now that’s unlikely.
But that's silly. Obviously "Apo" got that allele, and passed it on to his descendants in that town. Nothing unlikely about that. The only question under consideration is how Apo got it and why other relatives apparently don't have it, if a reasonable number of them have actually been tested, which is a question.
OK, next test of the explanations (#2). If it were a mutation, it would HAVE TO BE clearly and simply related to present genes.
If it were an existing allele, it could be very different. In fact, it should be very different, since the odds of that long a nucleotide matching perfectly are very low. It’s as if you picked two pages from different parts of an encyclopedia, and the middle paragraph was exactly word for word identical, except for one word, which was changed from, say, “herd” to “hard”.
Clearly the mutation hypothesis is much more likely for this point, since it predicts the similarity, while the Adam hypothesis must explain away this otherwise very unlikely word for word matchup. (unless we want to postulate a God that specifically tries to trick people so he can send them to hell and watch them burn).
If we had the nucleotide sequences, I could calculate the odds they would match up so perfectly, assuming no relation.
Sorry, you lost me in all this. I thought we were talking about a very short segment, a mere amino acid, which is why a mutation was considered to be such a likely explanation. I don't grasp what it is you are talking about having to match so perfectly.
Test number 3. Does this gene increase or decrease over time?
Humans have been eating artery-clogging meat for a long, long time. Even if reproduction happens prior to death, a longer post-reproduction life is selected for because one can help raise the kids and grandkids.
I really don't grasp this reasoning. Are there studies that prove that the long lives of grandparents contribute to reproductive success, which is "all evolution cares about" as I've been told SO many times, as if it were news. Parents makes sense, but then arteriosclerosis doesn't usually get to us until we're about grandparent age.
So the mutation explanation says that the allele has been selected for the few generations since it has arisen, and that coupled with population growth explains how we went from 1 to 33.
All it means is that it got passed down in the proportions that accord with Mendel's formula in a normally healthy reproducing family line. No selection is implied, it just got passed along in the normal course of things.
I’ve explained before why we know that it was just 1 back at Apo- the numbers otherwise are extremely unlikely. So the mutation explanation explains the data.
It could, but it just doesn't seem to me that you've covered enough territory. Just wait until a few years down the road the same allele is discovered in a family line in Turkey and it can be traced back to the 13th century or something like that.
The adam explanation somehow must have this gene being strongly selected against to go from at least a 0.25% frequency, to near zero (1 in 700000000 in 1750 or so), then for some reason must have the whole process reverse, where now it increases in frequency. I haven’t heard any explanation of this back and forth gene frequency from the adam explanation.
Well I gave a scenario above about how mutations could have zapped it here and there though it survived in some populations in very low frequency. There is nothing about it to select for or against that I can see, and again, I don't get the longevity-value argument since it seems to contradict the standard evolutionist formula of reproductive success. I'd simply expect that it was more frequent in earlier centuries and just got mutated out, or squeezed out by population decreases or some such. It's not as likely as your explanation, true. But again, wait until you discover someone out of that Apo family line with the same allele. In Italy.
In fact, if things continue to degenerate after the fall, then the frequency of this good gene should only have gone down since Apo, so it should only have a couple people at most, or not exist at all.
Nobody has argued that this is a uniform process. I would expect that there would still be people of extraordinary good health living here and there. If you want the spiritual explanation, it's all a matter of sin. Read the Book of Proverbs. Good health and long life are a matter of living according to God's Law. I believe the Tao gives the same advice in different words.
I’m sure more comparisons can be made, and we can discuss those as well. Based on 1, 2 and 3 above, it really doesn’t look like “two explanations that work equally well”.
Well, this isn't a crucial issue to me. I don't care if it's a mutation. I just seriously doubt that it is and really irrefutable evidence for it has not yet been given.
Edited by Faith, : No reason given.
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