What is the mechanism that prevents microevolution to become macroevolution?

Yes, it COULD be a mutation, but you are declaring that it IS a mutation though the evidence does not make that inevitable. More new information. What further new information are you going to drop on us? All his parents' and grandparents' descendants have been studied, you're really claiming that? OK, another way that can be explained is that those who are available for study all got the recessive allele, all aa's without a single Aa in the lot; he had an Aa and that got passed down according to Mendel's formula, producing more aa's as well, because of the rarity of the dominant A, but also a few with this protective A. It could happen this way, and in the other line, the line of his siblings, the dominant form would just never show up again. As for his grandparents' line, and descendants of his aunts and uncles, there may be some descendants that haven't been identified. But in any case a single dominant could be all that was ever available to pass on in this family.It could have been this way:Grandparents Aa - aaParent: Aa -- Parent's siblings: aa aa aa aa aa aa (it's possible)Parents together are Aa - aa and so on.The A is then passed on ONLY in this line, and only to some of the descendants. In other words the descendants don't *prove* mutation any way you look at it. Basic inheritance works just as well the way I laid it out above. He's the top of the pyramid for his own line of descendants, but he could have been the only one of his siblings to get the dominant A allele, while his siblings all got the recessive other form of the gene. That could have been the case a generation previous too, that only his parent got the A allele but no aunts or uncles got it. Of course the more siblings in each generation the more likely another of them got it too, but you haven't said how many there were. And again, likelihood is not inevitability.Edited by Faith, : No reason given.

SOME of the descendants kept it. Yes I'm saying that it could certainly have happened that way, that billions could have lost it. The inheritance scenario is quite reasonable. It only becomes of value past the reproductive age, since hypercholesterolemia normally catches up to us later on, so there'd be no selection factors working for it.This seems to me to fit the pattern of mutations doing us little good. That is, the known odds are that a mutation is either of no (recognized) function or it's deleterious. Edited by Faith, : No reason given.

I keep coming back to that thread to see if anybody is actually talking about macroevolution just to find out that you are still quibling about whether that was a case of benefical mutation or not. How does that connects to the macroevolution discussion?

It does, though. The alternatives are far, far too unlikely. It's far more likely that one man had one mutation that he passed on to some of his ancestors, than to suggest that more than six billion people all happened, coincidentally, to have the very same mutation that the decendants of that one man somehow didn't inherit. My, what a coincidence, that out of 6 billion people, the only ones that could be found to possess this dominant allele, which has profound and obvious effects on anybody with dietary risk factors, the only people who could be found all happen to be the direct decendants of one man who lived in the 18th century. The mind reels!Faith. Finding people with this gene would be as simple as sending an email out to cardiologists and geriatricians asking them if they've ever encountered any individuals who, despite eating cholesterol-heavy foods and smoking, stubbornly refuses to develop any arteriosclerosis. The effects of this gene are profound and obvious. It should be very easy indeed to find other people with the very same gene, but they don't seem to exist. The only people on Earth known to have this gene are the 33 people decended from that one guy.That's entirely consistent with a mutation emerging in a single individual. It's completely inconsistent with your model, where a beneficial mutation somehow, inexplicably, is outcompeted by detrimental mutations in every individual on Earth except for the direct decendants of one man.Your explanation doesn't make any sense. But how did the grandparent get the trait? And why didn't any of the grandparent's siblings have it? If they did, why didn't any of their children get it?Beneficial mutations increase in frequency over time. In this case, the gene has gone from one individual to 33. Beneficial mutations, almost as a rule, don't decrease. If a mutation goes from lots of people, to one person or less, by definition, that's not a beneficial mutation. Selection doesn't select like that. The way you say "it's possible" indicates to me that you understand how highly unlikely this would be to happen, even just in one generation.You're asking us to believe that, before Patient Zero back in the 18th century, that arrangement of offspring is exactly what happened every single time, in every single generation.How can you expect anyone to take you seriously with that? You're asking us to believe that an extraordinarily unlikely arrangment of alleles occured not just once, but thousands upon thousands of times, going all the way back to Adam. And what evidence to you provide to convince us that this extraordinarily unlikely sequence of genetic events actually occured? Why, none whatsoever. Faith doesn't need evidence, after all. It's sufficient for her to simply assert that a thing happened, and we're all completely unreasonable for simply taking her word on it. And his aunts/uncles? Greataunts/greatuncles? Greatgreataunts/greatgreatuncles? Why didn't any of them get it? We know they didn't, or else they would have passed it on and then we'd know of people that had it beyond this guy's direct ancestors. How many do you suppose there would be, if we're talking about the line of this guy's ancestors stretching back to the beginning of time?

Faith did point out that there may be very little selection on this allele since it might not affect anyone until after reproductive age.

Also the increase in the number of people carying the gene may reflect nothing more then the increase in overall population that happened last two centuries. I think crashfrog is right to believe that this is a case of benefical mutation but I don't blame Faith for feeling the need for a little more convincing evidence. Unadvertedly, though, Faith is making another point which is that even if it is a true case of benefical mutation, that is not easy to prove. Therefore the fact that not many cases of benefical mutations have been found so far cannot be taken as evidence that they do not exist or are to rare to be relevant, because it is so hard to prove that you have one (even when you are staring at one).

Maybe, but remember it's not about how many children you have, it's about how many grandchildren you have. Having babies that don't themselves survive to reproductive age is as much an evolutionary failure as never having babies at all.To the extent that this mutation extends the life of a person who can help in the raising of their offspring's offspring, it could easily have a beneficial effect.Faith has yet to specify a mechanism of negative selection, so her model that somehow this is the original and we all have the broken mutation is nonsense. The probabilities don't work out. Further she states that it's more likely that a protein will be broken than improved, and while this is true, it's irrelevant to this specific case.The mutation substituted one amino residue in the polypeptide, correct? So there's no difference in probability between a substitution occuring on Apo-AI that results in Apo-AIM, and a substitution occuring on Apo-AIM that results in Apo-AI. They're probably equally likely.So the only relevant probability is whether it's more probable that one person gains one mutation and passes it along, or that six billion people all coincidentally gain the exact same mutation and pass it along to everybody but 33 people.Imagine this. I walk out of a room and tell you that there's 50 quarters inside, laying on the floor. Before I entered they all were showing the same face up, but I don't tell you which. I also tell you that I flipped some number of them, but I don't tell you how many. And by "flip" I mean I picked some number of them up, one at a time, flipped them through the air, and set them back down with their new face up.You walk into the room and see 47 coins heads-up and 3 tails-up. Is it really so hard to reconstruct what side all the coins originally showed, and therefore which coins were changed because I flipped them? Certainly there's the possibility that I flipped all 50 coins. But the chances that 47 of them would be heads if I had done that are less than one in one trillion. You would have to have the mind of a child to emerge from that room and accuse me of flipping every single coin, or even most of them. You'd have to be pretty ignorant indeed to accuse me of flipping any more than 4-5 of the coins, max.Edited by crashfrog, : No reason given.

First-Faith, I have yet to respond to your response to my post last week. I’ll do so, I’m just too busy now. I’m taking a short break to jump in here to supply some numbers that have been sorely lacking.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.2. All 33 are direct descendants of a person who lived in the 18th century (call him Apo).3. The allele is different from an allele generally present in the human population by a single amino acid change.4. Both hetero and homozygous individuals appear to be healthy, and no disadvantage to the allele can be found.5. Mendelian genetics and general probability apply.6. The allele is dominant.Now, which explains these better?Test #1 - why are all 33 descended from Apo, and none found in, say, Chicago?If it was a mutation in Apo, then no one but his descendants should have it. That checks. 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.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)2Now that’s unlikely.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.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.
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. 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.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.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.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”.Oh, not that it’s important, but an Aa + aa mating has a 50/50 chance of producing an aa with each child. Thus the aa aa aa aa aa aafamily mentioned has a 1 in 2^6 or 1/48 = 2% chance of happening. Yes, it’s possible, in fact, it’s thousands of billions of billions of billions of billions of billions of billions (.....) of times more likely than getting all 33 in just that one town. But in reality, these kinds of numbers show how unlikely either thing is.Take care--Equinox

Crash, that's not the idea. The idea is that back say a few hundred years or few millennia, the good allele got mutated to the nonbeneficial amino acid. It's an easy mutation to occur it appears, affecting only that one amino acid, so it could occur now and then in different individuals. This way the nonbeneficial mutation would gradually work its way into the population more and more with each generation. In each generation there would still be a lot of people who had the good kind of allele too of course, but if the bad mutation continues to occur from time to time then more and more people will have it. By modern times most people have it. By very modern times only a few families here and there still have the good allele to pass on as the Italian family did. It could also be that it still survives in concentrated numbers in some parts of the world where it hasn't yet been identified. Edited by Faith, : No reason given.

Does every person *on earth* have a cardiologist, Crash? Even in this first world country a lot of us would not be identified even for having or not having arteriosclerosis because we don't go to doctors much, so we're not going to be chosen as subjects for a DNA study. If we up and die of something else nobody will ever know if we had that allele or not. It seems that quite a few people are living up into their hundreds. One lady just died at 117 I think it was in South America. Was her DNA studied? Is every individual who lives a long life being studied?

Well, nobody has told us how many siblings there were in the family that passed on the allele in question so I'm guessing. I guessed a large number because that was common a few centuries ago. {edit: But of course you're right about the 50% chance of passing on that dominant allele, I wasn't thinking. So maybe there weren't many siblings after all}, or maybe there were siblings who died young, because that also was common in those days. More information would clear this up easily, if it's available.And it's also still possible that other descendants of the family of that 18th century individual are still living somewhere with the good allele.Edited by Faith, : No reason given.Edited by Faith, : No reason given.Edited by Faith, : No reason given.

Selection, Faith. Why wouldn't those people be outcompeted by the people with the Apo-AIM, who live long enough to support several generations of children?You're proposing that a deterious allele overtakes a beneficial one. Why would I accept such a counterintuitive outcome absent any evidence? Here and where? Where else is it?

When a big fat smoker dies, and during his autopsy they see tar in his lungs, and his 300 lbs of fat, but they can't find any evidence of arterial plaque - which is pretty obvious in a chest exam - the coroner is going to notice.And he's going to think back to that email he saw, looking for candidates for genetic analysis to detect Apo-AIM. Just about. How hard do you think it is to do a DNA test?

I'd be surprised if many people of any sort are tested even partially. Do you have anything to back this up?

This is a pretty unusual idea of yours that the grandparents' merely living a long time contributes so much to the reproductive success of their grandchildren. Where, pray tell, does that show up in evolutionist thinking outside your own ruminations? Why is the fact that selection only affects the reproductive years hammered away at so aggressively if other completely circumstantial factors are so important? Well,
1) it's not lethal, not before reproductive success anyway, which is aggressively and loudly proclaimed to be "all that evolution cares about;"
2) and besides that, many who have it probably have had a long life in spite of it;
3) On its first appearance, were DNA analysis available, it would probably have shown up as one of those "nonfunctioning" mutations;
4) it is an acknowledged fact that most mutations are either "nonfunctioning" or deleterious, so why WOULDN'T you accept that this scenario fits the known evidence? Africa? Indonesia? Tibet? Rural or remote areas in Eastern Europe and Russia or South America -- or the US for that matter?{edit: And I'd guess that even all the relevant branches of that Italian family tree haven't been subjected to DNA analysis.Edited by Faith, : No reason given.Edited by Faith, : No reason given.Edited by Faith, : No reason given.Edited by Faith, : No reason given.