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Drug-induced PN due to tirzepatide

Neuropathy | Last Active: 6 days ago | Replies (30)

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@projfan I’m experiencing something similar. Why do you believe the damage caused until this point is essentially irreversible? Is this based on your experience, or something you’ve read? Thank you.

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Replies to "@projfan I’m experiencing something similar. Why do you believe the damage caused until this point is..."

@thebugshort Good question. I've found no indication in the medical literature of a path to reversing DIPN, although to be fair, almost all DIPN research that's published seems to concern cancer drugs, and no one seems to think that DIPN is a reason to withdraw the drugs -- all the work is about minimizing the drug side effects, not reversing them. If you find anything, I would love to see it.

I personally found that reducing dosages stopped the progression but failed to reverse the DIPN, and that switching forms of the drug after achieving a low maintenance dose made no difference. My neuropathy has now been stable for well over a year. It is possible that going off the drugs entirely rather that moving to a minimum dose would have worked, but I prefer the stabilized DIPN symptoms over knee replacement surgery -- I know better than to believe dropping the drugs and keeping the weight off using other means is a viable option for me personally.

I vaguely recall digging into the literature at the time concerning healing of the nerves after removing any stimulus driving PN, and finding nothing. Again, if you find any relevant studies, I'd be very interested in hearing about them.

In general, PN does not seem to be curable -- treatments seem to be focused on managing and reducing the symptoms, not on fixing the underlying problem.

Finally, although I have an automated search running in PubMed every week for DIPN, it's been months since I last dug elsewhere into this topic, so my reply here is based on aging data. The PubMed search has popped nothing of any use for a long time -- pretty much all of the work has been narrowly focused in ways that make it irrelevant to our specific problem. And if you look at the analyses of GLP-1 RA side effects, both beneficial and not, our problem barely emerges from the data at a population level. So really, what motivation does anyone have to go after it?