Fluoroquinolone (FLUORIDE!) antibiotics like Cipro and Levaquin have been getting plenty of negative press over the years for the mitochondrial damage that they can cause. The term “floxxed” has been used for the semi-permanent or permanent side effects of these antibiotics that some people have taken that have cost them their health. Fluoroquinolones are given out by the medical establishment like candy to treat bacterial infections. Instead of prescribing the antibiotic as a drug of last resort or at least “black-box” warning (the FDA finally assigned it to the antibiotics in 2016, “An FDA safety review has shown that fluoroquinolones, when used systemically, are associated with disabling and potentially permanent serious side effects that can occur together. These side effects can involve the tendons, muscles, joints, nerves, and central nervous system”) medication that should be used only when necessary. Between 1995 and 2002, fluoroquinolones became the most commonly prescribed class of antibiotics to adults in the United States. Fluoroquinolone prescribing rose from seven million visits in 1995 to twenty two million in 2002. Medicaid reimbursements for quinolones show that the prescribed amounts have maintained the same intensity. “The total annual number of quinolone prescriptions increased 402%, from 247,395 in the first quarter of 1991 to 1.2 million in the second quarter of 2015, peaking at 1.3 million in the first quarter of 2005.” In 2016, the FDA also recommended that the “serious side effects associated with fluoroquinolone antibacterial drugs outweigh the benefits for patients with acute sinusitis, acute bronchitis, and uncomplicated urinary tract infections who have other treatment options. For patients with these conditions, fluoroquinolones should be reserved for those who do not have alternative treatment options.” Many doctors still give it out for people with these conditions to this day, I see many clients and family members who have had these conditions, prescribed these antibiotics continuously. 1 2 3 4

Quinolone antibiotics have been used for a long time, but since the late 2000’s, mitochondrial severe side effects have been more frequently reported. For some, quinolones appear to be well tolerated, and the average side effects include systemic allergic reactions, headaches, insomnia, diarrhea, and nausea. The main issues associated with the use of quinolone antibiotics are the issues related to mitochondrial dysfunction and GABA inhibition. Central nervous system toxicity, spontaneous Achilles tendon ruptures that can occur a couple of months after use (the increase in risk is associated with people over the age of sixty and athletic males), psychosis, cardiac arrhythmias (mainly prolonged QT syndrome), seizures, worsen symptoms of myasthenia gravis, peripheral neuropathy (oral and injection versions only), and hypoglycemia have been reported in more significant quantities as serious side effects in the 2000’s. People with a SOD2 (superoxide dimutase two gene) mutation, might have a greater negative mitochondrial reaction to quinolone antibiotics.5 6

The following is a list of fluoroquinolone antibiotics that have a higher chance to cause a multitude of side effects:

  • Moxifloxacin carries a higher chance of causing long QT syndrome and is associated with uveitis. 7 8
  • Gatifloxacin (was voluntarily withdrawn from the market), clinafloxacin, and levofloxacin are linked to severely disturbed blood glucose regulation. 9 10 11
  • Clinafloxacin causes photosensitivity, is a mild photocarcinogen, and inhibits multiple liver CYP450 drug metabolizing enzymes, primarily CYP1A2. 12
  • Temafloxacin, gatifloxacin, trovafloxacin, were withdrawn from the market because of adverse side effects. 13
  • Like some antibiotics, C. difficile dysbiosis is caused more often by quinolone antibiotics, and the strains of C. difficile associated with fluoroquinolone caused dysbiosis might be more virulent. 14
  • Most fluoroquinolones chelate magnesium and calcium from our microbiome and our cells. Though fluoroquinolones would bind with the magnesium in endotoxins and weaken Gram-negative bacterial cell walls and biofilm, it can also affect cellular and mitochondrial calcium and magnesium availability, causing hypomagnesemia and hypocalcemia. 15

There are many different mechanisms associated with causing people to become “floxxed” when they take fluoroquinolone antibiotics. Fluoroquinolones block GABAa receptor complex within the central nervous system which can cause glutamate excitability and increased oxidative stress cause the associated negative neural and nervous system symptoms. Anxiety disorders, seizures, and even psychosis have been linked to quinolones because of its interference with the GABAa receptors and GABA production. Fluoroquinolones deplete mitochondrial DNA in humans, reducing mitochondrial function and biogenesis. Fluoroquinolones also decrease brain serotonin levels which can induce mood destabilization (more prone to mania and depression) and circadian dysrhythmia (poor sleep and lack of energy). 16 17 18

Our mitochondria are bacterial in origin, so it would make sense that many antibiotics that we use to target bacterial DNA would also to a lesser extent target mtDNA. Fluoroquinolones also interfere with the electron transport chain within our mitochondria and increase the formation of reactive oxygen species within our mitochondria and our cells creating unnecessary healthy mitochondria and cellular apoptosis. 19 20

“The loss in mtDNA was associated with a delayed loss in mitochondrial function. Here, we report that the 4-quinolone drug ciprofloxacin is cytotoxic to a variety of cultured mammalian cell lines at concentrations that deplete cells of mtDNA.” 21

“Studies have also suggested that 4-quinolones may interfere with cell growth by inhibiting mammalian mtDNA replication. Castora et al. found that the 4-quinolone drugs nalidixic acid and oxolinic acid inhibited mtDNA replication in isolated rat liver mitochondria. These investigators inferred that this effect might be mediated by the inhibition of a mitochondrial topoisomerase II activity related to the bacterial enzyme DNA gyrase.” 22

“We recently demonstrated that the 4-quinolone drugs nalidixic acid and ciprofloxacin cause a selective loss of mtDNA in drug-treated mammalian cells. The loss of mtDNA was associated with a decrease in mitochondrial respiration and an arrest in cell growth. These results suggested that inhibition of mammalian cell proliferation by 4-quinolone drugs might be caused by the selective depletion of mtDNA, resulting in compromised mitochondrial activity. We now report that ciprofloxacin causes delayed cytotoxicity in cultured mammalian cells at concentrations that deplete cells of mtDNA.” 23

“Quinolones target bacterial gyrases and mtDNA topoisomerases. First, we show that, regardless of their molecular targets, three major classes of bactericidal antibiotics – quinolones, aminoglycosides, and β-lactams—induce ROS production in mammalian cells, leading to DNA, protein, and lipid damage. Second, we demonstrate that these deleterious effects are produced by clinically relevant doses of bactericidal antibiotics, both in cell culture and in mice. These findings are analogous to our previous work in bacteria, in which we showed that clinically relevant doses of bactericidal antibiotics induce a common oxidative damage pathway.” 24

Tendon ruptures occur from a lack of proper collagen synthesis in the tendons and increased oxidative stress and inflammation. Athletes have been cautioned not to take quinolones if possible because it inhibits homeostasis and tissue repair in their tendons and can lead to ruptures.

“Normal tendon is primarily an extracellular tissue comprising mainly type I collagen fibers linearly arranged with proteoglycans and other noncollagenous proteins interspersed. The tendon cells (tenocytes) are specialized fibroblasts that produce collagen.

The pathways underpinning the tenotoxic effects of fluoroquinolones are unclear, but three main mechanisms have been proposed: ischemia, degradation of the tendon matrix, and adverse alteration of tenocyte activity. Matrix metalloproteinases are enzymes with degrading properties that are important in the homeostasis and response to injury of tendon tissue. Fluoroquinolones facilitate expression of matrix metalloproteinases in tendon tissue; ciprofloxacin, in particular, has been shown to increase the expression of matrix metalloproteinase-3 in human Achilles tendon-derived cells and to reduce collagen synthesis via inhibition of tenocyte proliferation.” 25

Fluoroquinolones in some people may induce hypoglycemia by increasing insulin release in the pancreas by blockading the ATP sensitive potassium channels in the beta cells of the pancreas. Improper insulin over release into the bloodstream metabolizes blood glucose dropping it to low levels creating hypoglycemia. The mechanism of action for quinolones to cause hyperglycemia is currently unknown. 26 27

I do not recommend using fluoroquinolone antibiotics unless necessary and if you do need to use them, follow the listed protocol to see if you can protect your mitochondria as much as possible when you are taking them. I also recommend that quinolones should only be used in children as a drug of last resort because of the potential risks associated with arthropathy (joint health issues) in children with proper studies. The FDA limits quinolones usage in children only for serious medical necessity:

“Currently, FQs that are approved by the U.S. Food and Drug Administration (FDA) for use in children include ciprofloxacin for the treatment of inhalation anthrax, complicated urinary tract infections, and pyelonephritis along with levofloxacin for inhalational anthrax and plague.” 28

Finally, work with your doctor on trying to use the lowest dose possible and avoid some of the fluoroquinolones listed above that are associated with severe side effects if you must use quinolones.

Recommendations to Help Reduce Quinolone Mitochondrial Toxicity

  • Jarrow Ubiquinol – 100 – 300 mg daily. 29
  • Jarrow PQQ – one capsule daily with food. 30
  • Increase Omega 3 fatty acid ingestion.
  • Maintain proper sunlight exposure and sleep hygiene.
  • Supplement with magnesium regularly. Magnesium will increase mitochondrial function and ensure proper GABA production and reduce glutamic acid neurotoxicity. Take magnesium separate from quinolones because of their magnesium chelation effect.
  • Quinolone antibiotics deplete glutathione, so you might want to supplement with it to protect the liver and mitochondrial health.
  • Change your diet; try to follow the Perfect Health Diet and make sure you consume a right amount of pure water.

  1. https://www.fda.gov/Drugs/DrugSafety/DrugSafetyPodcasts/ucm503021.htm
  2. https://www.fda.gov/Drugs/DrugSafety/ucm500143.htm
  3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5691846/
  4. https://www.ncbi.nlm.nih.gov/pubmed/15745724
  5. https://www.fda.gov/Drugs/DrugSafety/DrugSafetyPodcasts/ucm503021.htm
  6. https://www.fda.gov/Drugs/DrugSafety/ucm500143.htm
  7. https://jamanetwork.com/journals/jamaophthalmology/fullarticle/1913582
  8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4070463/
  9. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3696308/
  10. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC90322/
  11. https://www.ncbi.nlm.nih.gov/pubmed/22456302
  12. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC90322/
  13. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2094848/
  14. https://www.ncbi.nlm.nih.gov/pubmed/22921930
  15. http://fluoroquinolonethyroid.com/wp-content/uploads/2015/04/Musculoskeletal-Complications-of-Fluoroquinolones.pdf
  16. https://academic.oup.com/cid/article/41/Supplement_2/S144/308000
  17. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3175508/
  18. https://www.ncbi.nlm.nih.gov/pubmed/25902267
  19. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3760005/
  20. https://floxiehope.com/2014/11/10/fluoroquinolone-induced-gene-upregulation-and-ros/
  21. https://www.ncbi.nlm.nih.gov/pubmed/8913349
  22. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3985860/
  23. https://floxiehope.com/2015/02/24/study-finds-that-ciprofloxacin-depletes-mitochondrial-dna/
  24. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3760005/
  25. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4080593/
  26. https://www.ncbi.nlm.nih.gov/pubmed/24284031
  27. https://www.ncbi.nlm.nih.gov/pubmed/15321742
  28. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3668199/
  29. http://journals.sagepub.com/doi/full/10.1177/2326409817707771
  30. https://www.ncbi.nlm.nih.gov/pubmed/24231099
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