Anyone used those bloodsuger control medications?

Hufsamor

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Someone in a Norwegian Facebook group posted this question, and I thought I’d ask here:

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Our heroes from Haukeland — Fluge, Mella, and Moreau from Canada — believe that these type 2 diabetes medications might help with ME!


If you’re testing these medications, could you please share here whether they’re working for you?
 

bad1080

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oh and somebody said regular doses wouldn't be enough to achieve the concentrations used in the study, so even if you find somebody who takes these for diabetes it wouldn't be meaningful for me-cfs
 

Oliver3

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There's a link I think tho. Like I've read gastroparesis is due to blood sugar issues.
I've really been helped by berberine.
My sister has pcos . These blood sugar/ fatigue issues run in different illnesses I believe
 

cfs since 1998

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Hufsamor

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If you don't have sugar problems or diabetes and take these medications wouldn't that lead to serious problems like a dangerously low blood sugar?
You’re right. :thumbsup:
I wouldn’t recommend anyone to try the medication. But I don’t think it’s much used, everyone I know are on metformin and /or ozempic.
So I was just curious to know if anyone with me/cfa and diabetes had used any of those medications and if they had, if they felt any difference.
If I had tried, and felt better on the medication, I would have believed it to be because of better bloodsuger control.

But, as it seems the doses Fluge/Mellar used will be much higher than an ordinary dose, I doubt we will have any patients coming forward with a good story.
 

Hufsamor

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The paper also mentioned trying to find more bioavailable forms or using a transdermal patch...it was kind of buried in the text. From what I've seen typical doses result in concentrations of 1 µM or less.
Let me see if I’ve got this right-
What this medication does has nothing to do with bloodsuger control.
It’s more of a side effect?
(I got chat gtp to explain a little bit, but as it’s not a hundred percent trustworthy and I know a lot of people really dislike it, I didn’t want to post the answer here)
 

kushami

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Am I understanding correctly that they didn't actually give the drugs to the subjects, but tried them on plasma taken from some of the subjects?

This paper is not very easy to read. I know it's very technical, but the outline of the study, as in what they actually did, is hard to dig out.
 

wabi-sabi

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Like I've read gastroparesis is due to blood sugar issues.
Uncontrolled diabetes can cause nerve damage in many parts of the body including the GI tract. But lots of other things can cause nerve damage too. Gastroparesis in pwME does not necessarily mean that there are sugar issues, due to the nervous system problems caused by ME/CFS. Gastroparesis is part of the dysautonomia picture, like the problems with heartrate and blood pressure regulation.

Of course, there's nothing stopping you from having type 2 diabetes and ME/CFS. Losing muscle mass as tends to happen in ME/CFS is a risk factor for type 2 diabetes and insulin resistance.

If I had tried, and felt better on the medication, I would have believed it to be because of better bloodsuger control.
This would be my explanation as well.

What this medication does has nothing to do with bloodsuger control.
It’s more of a side effect?
No. These medications are intended for type 2 diabetics to help them control their sugar. If they help us, that's the side effect. My guess is that these researchers are trying to repurpose other drugs for ME/CFS, because that's faster than trying to make a drug from scratch just for us. It also looks like these drugs don't carry much risk for low blood sugar (compared to other diabetes drugs). This explains briefly how the drugs work:
https://hopkinsdiabetesinfo.org/medications-for-type-2-diabetes-dpp-iv-inhibitors/
 
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wabi-sabi

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My best stab at explaining this paper. The authors have a protein in cell membranes that plays a very complicated role in inflammation and seems to be messed up in pwME. I am not up to explaining that part. In a nutshell, the protein, called SMLDP3B, lives mostly in cell membranes. Sometimes they are chopped out of the cell membrane by an enzyme, called PI-PCL, and this causes problems when the protein is released into the bloodstream (at least I think that's where it's being released. Maybe it's intracellular. At any rate, when this protein is chopped out of the cell membrane bad things ensue.

How to stop this? Well, with a drug that inhibits the chopping enzyme. For some random reason, that turns out to be this diabetes drug. Saxagliptin inactivates the enzyme in a bacteria, and it turns out it does so in human peripheral mononuclear blood cells as well. Note that this experiment was done on blood samples, not people! We don't know what effect turning off this enzyme will have on the immune system in a whole person. I'm not sure what dose you would use in a person instead of some cells in a petri dish either. And maybe the bigger problem: we don't seem to know exactly if SMLDP3B being messed up is a cause or effect of ME/CFS. Without knowing that, it's hard to know what the effect of the drug would be on the illness...
 
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kushami

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By the way, I didn't mean it as a criticism that the authors had only tried the medications on serum. Obviously that is a good and cautious way to start. Apologies if it came across as a negative.
 
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