That begs the question of how did the original mutation spread to X percentage of the population.
Spontaneous mutations and random genetic drift. (There’s also the case where X is the original variant and has been decaying for a long time, but that’s not relevant to homosexuality.)
A spontaneous mutation produces 1 (one) individual and pure genetic drift is unlikely to get to noticeable percentages of the population (with some exceptions, of course).
pure genetic drift is unlikely to get to noticeable percentages of the population
The random walk will either lead to fixation or extinguishing the spontaneous mutation, and the probability of fixation for a neutral mutation is meaningful: “the rate of fixation for a mutation not subject to selection is simply the rate of introduction of such mutations.” Hence, genetic drift is powerful enough that it can separate isolated populations.
Well, the rate of fixation of any neutral mutation is the rate of neutral mutations in general and so is meaningful. The chances of fixation of a particular neutral mutation are the chances of this particular mutation happening and so are very very small.
So if you look at a newborn baby and go “Hmm, this baby has a novel mutation X, it looks to be neutral, what are the chances that this specific mutation X will fix itself in the population?”, the chances are very low.
On the other hand, if you aggregate all novel mutations of all babies born, say, during this year, then the chances that one (and we don’t know which one) of these mutations will survive and get fixed are more meaningful.
So if you look at a newborn baby and go “Hmm, this baby has a novel mutation X, it looks to be neutral, what are the chances that this specific mutation X will fix itself in the population?”, the chances are very low.
if there is no advantage whatsoever, the proportion X can only go down—there is nothing which can increase it
This is totally wrong. It can easily increase: genetic drift/random walk. Not only is it possible, all sorts of neutral mutations reach fixation all the time. It’s true any particular instance of any mutation may not win the lottery, but it’s quite different to argue that there is no such thing as a lottery and no one has ever won a lottery!
That begs the question of how did the original mutation spread to X percentage of the population
There is no question to beg; the gene in question may simply be yet another lottery winner like what regularly happens. At any time, there are countless variants which are slowly working their way up to fixation or down to extinction.
It is entirely meaningful to ask about the probability they will make it to either endpoint and how fast, and if you are looking at an existing variant with a particular prevalence, weird to object to it on the basis that each time the novel mutation appeared (and it could have appeared many times before succeeding in spreading as much as it did) it had little chance of spreading; perhaps, yet, it did.
Read the comment you linked more carefully. I’m not talking about reality—I’m talking about the model which RichardKennaway proposed. Specifically, I find this model too simple because it has a single force acting on the spread of a gene—the “selective disadvantage D”. Note, by the way, that it’s not about neutral mutations at all, presumably D is not zero and we are talking about mutations which are actually selected against.
Given that, the expected value of X (I’ll grant you that I should have been more clear that I’m talking about the expected value and not about what one instantiation of a random process could possibly be) must decrease.
Spontaneous mutations and random genetic drift. (There’s also the case where X is the original variant and has been decaying for a long time, but that’s not relevant to homosexuality.)
A spontaneous mutation produces 1 (one) individual and pure genetic drift is unlikely to get to noticeable percentages of the population (with some exceptions, of course).
The random walk will either lead to fixation or extinguishing the spontaneous mutation, and the probability of fixation for a neutral mutation is meaningful: “the rate of fixation for a mutation not subject to selection is simply the rate of introduction of such mutations.” Hence, genetic drift is powerful enough that it can separate isolated populations.
Well, the rate of fixation of any neutral mutation is the rate of neutral mutations in general and so is meaningful. The chances of fixation of a particular neutral mutation are the chances of this particular mutation happening and so are very very small.
So if you look at a newborn baby and go “Hmm, this baby has a novel mutation X, it looks to be neutral, what are the chances that this specific mutation X will fix itself in the population?”, the chances are very low.
On the other hand, if you aggregate all novel mutations of all babies born, say, during this year, then the chances that one (and we don’t know which one) of these mutations will survive and get fixed are more meaningful.
This is irrelevant to the original claims you were making, which I was responding to: http://lesswrong.com/r/discussion/lw/mbl/when_does_heritable_low_fitness_need_to_be/cgrk?context=1#cgrk
You claimed:
This is totally wrong. It can easily increase: genetic drift/random walk. Not only is it possible, all sorts of neutral mutations reach fixation all the time. It’s true any particular instance of any mutation may not win the lottery, but it’s quite different to argue that there is no such thing as a lottery and no one has ever won a lottery!
There is no question to beg; the gene in question may simply be yet another lottery winner like what regularly happens. At any time, there are countless variants which are slowly working their way up to fixation or down to extinction.
It is entirely meaningful to ask about the probability they will make it to either endpoint and how fast, and if you are looking at an existing variant with a particular prevalence, weird to object to it on the basis that each time the novel mutation appeared (and it could have appeared many times before succeeding in spreading as much as it did) it had little chance of spreading; perhaps, yet, it did.
Read the comment you linked more carefully. I’m not talking about reality—I’m talking about the model which RichardKennaway proposed. Specifically, I find this model too simple because it has a single force acting on the spread of a gene—the “selective disadvantage D”. Note, by the way, that it’s not about neutral mutations at all, presumably D is not zero and we are talking about mutations which are actually selected against.
Given that, the expected value of X (I’ll grant you that I should have been more clear that I’m talking about the expected value and not about what one instantiation of a random process could possibly be) must decrease.
In the model proposed there is.