Fluoroquinolone antibiotics, like ciprofloxacin, are well documented to cause permanent nerve damage (and chronic fatigue). One of the symptoms/causes is demyelination of the nerves. Similarly in MS, as the article states:
> Myelin is the very thing that is destroyed in MS
While it seems unlikely that FQ nerve damage is caused by the immune system attacking its own nerve cells, the mechanism by which these antibiotics cause nerve damage is unknown. This makes them higher risk to take, because your doctor has no idea what to look for to make sure you don't get nerve damage. Most doctors aren't even aware of the link, the FDA forced manufacturers to add permanent neuropathy as a black box warning to the drugs, long after most doctors learned about them in medical school.
If two conditions lead to the same outcome, I wonder if there's any utility in looking for links, either in treatment or prevention, between them.
Fluoroquinolones are also completely contraindicated in patients with connective issue disorders (e.g. Marfan, EDS, Loeys-Dietz.) It can lead to organ rupture, torn arteries, aneurysms etc. CTDs often remain undiagnosed for a long time, so a small percentage of the population are ticking time bombs for this interaction.
I have EDS, and cipro spooked me so I didn't fill my Rx for it in college. If I had I'd likely be even more disabled than I already am.
This seems to be a common thread, my wife's EDS diagnosis took more than a decade. It's a straightforward and obvious physical ailment. Even after her diagnosis she ran into problems - she once had to leave an ER without treatment for an unrelated problem, because the attending refused to treat her until she admitted that she was lying about her diagnosis. Hearing her stories and seeing first-hand how her medical interactions go has really shaken my faith in the medical system.
EDS has a bizarre stigma attached to it for some reason. I'm pretty noticeable (I can fully dislocate my shoulders, for example), so I was immediately diagnosed with HSD, and finally with hEDS a year later. I haven't had issues with doctors since that, but I got treated terribly in the interim.
I've heard that MS was stigmatized like that before the neurology was appreciated. But EDS has one of the highest disability-to-stigma ratios of any disorder I've known. It gave me a spinal cord injury, for Pete's sake.
I think it unfortunately boils down to externalized shame from MDs who can't admit they don't know something, mixed with old biases about neurotic women who make up ailments. Nearly all medical knowledge is based on rote memorization in med school and received tribal wisdom during residency. MDs aren't given the time and mental space to really sort out which things are true and which are superstition while they are in training.
Ideally the check from a knowledge perspective is CMEs and a separate group of medical researchers that inform med school curriculum, but there is no real check on the eye-rolling and "oh, you have to deal with one of THOSE" that they are exposed to during residency.
This is how a number of cell / animal models of diseases are done. For example DSS induced colitis in mice.
Pharmacogenomics is a thing. There are companies out there that do PGx testing. The problem is that frontline clinicians mostly haven’t adopted / integrated it into their practices.
> Myelin is the very thing that is destroyed in MS
While it seems unlikely that FQ nerve damage is caused by the immune system attacking its own nerve cells, the mechanism by which these antibiotics cause nerve damage is unknown. This makes them higher risk to take, because your doctor has no idea what to look for to make sure you don't get nerve damage. Most doctors aren't even aware of the link, the FDA forced manufacturers to add permanent neuropathy as a black box warning to the drugs, long after most doctors learned about them in medical school.
If two conditions lead to the same outcome, I wonder if there's any utility in looking for links, either in treatment or prevention, between them.