We don’t wonder how it is possible that selection pressure allows anencephaly to occur in 1 in 4859 births.
Oh, but we do.
I’d recommend a couple of West Hunter posts: this and this.
Sample:
Probably the biggest well-understood case involves two common variants of APOL1, a gene that mostly transports lipids, but also zaps trypanosomes – the cause of sleeping sickness. Humans with the standard form of APOL1 are immune to most trypanosomal infections, but two strains have evolved resistance to the standard form of APOL1 – they’re the ones that cause sleeping sickness in humans In response, two variants of APOL1 that block one of the strains of sleeping sickness that infects humans (Trypanosoma brucei rhodesiense) have become common in central and west African populations, and their diaspora.
Unfortunately, these protective variants are hell on your kidneys. And they’re common: > 30% of African-Americans carry a risk variant. It increases the risk of kidney failure ( by a lot) in several conditions (focal segmental glomerulosis(FSGS), HIV-associated nephropathy (HIVAN), and diabetes-associated nephropathy). Altogether, African-Americans develop kidney disease at a rate 4-5 times higher than other groups. It is worth noting that African-Americans that don’t have these APOL1 variants appear to have a risk similar to that of whites.
These don’t seem to be related to anencephaly in particular? Not sure if you meant to imply that they do.
Certainly some mutations trade off a harm against a benefit, sickle-cell anemia is the classic example, but that doesn’t mean all or even most of them do.
No, I don’t imply any connection to anencephaly. The point is just that many deleterious outcomes that we observe are a trade-off against something. In some cases we know against what—as you mentioned, sickle-cell anemia is an example. But in most cases we do not know. I would expect that a prior of “it’s a trade-off against some advantage, we don’t know yet which one” to hold as a rule, but I also expect to find some exceptions to it as well.
Not all but most very common obviously harmful mutations involve some kind of tradeoff or somehow fails to affect reproduction.
If something kills you in older age it’s free to spread, if something isn’t so terrible it can also spread through founder effects in a population but if some trait obviously hurts people at a young age but is still common it’s a good sign that it’s giving or did give some kind of advantage. .
Oh, but we do.
I’d recommend a couple of West Hunter posts: this and this.
Sample:
These don’t seem to be related to anencephaly in particular? Not sure if you meant to imply that they do.
Certainly some mutations trade off a harm against a benefit, sickle-cell anemia is the classic example, but that doesn’t mean all or even most of them do.
No, I don’t imply any connection to anencephaly. The point is just that many deleterious outcomes that we observe are a trade-off against something. In some cases we know against what—as you mentioned, sickle-cell anemia is an example. But in most cases we do not know. I would expect that a prior of “it’s a trade-off against some advantage, we don’t know yet which one” to hold as a rule, but I also expect to find some exceptions to it as well.
Not all but most very common obviously harmful mutations involve some kind of tradeoff or somehow fails to affect reproduction.
If something kills you in older age it’s free to spread, if something isn’t so terrible it can also spread through founder effects in a population but if some trait obviously hurts people at a young age but is still common it’s a good sign that it’s giving or did give some kind of advantage. .
Is homosexuality very common, at 1-3%? This requires quantitative analysis.
1 in 30 of the population counts as very common in genetics terms.