Fluoroquinolone Toxicity Mimics Benzodiazepine Withdrawal – Beware

GABA “is the chief inhibitory neurotransmitter in the mammalian central nervous system. Its principal role is reducing neuronal excitability throughout the nervous system. In humans, GABA is also directly responsible for the regulation of muscle tone” (source). Fluoroquinolones “are known to non-competitively inhibit the activity of the neurotransmitter, GABA, thus decreasing the activation threshold needed for that neuron to generate an impulse.” (sourcesourcesource) Fluoroquinolones have also been shown to have similar effects on GABA neurotransmitters as benzodiazepine withdrawal (source).

The effects of fluoroquinolones on GABA-A neurotransmitters are the exact opposite of the effects of benzodiazepines, and, on a neurotransmitter level, they are the same as the effects of benzodiazepine withdrawal.

Symptoms of benzodiazepine withdrawal, AND fluoroquinolone toxicity, include:

  • sleep disturbances
  • irritability
  • increased tension and anxiety
  • panic attacks
  • tremors
  • difficulty with concentration
  • confusion and cognitive difficulty
  • memory problems
  • nausea
  • heart palpitations
  • headaches
  • muscular pain and stiffness
  • psychosis

And many other symptoms.

Both fluoroquinolone toxicity and benzodiazepine withdrawal are multi-symptom, chronic illnesses, for which there is no cure, and, despite significant research into both, the severity and complexity of both SYNDROMES is rarely acknowledged.

The following article does a brilliant job of connecting fluoroquinolone toxicity (syndrome) and benzodiazepine withdrawal (syndrome), and it gives a thorough explanation as to why people who have gone through benzodiazepine withdrawal should NEVER be prescribed fluoroquinolones. The article was originally published on the Benzodiazepine Information Coalition web site, www.benzoinfo.com, in October, 2016. It was written by Brad Verret, and I am grateful to him for the wonderful article.

Tragically, Brad Verret has passed away. I asked the editor of benzoinfo.com if I could re-publish it on floxiehope.com, and she said yes and noted that, “Brad wrote his articles to help as many people as possible. His intentions were to sound the alarm for benzodiazepine affected people to avoid that awful class of antibiotics, and he would have been pleased to help floxies avoid getting benzodiazepine injured.” She also noted that Brad was kind and smart and that he is missed dearly. I hope that his loved-ones see the use of his wonderful article as a tribute. Brad synthesized and interpreted the data about the effects of fluroquinolones and benzodiazepines on GABA-A thoughtfully and insightfully. This is a wonderful article, and Brad’s work is greatly appreciated! Please share it (or this entire post) far and wide – thank you!!

Hidden Dangers of Fluoroquinolone Antibiotics in the Benzodiazepine-Dependent Population

By Brad Verret

Whether it was for a sinus infection or bronchitis, most people have taken an antibiotic at some point in their lives. Antibiotics can be lifesaving medications but, like all other drugs, they come with risks. In particular, one specific class of antibiotic drugs called the fluoroquinolones carry serious risks that few people are aware of. In light of the growing epidemic of antibiotic resistance, each new generation of antibiotics has bolstered an enhanced degree of potency which can be viewed as both an asset and a liability. The fluoroquinolone class features a robust, broad-spectrum antibiotic effect and includes many popular drugs such as ciprofloxacin (Cipro), ofloxacin (Floxin), norfloxacin (Noroxin), levofloxacin (Levaquin), moxifloxacin (Avelox), and gemifloxacin (Factive).

Chemically speaking, the mechanism of action of the fluoroquinolones closely mirrors that of certain chemotherapy drugs, so it is rather unsettling that these powerful agents are sometimes prescribed for relatively benign infections that would probably resolve on their own or with a milder drug. One notable and unique risk of the fluoroquinolones is that, unlike most other antibiotics, they are neurologically active at commonly prescribed dosages. As an action secondary to their primary antimicrobial effect, they are capable of binding to certain receptors in the brain, spinal cord, and peripheral nervous system. The primary receptor type affected is the GABA-A receptor, which is the exact same receptor that benzodiazepines act on.[1]

When a fluoroquinolone binds to a GABA receptor, the result is the polar opposite of the effect of CNS depressants like benzodiazepines. Fluoroquinolones are antagonists of the GABA-A receptor, meaning that they prevent the binding of GABA and can displace other molecules bound to the receptor, such as benzodiazepines.[1] GABA is an inhibitory neurotransmitter and drugs which enhance its action, like benzodiazepines, cause sedation. The GABA receptor blockade caused by a fluoroquinolone results in a CNS stimulant effect, with neurological manifestations ranging from mild insomnia and agitation to hallucinations and seizures.[2] Anyone can suffer these side effects, but individuals prescribed benzodiazepines are notably much more prone to experiencing these adverse neuropsychiatric reactions.

The culprit is the GABA receptor downregulation imposed by benzodiazepine tolerance. When a benzodiazepine is given chronically (beyond 10 days) there are a series of downward compensatory mechanisms which seek to restore a neurological equilibrium in light of the overstimulation of GABA receptors by the drug. This results in GABA receptors becoming progressively less receptive to GABA over time following prolonged exposure to benzodiazepines.[3] Over time, the brain’s GABA-dependent systems are weakened and there is a heightened vulnerability to external influences which decrease the action of GABA.

A storm neural excitation ensues when a fluoroquinolone “unmasks” the GABA receptor downregulation associated with benzodiazepine tolerance. In addition, since they share the same target, fluoroquinolones are capable of competing with benzodiazepines for GABA receptor binding in a concentration-dependent manner. Studies have shown a complex interaction when a fluoroquinolone and a benzodiazepine are simultaneously bound to a GABA receptor. At high concentrations, fluoroquinolones are capable of displacing a portion of the benzodiazepine molecules bound to GABA receptors.[4]This displacement can precipitate an acute benzodiazepine withdrawal syndrome which is identical to that which would normally happen if an individual were to suddenly reduce their benzodiazepine dosage.

Imagine each GABA receptor as having a gas pedal and a brake pedal. The entire GABA receptor, with its imaginary gas and brake pedals, is anchored into the neuron whose pace it controls. GABA agonists like benzodiazepines act on the brake pedal and GABA antagonists like fluoroquinolones act on the gas pedal. When an agonist acts on the brake pedal, chloride ions flow through the receptor into the neuron. Chloride ions are like an electrostatic glue which slows the neuron down. When an antagonist acts on the gas pedal, the flow of chloride stops and the neuron speeds up.

When an agonist is present for a prolonged period of time, the brake pedal gradually becomes worn out. Additionally, the neuron will recruit chemical messengers to tune up the gas pedal so that the neuron can continue to move along at its desired pace. It might be a pace that provokes anxiety, but it is the precise pace which will allow the neuron to fulfill its purpose within the unique neural circuit it belongs to. After being chronically slowed down by benzodiazepines, neurons want to break free but are held back by the presence of the drug. They will progressively fight back harder and harder to overcome this pharmacological oppression. Fluoroquinolones unleash neurons from their chemical bondage by disengaging the brake and stepping on the gas pedal, causing a sort of neural short-circuit as the freed neurons begin to race out of control.

It has been shown that certain non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen are capable of enhancing the GABA receptor blockade cause by fluoroquinolones, potentiating their neurotoxicity and exacerbating their CNS side effects.[5] NSAIDs are frequently co-prescribed with fluoroquinolone antibiotics for painful infections like sinusitis and urinary tract infections. Adding further insult to injury, some fluoroquinolones including ciprofloxacin (Cipro) are inhibitors of the CYP1A2 liver enzyme which is responsible for metabolizing caffeine and other xanthine alkaloids found in coffee, tea, and chocolate.[6] This commonly results in an increased sensitivity to the stimulating effects of caffeine when ciprofloxacin is taken. Hence, it is hardly a surprise that coffee drinkers who are prescribed a benzodiazepine are at an even higher risk for fluoroquinolone-induced seizures and neuropsychiatric disturbances.

It is an unfortunate truth that many healthcare practitioners outside the realm of neuroscience are unaware of these lesser-known facts about fluoroquinolone antibiotics. The fluoroquinolone-caffeine interaction is well documented but the fluoroquinolone-benzodiazepine interaction is not currently recognized in any of the current web-based drug interaction cross checking systems commonly used by healthcare consumers. Most pharmacists are not aware of the issue either, and will readily dispense fluoroquinolone prescriptions to benzodiazepine-dependent patients. This interaction is not consistently recognized yet it very consistently gets benzodiazepine-tolerant individuals into deep trouble. Studies have found that benzodiazepine-dependent individuals frequently experience depression, anxiety, psychosis, paranoia, severe insomnia, paraesthesia, tinnitus, hypersensitivity to light and sound, tremors, seizures, and suicidal thoughts upon exposure to fluoroquinolone antibiotics.[7] 

These symptoms are all consistent with acute benzodiazepine withdrawal syndrome. Furthermore, it may take several weeks or even months after discontinuing the fluoroquinolone for the affected individual to become symptom-free. This may be due to the long-term potentiation that occurs when excitatory glutamate-containing synapses are overstimulated by a deficit of GABA activity. Some individuals never return to their pre-fluoroquinolone state and they are commonly referred to as having been “floxed”. They are left with conditions including peripheral neuropathy, muscle weakness, cognitive dysfunction, new or worsened mental illness, and even paralysis which are all consistent with excitatory neurotoxicity (excitotoxicity) and brain damage.[8][9][10]

Taking all this into account, it is imperative that moving forward more healthcare professionals will become aware of and publicly acknowledge this dangerous interaction which has rendered normal, healthy people disabled. However, this alone is not enough. It is equally important that benzodiazepine-dependent individuals become aware of this interaction so that they can better advocate for themselves. It is well known that chronic benzodiazepine usage often creates chemical sensitivities which require the affected individuals to avoid a variety of foreign substances which most normal people can tolerate, and fluoroquinolones probably fall at the very top of that list.

All doctors should be aware that prescribing a fluoroquinolone to a benzodiazepine-dependent individual carries a serious risk for disability which could potentially be permanent. Fluoroquinolones should be contraindicated with chronic benzodiazepine exposure in nearly every scenario, including nonmedical benzodiazepine abuse. Clinicians should explore all alternatives before fluoroquinolones are considered. In rare cases where it has been determined that failing to administer a fluoroquinolone could result in death, benzodiazepine-dependent individuals should have their benzodiazepine dosages increased for the entire duration of fluoroquinolone therapy and until the drug is completely cleared from their system.



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13 thoughts on “Fluoroquinolone Toxicity Mimics Benzodiazepine Withdrawal – Beware

  1. Honestly October 9, 2017 at 7:56 am Reply

    I was on a benzo then Cipro, and two years later Cipro again. The sleep issues were through the roof. The verbal and psychological abuse in my marriage was the worst, and I was gaslighted. Please don’t allow “new” information to reduce those horrible years many went through as only drug related. I’m not the only one who had this response but a doctor who prescribes these drugs and is downright mean and insinuating mental issues as a response to your side effect complaints knows what he is doing. Only wish I had been clear headed enough to ask, “If it’s not Cipro, then what is it?” Labrat no more.

  2. L October 9, 2017 at 10:16 am Reply

    Wow. “Studies have found that benzodiazepine-dependent individuals frequently experience depression, anxiety, psychosis, paranoia, severe insomnia, paraesthesia, tinnitus, hypersensitivity to light and sound, tremors, seizures, and suicidal thoughts upon exposure to fluoroquinolone antibiotics.” I was not a benzo-dependent person, but I experienced ALL (except the seizures.) Interestingly I was recently prescribed some (anti-anxiety meds) pre-dental work and seemed to do just fine. I suspect there is a difference between being on them all the time as opposed to on occasion. I also was able to add back in a cup of coffee with no ill effects, after about 1 1/2 years.

    • Rob November 5, 2017 at 9:03 am Reply

      L–I’ve seen you comment on this page a lot. Do you have a full story on here somewhere? How are you doing now?

      • L November 5, 2017 at 10:55 am Reply

        Hi Rob. I never did an official full story, but I described what happened a number of times at length in the posts. I just never wanted to go back and dredge it all up again. It was terrifying and I still have PTSD from it. Whenever I try to warn someone, inevitably the tears come. But here is the abbreviated version.

        Within hours of taking the first Cipro (and I was on prednisone as well which I believe exacerbated everything) I had blurred vision, lots of floaters and a couple numb fingers. I did not connect it to the Cipro. At first I thought I had slept funny and pinched a nerve. I continued taking 3 more Cipro before I made the connection.

        Within days all my toes were numb, my vision worsened significantly, and I just started feeling really ill, like if I had pneumonia. My gut was ravaged. I couldn’t eat and I lost 36 pounds in 6 weeks. I became very weak and could only walk with assistance. A couple fingers started spasming wildly out of control, my hair started coming out in chunks, my skin got like carboard, I got rashes all over my body. At one early point I got the most horrific pain imaginable in my mid-back. I have had cracked ribs and a fractured scapula before and they are extremely painful, but they paled in comparison to this pain. It was just excruciating and felt like it was buried deep in the bone. I had anxiety 24/7 of the fight or flight variety, and paranoia. I also had terrible insomnia, where I didn’t sleep more than an hour or two for am month or more.There was also popping in my joints…my knees especially and back.

        Next to the vision issues, which continued to worsen (sometimes if I looked at a wall or a light colored floor, it would literally be filled with little black specks, and the floaters were so large and so unmoving, that it was like looking through gauze) I had two other “deal-breaker” issues which made me suicidal. Had they not resolved I would not be here today. The first was olfactory nerve damage. This one is SO difficult to explain because it is so out of the realm of our normal experiences. My nerves were so damaged that EVERYTHING in the world asphyxiated me. I couldn’t go outside. If someone came to take me to the appointment, they could not have any lotion on at all. Even scents lingering that had been applied the day before I could smell. A baking potato would choke me because it smelled so strong. It was painful to smell anything. It was like everything in the world smelled as strong as an open vat of bleach. It was hideous.

        The other and biggest threat for me was I started gasping for breath. They call it dyspnea which translates appropriately to “air hunger.” It began just a week or so in. Suddenly, I couldn’t breath. Every breath was a struggle. I remember thinking “I don’t know how I am going to make it through the next ten minutes.” I ended up like that for several months. I just wanted out. It was suggested by a researcher that it was mitochondrial damage to the heart muscle, and a doctor suggested autonomic nervous system damage. TO make matters worse I would also intermittently get a sensation around the outside of my throat like I was being strangled. That jolted me up out of bed a number of times, thinking I was choking.

        There were dozens of other side effects, some of which I cannot even readily recall right now. I was thrown under the bus by a dozen doctors, most of which believed it could not possibly all be from the Cipro. (Just a HUGE coincidence that someone in great shape suddenly has all this happen within hours/days of the Cipro.) I really wanted “out.” I was in so much pain; I could barely see; the olfactory nerve damage was nightmarish and I couldn’t imagine spending my life struggling with every single breath. To add insult to injury, I was also on asthma inhalers that contain both steroid and fluoride. MY greatest fear (aside from never recovering,) was this: if I stay ON the inhalers I am only further damaging myself but if I GO OFF and have an asthma attack, on top of the already gasping situation—-unimaginable.

        Then I finally went to an ND whose name I found on this site. He was the first one to give me any hope. He had seen a few floxies before me so he needed no convincing that all the damage was indeed from the Cipro. He wanted to put me on H2O2 IVs to get off the asthma meds. A physician had told me that was dangerous, but at this point I just didn’t care. I did the H2O2, eventually weaned off the asthma meds. I also did phosphytidylcholine (A LOT—40 total, although I think the first 20 would have sufficed). I did hig dose vitamin c (50,000 mg) an ocassional Myers and with the exception of the H2O2 I got a push of glutathione with each IV.

        Since this is the “short” version I won’t go through the phases but this is where I am today.
        The breathing has almost completely resolved. I still get an ocassional “glitch” where the breath doesn’t seem to complete, but it goes away fairly quickly. The hyperosmia (olfactory damage where everything was grotesquely exaggerated) is gone but I still am sensitive to smells (had to be moved after being seated next to someone with perfume a few nights ago at a theatre) and I get occasional phantom scents, like dirty ashtray or chemical smell.) The strangling sensation is mostly gone. It reappears sometimes but is much less pronounced when it does. My vision in my right eye went from 20/25 to 20/65 and I was diagnosed soon after with early stage macular degeneration. I still have some floaters but WAY better than it was ( I had done NAC eye drops 4x day for a year which I think helped.) and once and a while I will see that little black dot type of floaters but rarely. I still have light sensitivity where it’s almost like a shade pulls down over my right eye in bright sunlight and also problems under fluorescent lighting. I also have really annoying non stop tinnitus (buzzing/hissing/humming sound that is constant) I continue on occasion to have pelvic area pressure and my toes are numb still, but the numbness had at one point started to move into the rest of my feet and my calves. It is now only the toes and a couple wonky fingers.

        I ended up with torn meniscus where the knee popping was and I did prolozone injections for those. So far so good! I gained the weight back, but my skin is in bad shape. My energy is back to almost normal. I continue to have fluid around my heart, and at my last visit was told it appears to be permanent so now I have to always continue to get EKG/Echo to make sure it hasn’t grown;.

        So, where I was at my worst: a gasping, mentally confused, and frightened, suicidal, blurried eyed, shuffling, barely able to get off the couch shell of a person. Where I am today: Back to doing most things I did before being floxed, albeit not seeing as clearly and dealing with some residual issues. I am 2 years and 9 months out, and I never believed I would get to this place. I continue to try to find fixes for the tinnitus, vision, and a couple other things—but the difference between where I was and where I am is phenomenal. (MY ND told me he thought I was 20 years older than I was when I first went to him.) So….there is hope.

        • Rob November 5, 2017 at 12:03 pm

          Thank you so much for responding. It sounds like you’ve had it worse than most, I am so thankful you have most recovered and are living your life again. I pray that I will also have a swift recovery, it’s just too early to tell (1.5 weeks post floxing but symptoms are only moderate right now except nightly insomnia).

  3. Carly October 9, 2017 at 9:35 pm Reply

    This is a HUGE missing link to the FQ puzzle. I took Cipro for 3-days in 2013 along with my nightly dose of Xanax and it was as many say, “a bomb went off in my body and brain”. At the end of my career and at the top of my game as a technology project manager, I could no longer function well enough to make sense, and I left my profession. A year ago I realized that the Xanax played a part in the suffering and I weaned off xanax completely. I experienced all the symptoms except seizures and psychosis. In order to continue to heal, I have to eat all organic food, NO supplements except for magnesium, vitamin D and C and meditate/breathing exercises daily – if I don’t meditate for a few days and have stress – I’ll relapse which for me is insomnia, gut dysbiosis (sibo), headache and fatigue. The symptom that at relapse is coming is eye discomfort/pain. There are so many people, normal people just like me who take benzos. There needs to be awareness raised — the road back is very long but not impossible. Thank you for sharing this information.

  4. Brian October 10, 2017 at 10:14 am Reply

    Great post. I was taking benzos when I was floxed. While I was still taking Cipro, I limped into my doctor’s office saying something was wrong. He never acknowledged that FQs could cause the kind of symptoms I was having, but sometime later mentioned to me that he thought I was going to have a “psychotic break” in his office that day. I wonder why…

  5. Joseph Rosen November 23, 2017 at 9:35 am Reply

    Been floxed since June 2015. 90 days after treatment, I experienced severe pain so throughout my entire body (joints, tendons, and muscles), memory loss, anxiety and depression. None of the Army doctors believed the research I presented to them. This website was very helpful and informative. I tore my labrum and 2 tendons in October 2015; surely in July 2016. The pain has decreased, but have permanent joint damage. Nothing helped until recently. A fried recommended CuraMed’s blend of Curcumin with Turmerones. After a month, I felt so much better. Was actually able to jog for the first time in 2 years without excruciating pain. This may not work for you, but I believe it has made a difference for me.

    • L November 23, 2017 at 10:22 am Reply

      So glad that helped joseph. Something else you can try is prolozon injections. It is a combination of ozone and procaine (not to be confused with prolotherapy…another treatment that I really am not to familiar with, but apparently works on same principal.) Anyhow, it takes a few months from the time of injection, while it helps the body heal itself. It is used on tendons, meniscus, etc, wherever there is connective tissue damage. Used for arthritis. I got mine from an ND but many sports medicine doctors are now offering it.\

      Surprised your army doctors didn’t believe you. IT has long been known that gulf war syndrome is linked to the prophylactic use of Cipro….https://www.militarytimes.com/2013/11/01/new-fda-warnings-on-cipro-may-tie-into-gulf-war-illness/

  6. Anja December 23, 2017 at 6:13 am Reply

    Please read Marc’s story. He was poisened and hurt by levaquin and Valium (benzo). He is bedridden in severe pain for two and a half years. He needs support. Please share his story and help him.

    Thank you.


  7. […] via Fluoroquinolone Toxicity Mimics Benzodiazepine Withdrawal – Beware […]

  8. J Snow June 16, 2018 at 4:28 pm Reply

    Should be able to take legal action against medical professional that prescribed this. In my case I was never asked what meds I was currently on nor was I told about a BLACK BOX WARNING, FROM DOCTOR OR PHARMACIST! Plus my prescription bottle and print out says nothing about a black box. Very unfair that an individual with a medical professional degree doesn’t care what he/she gives the patients. I’m not alone as far as having permanent peripheral neuropathy, body tendonitis and eye problems quickly advancing. A doctor and pharmacist ruined my life. I don’t live to blame, but these two are definitely at fault for my permanent disabilities. Thank you for the article.

    • L June 16, 2018 at 5:09 pm Reply

      Yeah, welcome to this awful club. I had/have neuropathy, major eye issues, heart issues, and dozens more issues. And yes, the medical community. including the pharmacists are all negligent.

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