Well, I think homosexuality is a disorder or sorts, but I'll see what I can find.
The history of CF does not date back far enough to claim that the numbers in the population are remaining constant (or so it appears to me). It would take many generations to see the effect. Starting with 2 carriers (1 to zero ratio) they would produce a 2 to one ratio (assuming the one with the disease is left out of the mix). They would then produce a 1 to one ratio, followed by a 2 to 3 ratio (carrier to non-carrier). I do not see how that math would be different depending on the size of the population. You can show me where I am wrong. I don't mind (lol).
History of the Disease
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For centuries in northern Europe, the adage went: Woe to that child which when kissed on the forehead tastes salty. He is bewitched and soon must die. (Welsh, Smith). Cystic fibrosis developed in the northern European poplulation as a reaction to typhoid fever, in much the same way that the sickle-cell mutation developed in Africa (Cooke). However, we did not know of cystic fibrosis (CF) as a disease until the early part of the 20th century.
In 1938, Dorothy H. Andersen of Columbia University provided the first comprehensive description of the symptoms of cystic fibrosis and its effects in organs. She gave the disease its name, calling it "cystic fibrosis of the pancreas". By the late 1940s, doctors learned of the thick mucosal secretions that can clog ducts and passageways. And in 1946, doctors examining inheritance patterns in families deduced that cystic fibrosis was probably caused by the mutation of a single, recessive gene. Nearly seven years later, Paul di Sant'Agnese and colleagues at Columbia discovered that CF patients lose an inordinate amount of salt in sweat (Welsh, Smith).
Fast forward to the 1980s, when scientists learned that epithelial tissue malfunction occurred in every organ affected by cystic fibrosis. Of note are Paul Quinton of UC Riverside, who discovered chloride uptake problems in the sweat glands of the skin, and Michael Knowles and Richard Boucher of UNC Chapel Hill, who found similar problems in the epithelia and passageways of the lungs. In 1989, a genetic breakthrough occurred. Researchers led by Lap-Chee Tsui, John Riordan, and Francis Collins isolated the gene responsible for CF. They named it CFTR - cystic fibrosis transmembrane conductance regulator (Welsh, Smith).
Researchers today continue to try to deduce exactly how CFTR influences cells, and come up with new and better treatments for cystic fibrosis.