Wikipedia: "Essentially, CFTR is an ion channel that evolved as a 'broken' ABC transporter that leaks when in open conformation."

You: "That is interesting to me. CF is basically a salt-wasting condition. There are various forms of defect in the CFTR, but knowing that it basically leaks may explain why it is basically a salt wasting condition."

Errr, that was referring to normal CFTR. The class of proteins it belongs to normally require ATP, the ready energy source in cells, to actively transport stuff, e.g. use up one molecule of ATP to transport one molecule of whatever. CFTR is 'broken' in that it looks a whole lot like one of these proteins, but instead of ATP being used to transport a molecule, i.e. against an osmotic gradient, the ATP just "opens its door" (or the reverse, I didn't check), and then ions and water go whichever way the gradient favors. I.e. if there's lots more water in the cell than outside the cell, it goes out.

So one of the things I found was that there are two conditions that cause higher misfolds of proteins within the cell: Derangement of PH level and derangement of salt level. You see both of these things happening with CF.

Ah, I see where there's usefulness here, given the variety of CFTR mutations (and note that one person might have two different mutations, one contributed from each parent, or arising from very early stage embryo mutations). There will be mutations that as you describe, where if you can adjust the conditions under which the protein is created and initially folds, and or preforms afterwards, you get a more favorable outcome.

As for acid, well, it depends on where the acid is. Acidosis is a condition outside the cell, per the Merck Manual "Acidosis is excessive blood acidity caused by an overabundance of acid in the blood or a loss of bicarbonate from the blood (metabolic acidosis), or by a buildup of carbon dioxide in the blood that results from poor lung function or slow breathing (respiratory acidosis)."

So to refine your hypothesis, once the protein is in the cell membrane, a greater concentration of hydronium ions (https://en.wikipedia.org/wiki/Hydronium) outside will damage it. And if the outside is more acid than the cell, they'll flow in through the channel, where they can donate a proton (bare hydrogen atom), doing mischief to CFTR or even the cell.

So I have concluded that there is a vicious positive feedback loop where the more acid you get, the more you see protein misfolds and the more you see protein misfolds, the more acid you get. I believe this is why it is a degenerative, progressive condition.

That would only happen if your as blood gets more acid, it stays more acid, but short of requiring intervention. Note also that proteins tend to? often? have have a life cycle, they get produced, work for a while, often get zapped one way or another, and then get recycled. That mutation class I mentioned of premature degradation implies this is true for CTFR; the cell would fail to keep up production sufficient to counter that. Note also there should be a signaling mechanism that tells the cell to produce more or less of CTFR, I'm assuming that even if the signal is "I really need more!", the cell has a limit to how much it can produce, and still survive, it can't under-produce other vital stuff too much ... and that also might have an effect.

Sounds like there's cumulative damage elsewhere that can't be reversed in this way, e.g. the stated pancreas scarring that causes Type 1 diabetes, or the classic clubbed fingers per the Wikipedia picture.

But most people with CF are prescribed a high salt, high fat, high calorie diet. This means they are actively encouraged by medical professionals to eat a junk food diet. I went the other way. I pay very close attention to the quality of my food, not the quantity. I went looking for good quality fats and salts and other foods. I think the current practice of prescribing a junk food diet because it is high in fat and salt without caring that it is low in quality is part of what is killing people with CF.

Well, salt is salt, and it might help to increase the saltiness of your blood (not sure how much that's possible or practical), you'll end up with more salt inside the cells (or that sounds likely, but there are surely other proteins that also can transport salt in and out), and outside the cell, the former probably not so good, the latter perhaps in balance for the best for many people.

More later if you wish when you have time, on this HN topic, or you're welcome to email me (see the address in my account info).