First of all, you should distinguish between the fitness of the gene and the fitness of the people. Second, I am using as input the empirical observation that the fitness of the achondroplasia gene is 1/4. Third, and tangentially, you should distinguish between the fitness of the children and parents.
(1 gene vs parents) Let us consider the 3 surviving children. Out of the 6 copies of the gene, 4 are wild type and 2 are achondroplasia. But in the parents, half of the genes are achondroplasia. Thus, regardless of how many children the parents have, the fitness of the gene is 2/3 the fitness of the parents.
(2) Empirically, 1/4 of achondroplasia births are inherited and 3/4 are de novo. Assuming equilibrium, the gene is producing 1/4 of replacement fertility, so it has a fitness of 1/4. If dwarfs only reproduce with non-dwarfs, they, too, have a fitness of 1/4. But if they only reproduce with dwarfs, they have a fitness 3/2 of the gene, thus 3/8.
(3 parents vs children) The 3/4 you compute is the reduction in the proportion of pregnancies yield children. This is a kind of infertility, though more emotionally difficult. It is only relevant if the parents are trying to reproduce as fast as possible. In the modern world, parents usually target a small fixed number of children and infertility has little effect. In both farmer and forager societies, children were probably modulated to available food supply. Such a wasted pregnancy does not reduce the number of children by 1, but probably delays future children by a year. If the usual interval is 4, this might reduce fitness by 1/4. But the effect is probably significantly smaller. If people are reproducing at the optimal speed, taking into account risk of famine, a small perturbation probably has little effect.
(2) Empirically, 1/4 of achondroplasia births are inherited and 3/4 are de novo.
sorry; point 2 again, (Aa x aa should product a 1/2 not a 1/4)
acondroplasia X normal
............A.............a
...a.......Aa..........aa
...a......Aa...........aa
50%Aa acondroplasia
50%aa normal
or am I confused somewhere? Is that not the punnet square?
Epistemic status: speculating about things I'm not familiar with; hoping to be educated in the comments. This post is a question, not an answer.
ETA: this comment thread seems to be leading towards the best answer so far.
There's a question I've seen many times, most recently in Scott Alexander's recent links thread. This latest variant goes like this:
Obligate male homosexuality greatly harms reproductive fitness. And so, the argument goes, there must be some other selection pressure, one great enough to overcome the drastic effect of not having any children. The comments on that post list several other proposed answers, all of them suggesting a tradeoff vs. a benefit elsewhere: for instance, that it pays to have some proportion of gay men who invest their resources in their nieces and nephews instead of their own children.
But how do we know if this is a valid question - if the situation really needs to be explained at all?
For obvious political and social reasons, it's hard to be sure how many people are homosexual. Note that we are interested only in obligate homosexuality - bisexuals presumably don't have strongly reduced fitness. The Wikipedia article doesn't really distinguish obligate homosexuality from bi-, pan- and even trans-sexuals. The discussion in the SSC comments used an (unsourced?) range of 1%-3%, which seems at least consistent with other sources, so let's run with that.
The rate of major birth defects in the US, as reported by the CDC, is also about 3%. This counts both developmental and genetic problems, and includes everything from anencephaly (invariably fatal) through Down syndrome (severe but survivable) to cleft palates (minor). But most of these, at least 1.5% of births, were always fatal before modern medicine, and many of the others reduced fitness (via mate selection, if nothing else). Various other defects and diseases, which only manifest later in life, are also thought to be influenced or determined during early development. And so is sexual preference.
(Whether homosexuality is a developmental disorder is not the point; I'm comparing the effect of selection pressure on fatal teratology with its effect on reduced-fitness homosexuality.)
Embryological development is a complex and fragile process, and there are many ways for it to go wrong. We don't wonder how it is possible that selection pressure allows anencephaly to occur in 1 in 4859 births. There are certainly direct causes of anencephaly, explanations of why it happens when it does, but (I think) we don't a priori expect them to be due to tradeoffs yielding benefits elsewhere. It's just as plausible that the tradeoffs involved are against even worse (counterfactual) problems elsewhere - or that there are just no available mutations that don't have these or equally severe problems.
Could it be that linking sexual preference to the biological gender is, for some complex developmental reason, fragile enough that it goes wrong despite all selection pressure to the contrary, that it has no redeeming qualities from the viewpoint of evolution, and that is all there is to it?
When faced with any phenotype with reduced fitness, how can we judge if there is something to be explained - a beneficial tradeoff elsewhere to search for - or merely a hard problem evolution couldn't solve completely? And is there a way to quantify this question, relating it to the known mathematical models of genetics?
Notes:
1. I'm posting this in the spirit of recent suggestions to post more and accept lower quality of (our own) posts to Discussion.
2. I'm going to sleep now and will start replying to comments about 10 hours from now; sorry for the inconvenience.