It's not anemia that gives you advantage, but the gene that gives you anemia. People who carry one copy of the gene (who are heterozygous), don't have anemia but have the advantage, while people who carry two copies (are homozygous) are at a huge disadvantage due to anemia. This is a classic example of heterozygosity advantage.
Sickle cell anemia is Mendelian and recessive. So if 2 carriers (Rr and Rr) have kids, 50% of the children will be strictly superior (carriers), 25% will be normal, and 25% will die young. Not a bad outcome, especially if you have a lot of kids to reduce the variance.
> 50% of the children will be strictly superior (carriers)
Is that domain nomenclature? Because I wouldn't call having to be careful who procreate with otherwise risk losing 25% of my children from that relationship as "strictly superior"...
According to the article, the evolutionary choice at work here was isolation-induced. It was each blue family member choosing to reproduce with another blue individual that propagated the recessive gene.
This is a joke right? Evolution doesn't choose anything.
In this case, the family had a hemoglobin variation, that resulted in a different kind of non-functional hemoglobin being produced. This hemoglobin has a blue tint. This, combined with their pale coloration, meant they had a blue tint.
This is not too dissimilar to how other hemoglobinopathies come about in nature. For example, the thallassemias and sickle cell anemia are two common hemoglobinopathies. Unlike the Fugate family's hemoglobinopathy, which likely did not provide any benefit, these two do provide some benefit to heterozygotes, and thus end up existing at a steady state in the population. The Fugate family's would likely disappear if it caused any issue in reproductive fitness (even a minor one), and the family reproduced among a sufficiently large population. However inbreeding combined with genetic drift means that there simply does not end up being a large enough population for the law of large numbers to take effect.
On the other hand, if the condition causes no reproductive fitness deficiency or increased reproductive ability, then the gene could potentially continue to exist in some very small number of the population. It could die out due to the simple fact of not having many affected people able to reproduce enough to make statistics matter.