What if a loved one must take a fluoroquinolone because it is the only option available to save their life? How do they avoid getting “floxed” and experiencing the devastation that fluoroquinolones have brought to too many lives?
Undeniably, there is a range of reactions to fluoroquinolones – from people not reacting badly at all, to people being permanently disabled and in excruciating pain, and everything in between. If a loved one must take a fluoroquinolone because it is the only viable option, is there any way to push them toward the “not hurt” end of the spectrum?
Who Gets Floxed?
At this time, no one knows what makes someone susceptible to getting “floxed.” No one knows why some people tolerate fluoroquionlones well but other people don’t. No one knows why an individual can tolerate fluoroquinolones fine at one time, but have a horrible reaction another time. No one knows what genetic predispositions contribute to some people getting hurt by fluoroquionlones.
The epidemiologists say that the risk of fluoroquinolone-induced tendon ruptures is higher in those over the age of 60. However, there are many “floxies” under the age of 60, and many of them suffer from tendon ruptures and other musculoskeletal problems.
It is hypothesized in, “Fluoroquinolone Antibiotics and Thyroid Problems: Is there a Connection?” that, “anyone with any underlying genetic predisposition, or possibly harboring a subclinical, latent, or silent endocrinopathy might be ‘pushed over the edge’ into full blown clinical pathology” by fluoroquinolones. But I have a friend who is over the age of 60 and who has thyroid problems, as well as osteoporosis, who recently took a course of Cipro and was fine afterward. I saw her yesterday and she is doing well. I would have thought that she would have been predisposed toward an adverse reaction… but she wasn’t.
As a strong and athletic 32 year old who had no history of illness, I certainly didn’t think that I was predisposed to having an adverse reaction to Cipro, but it happened. Cipro made me sick for a while.
There seems to be a certain amount of “Russian Roulette” going on when one takes a fluoroquinolone. There aren’t any tests to determine who will react poorly to fluoroquinolones, and even known risk factors only sometimes make a difference. Some people seem to get lucky, while others get very, very unlucky. I realize that attributing adverse reactions to bad luck and “Russian Roulette” is a frustrating non-answer, but, unfortunately, that’s where we’re at right now – the land of frustrating non-answers. Welcome to being a floxie.
Despite the seeming randomness of adverse reactions, there is sufficient evidence that people who are over the age of 60, athletes, those who have a history of psychiatric illness, those with a history of benzodiazepine withdrawal, people who regularly use NSAIDs, people using corticosteroids, people who have an existing autoimmune or endocrine disorders, those who are immunocompromised, and people who have a mitochondrial disorder (in any of its manifestations, including ME/CFS and fibromyalgia) should avoid fluoroquinolones if at all possible. (More about this can be found in the post, “Don’t Take Cipro, Levaquin or Avelox If….” on Hormones Matter.)
When it’s the Only Option
Given that few people think that an adverse drug reaction will happen to them, and that antibiotic resistance is reducing the number of safe antibiotics available to treat many infections, many people are stuck with fluoroquinolones being the only option available to them.
If this is the situation for you (yes, I do realize that many/most floxies would rather die than take a fluoroquinolone again, but that’s not the case for everyone) or a loved one, is there anything that can be done to mitigate the damage done by the drug?
Mitigating Fluoroquinolone Damage
Studies have noted that magnesium and vitamin E can mitigate some of the damage done by fluoroquinolones. In, Musculoskeletal Complications of Fluoroquinolones: Guidelines and Precautions for Usage in the Athletic Population, it is noted that:
“Pfister et al  studied the effects of oral vitamin E (tocopherol) and magnesium supplementation on ciprofloxacin-associated chondrotoxicity. Juvenile rats were divided into 4 groups: those fed a normal diet, a vitamin E– enriched diet, a magnesium-enriched diet, or a diet enriched with both vitamin E and magnesium. These diets were initiated 10 days before the rats were given ciprofloxacin. Two days after fluoroquinolone exposure, cartilage samples from the knee joints were histologically examined, and cartilage and plasma concentrations of magnesium, calcium, and vitamin E were measured. Fluoroquinolone-associated cartilage changes were observed in all groups, but the supplemented groups showed significantly less change, with the magnesium and vitamin E combination group demonstrating the least change. Both plasma and cartilage concentrations of magnesium and tocopherol were significantly higher in the supplemented groups than in the animals that received the normal diet, which supports the potential role of magnesium deficiency in the pathogenesis of fluoroquinolone-associated chondrotoxicity.”
Does that mean that magnesium and vitamin E should be taken along with fluoroquinolones to mitigate damage? Maybe. It should be noted that magnesium inhibits fluoroquinolones both for better and for worse, and that the magnesium may decrease the ability of the FQ to fight the bacterial infection.
Additionally, it is noted in “Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells,” that:
“Mice treated with clinically relevant doses of bactericidal antibiotics similarly showed signs of oxidative damage in blood tests, tissue analysis, and gene expression studies. This ROS-mediated damage could be reversed by the powerful antioxidant N-acetyl-l-cysteine (NAC) without disrupting the bacteria-killing properties of the antibiotics.”
Since NAC doesn’t disrupt the bacteria-killing properties of the antibiotics, it’s a better bet (IMO).
“A mitochondrial-targeted form of ubiquinone (MitoQ) demonstrated a larger protective effect than did untargeted ubiquinone. Oxidative stress frequently occurs in the mitochondria , and fluoroquinolone-induced oxidative damage to mitochondria in tenocytes and chondrocytes has been reported .”
Some “floxies” have found MitoQ to be helpful in healing fluoroquinolone-induced damage. Perhaps it can also prevent the damage from occurring.
If a loved one of mine had to take a fluoroquinolone, I would try to get him or her to load up on magnesium before-hand, and I would try to get vitamin E, NAC, and MitoQ into him/her while the FQ was being administered.
I certainly wouldn’t claim to know for sure that they would be safer while taking those antioxidants, but it’s worth a try.
People should be aware of the dangers of fluoroquinolones, and they should know that there is a certain amount of Russian Roulette that is being played with every pill administered. For better or for worse, I don’t think that people really understand fluoroquinolone toxicity until it happens to them. As scary as it is for those of us who have been hurt by fluoroquinolones to stand by and watch while our loved ones take these pills, some of us will have to do just that at some point. Maybe some of the fluoroquinolone-induced damage can be mitigated by the supplements mentioned above. I hope so.
Tagged: adverse reactions, Cipro, cipro adverse reaction, ciprofloxacin, Flox, Fluoroquinolone toxicity, magnesium, mitochondrial supplements, MitoQ, NAC, risk factors for floxing, supplements, tendon ruptures, Vitamin E