And, Dr. Titze said, high glucocorticoid levels are linked to such conditions as osteoporosis, muscle loss, Type 2 diabetes and other metabolic problems.
And cystic fibrosis, which is perhaps best tldr'd as a salt wasting condition, frequently leads to Cystic Fibrosis Related Diabetes, which is neither type 1 nor type 2 diabetes.
CFTR, being a chloride channel, most likely leads to diabetes as a consequence of its effects on the voltage-regulated insulin release in beta cells from glucose sensing. [1]
It strikes me as unlikely to be related to the salt-wasting that occurs from failure to reabsorb chloride in the epithelium.
I think it is probably a lot more complicated than that. CF does a great many things to the body. It is an inflammatory condition and I have seen multiple articles linking diabetes and inflammation. People with CF tend to be seriously underweight and I have recently seen articles that link inadequate muscle protein to insulin resistance. There is no doubt more than that going on, those are just a couple of things that occur to me off the top of my head.
I have CF. About 2009 (age 32) I developed diabetes (commonly known as CFRD, CF related diabetes). CF patients early on have the ducts in their pancreas blocked from producing digestive enzymes, causing low weight. We take digestive enzyme supplements to (inefficiently) counter this. (I realize you have CF too - laying out background for the non-CF reader) My understanding is that the eventual diabetes is caused by gradually decreasing pancreas function.
I genuinely think it is a lot more complicated than that. My blood sugar is more stable than it has ever been and I have gotten off digestive enzymes. I wasn't doing anything to specifically try to fix my blood sugar issues. I was doing things like trying to get inflammation and infection under control based on the success of therapies like daily ibuprofen. I read up on that, inferred that if you can reduce inflammation, you can be less symptomatic, and used a dietary and lifestyle approach to do that. I did take ibuprofen daily for something like 5 or 6 years, but was eventually able to successfully control symptoms such that I no longer needed it. Somewhere along the way, I happened to see articles about the link between diabetes and inflammation. Inflammation and infection go hand in hand, so I think very likely infection plays a role in the collapse of pancreatic function in pwcf.
The low weight is also from the gut being all kinds of out of whack and just not absorbing nutrients. There are things that can be done to improve gut function. The gut is about 70 percent of your immune system, so I think efforts to repair the gut lead to many different good things, including better nutritional status and a more functional immune system.
Though the degree to which you can correct these problems no doubt will be influenced by which specific alleles you have, I think there is a lot of room for improvement for most people with CF. Maybe it won't make much difference if you have one of the variations where the CFTR just basically doesn't work at all.
I used to jokingly talk about "Pale Skin Disorder" as a metaphor for special needs in my kids. It works well as a metaphor for what I mean here too. If you have pale skin (low melanin production) and are easily sun burned, there are things you can do to protect against sunburn. You aren't doomed to simply be sunburned to the point of peeling all the time. But if you are an albino and totally lack melanin, it is a whole different ball game.
So, if you have a form of CF that is the equivalent of albinism where the CFTR simply does nothing or is outright absent, instead of one of the many variations where it has one of a number of different types of impairments, my assumption is that would be less responsive to dietary and lifestyle changes. Though I don't actually know.
Anyway, my apologies if I have offended. I rarely engage pwcf in discussion anymore as it tends to go bad places. Thank you for commenting.
> Though the degree to which you can correct these problems no doubt will be influenced by which specific alleles you have, I think there is a lot of room for improvement for most people with CF. Maybe it won't make much difference if you have one of the variations where the CFTR just basically doesn't work at all.
I'm delta-f508 homozygous, so I suspect there's less CFTR function. I lose a tremendous amount of salt when I sweat, so I suspect that's an indicator of function level. Oddly enough, I've always had less respiratory issues for CF, but my stomach pain and weight have been pretty severe as long as I can remember. (I wasn't diagnosed about age 13, and I can remember intense pain before then. When I'm religious about enzymes it's usually not an issue however.) My A1C these days is poor, and my BGC always runs high. I could probably counteract with diet, but then I have to contend to with keeping my weight up. I suspect I may be a much lower pancreas function than what you're describing.
> Anyway, my apologies if I have offended.
Not at all! I'll definitely look into inflammation etc.
It would be nice of you to provide some sources for your claims. I don't know if you are right or not, but at least providing links to the articles you are referring to would be appreciated.
There is a long and wordy section about muscle and insulin resistance, some choice outtakes:
However, over the past few years it has become evident that changes in the metabolic function of muscle itself plays a more direct role in the genesis of insulin resistance than previously appreciated. (This is rebutting the idea that higher fat levels explain insulin resistance.)
as little as a single bout of exercise [thereby stimulating triacylglycerol deposition in muscle intramuscular triacylglycerol (IMTG) oxidation] can transiently reverse insulin resistance (44).
The section concludes with:
Regardless of the specific intracellular mechanisms
at the molecular level, it is clear that insulin resistance is not simply the result of increased fat mass and release of FFAs into plasma at an accelerated rate, with the muscle responding to elevated plasma FAA concentrations. Rather, alterations in the metabolic function of muscle are central to the development of insulin resistance and ultimately diabetes.
I am not finding an exact point at which it explicitly says "Muscle loss causes insulin resistance" but that was my personal takeaway from reading this some time back. (On the other hand, maybe it does explicitly say that and I am just rushed for time and have crap eyesight, so maybe I am just not finding it. Whatever.)
And cystic fibrosis, which is perhaps best tldr'd as a salt wasting condition, frequently leads to Cystic Fibrosis Related Diabetes, which is neither type 1 nor type 2 diabetes.