Monthly Archives: December 2013

Bring on 2014 – Happy New Year!

NYE 2013-2014.


Congratulations!  You made it through 2013!  For those of you who were sick in 2013, there were probably moments that you didn’t think you’d make it through.  You made it though.  You made it to 2014.  Congratulations and may there be many more years for you to look forward to!

I wish you all hope and healing in the new year!  I have no idea how long your road will be, or if 2014 will be better or worse than 2013 for you, but I sincerely hope that it is better in every possible way.  I hope that it is a year of healing for you.  I hope that your pain subsides.  I hope that you get the support you deserve.  I hope that you either gain back what you have lost due to your illness, or that you come to appreciate what you still have.  I hope that you are able to access the people, methods or techniques that help you to move on from your illness.  I hope that you find peace, healing, love, happiness, patience, hope, etc.

For myself, I haven’t thought of any specific New Year’s resolutions quite yet, but I hope that this picture sums up my 2014:

Always wondered

2013 was an empowering year for me.  I started writing about FQ toxicity in June of 2013.  I truly had no clue that anyone would want to read the things that I wrote, but it turns out that people like what I have to say.  I don’t think that they like what I have to say because it’s pretty or because I’m anyone special (I’m not).  I think that they like what I have to say because what I write about is important.  It’s important that the word get out about the dangers of fluoroquinolones.  It’s important that people stop being hurt by the frivolous and foolish over-use of DNA damaging chemotherapy drugs that are being pushed as “safe” antibiotics.  It’s important that people make the connections between many of the mysterious modern diseases that plague us and fluoroquinolones.  Fibromyalgia, Chronic Fatigue Syndrome, all autoimmune diseases, anxiety, depression, dietary intolerances, autonomic nervous system dysfunction, mitochondrial dysfunction, diabetes, Gulf War Syndrome and even autism can be tied to fluoroquinolones.  These are not little problems.  They are serious concerns and it’s important that they be addressed and fixed.  In bringing attention to the role that fluoroquinolones play in each of these diseases, I’m bringing attention to something important.

It’s quite empowering and, though I’m sure that what I just said sounds egotistical, I am humbled by it.  The over-use of fluoroquinolones is a big problem that leads to multiple levels of other serious problems.  The problems are systemic and difficult to bring attention to, much less solve.   Paradigm shifts and systemic changes are needed in order for meaningful change to come about.

It’s a big task, but someone has to do it.  That someone may as well be me.  It may as well be you too.  Even better, it should be all of us together.

We can do this.  We can make change happen.  We can stop people from getting hurt by fluoroquinolones.  We may not be able to save everyone today or even tomorrow, but we can try.  And in trying, we are doing something.  We are making the world a safer and more just place.

“Trying” can be something little or something big.  It can be handing out cards warning people about FQ toxicity, it can be attending the FQ Awareness Rally in Washington D.C., it can be starting a blog, it can be talking to your friends about what happened to you, it can be filing a lawsuit, it can be enacting legislation, etc., etc.

In 2014, I resolve to DO SOMETHING about fluoroquinolone toxicity.  I hope that change comes about.  But if it doesn’t, well, I have my 2015 resolution set, and I’ll keep trying until people know about the causal links between fluoroquinolones and chronic diseases, until the frivolous over-use of fluoroquinolones is stopped, and until they stop giving these poisonous drugs to children.

If you feel inclined, I hope that you feel empowered enough to do something about fluoroquinolone toxicity in 2014 too.  It will take all of us to bring about change.  We can do it though.  We have to be able to.  No one else will and it’s important.  So, bring on 2014.  Let’s get ‘er done.


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How I Lost my Faith in Scientists

Hormones Matter Logo

I just want scientists to step up and scream about what they know.  Some of them, maybe many of them, fully realize that fluoroquinolones are dangerous.  Where is the outrage?  Where is the change?  I am deeply saddened by this list.  Thank you for reading the post!

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Is FQ Induced Insomnia an Autoimmune Problem?

insomnia math

In the December 9, 2013 issue of The New Yorker, there was an article by Ian Parker entitled “The Big Sleep” about Merck’s new sleeping pill called Suvorexant.  The article is interesting and I recommend that you check it out –

There were a couple of things that I found to be of interest in the article, from a Floxie perspective.

First, Parker noted that, “In narcoleptic humans, the cells that produce orexin have been destroyed, probably because of an autoimmune response.”  This is a really interesting assertion/finding.  Narcolepsy may be an autoimmune response/dysfunction/disease.  I wonder if insomnia is also an autoimmune response/dysfunction/disease.  I wonder if the cells that produce orexin (“Orexin neurotransmitters, first identified fifteen years ago, promote wakefulness.”) are over-stimulated in some Floxies, hence the horrible insomnia that some people suffer from.  Or, another possibility is that an autoimmune response in Floxies destroyed the cells that produce melatonin, or other hormones/neurotransmitters that are necessary to induce sleep.

My thinking at this time (subject to change with the introduction of more information), is that much of floxing is an autoimmune response/dysfunction/disease that results from a loss of mitochondrial DNA (mtDNA) from lymphocytes (immune system cells).  Here are some articles on the effects of fluoroquinolones on lymphocytes:

Perhaps, if the insomnia that Floxies suffer from is an autoimmune response of some sort, a pill that is an orexin antagonist, like Suvorexant, can help relieve, or even cure their insomnia.

The experience of getting floxed has made me VERY averse to pharmaceuticals (I intend to never take a drug again).  I empathize with anyone who is wary of trying a new drug.  But insomnia is horrible and when these orexin antagonist drugs are released into the market, if any Floxies are willing to try it, please let me know how it works for you.

Insomnia is one of those disorders that is easy to blame on the victim.  It is thought that everyone should be able to simply turn their mind off and sleep.  If it turns out that insomnia is an autoimmune response/dysfunction/disease, perhaps it will be recognized that, a) sleeping is not a simple condition to treat, and, b) a lot of people have autoimmune dysfunction and disease.  If even 10% of insomniacs are suffering from insomnia because of autoimmune dysfunction, the number of people with autoimmune problems is significantly larger than it is thought.  What could cause so many people (those with official autoimmune diseases, narcoleptics, insomniacs and those with chronic mysterious diseases like fibromyalgia) to have malfunctioning lymphocytes?  FLUOROQUINOLONES!  The articles above go into more detail and actually build a case, and there are more to be found on the internet and in the library (search for “fluoroquinolone or ciprofloxacin and lymphocytes”).  There are probably other factors at work too, but the role that fluoroquinolones play in inducing dysfunctional lymphocytes is large and it has been systematically overlooked.

The other interesting point in the article was this:

“In a recent paper in the online edition of the British Medical Journal, Daniel Kripke, a professor emeritus at the University of California San Diego School of Medicine, examined five years of electronic medical records collected by a health system in Pennsylvania. He compared more than ten thousand patients who had been prescribed a sleep medicine—most commonly Ambien—and more than twenty thousand patients who had not. After adjusting for age, gender, smoking habits, obesity, ethnicity, alcohol use, and a history of cancer, and after controlling, as much as possible, for other diseases and disorders, Kripke found that people who had taken sleeping pills were more than three times as likely to have died during the study period as those who had not. Those on higher doses of the drugs were more than five times as likely to have died.”

I wonder if Dr. Kripke could do an analysis of health outcomes among people who have taken fluoroquinolones versus those who have taken other kinds of antibiotics (or no antibiotics).  I would bet quite a bit of money that those who have taken a fluoroquinolone are significantly more likely to be diagnosed with an autoimmune disease, fibromyalgia, chronic fatigue syndrome, insomnia, leaky gut syndrome, lymphoma, etc. and that they are more likely to have children with autism, ADD, ADHD, allergies, etc.  I’m going to write him a letter requesting that he look into doing a study of health outcomes for people who take fluoroquinolones.  It can’t hurt to ask.  Besides, he’s a colleague of Dr. Beatrice Golomb, who is conducting the UCSD Fluoroquinolone Effects Study.  Dr. Golomb will almost certainly have enough evidence to conclusively show that Gulf War Syndrome was caused by Cipro soon.  When that news is released to the public, people will want to know what the consequences of 20+ million prescriptions for fluoroquinolones being given to American civilians each year for the past two decades has done to human health.  If Dr. Kripke is prepared with the answer, maybe this ridiculousness of prescribing fluoroquinolones for any situation other than a life-threatening emergency will stop.


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A Return to Hope

CS Lewis

I’ve been doing a lot of research into the mechanisms of action for fluoroquinolones lately.  I’ve been passing what I’ve learned on Floxie Hope.  Unfortunately, much of what I’ve learned hasn’t fallen into the “hopeful” category.  Most of what I’ve learned has been pretty grim.  Fluroquinolones deplete DNA, damage mitochondria, stimulate lymphocytes (immune system cells) deplete irreplaceable enzymes and produce neurotoxins.  Bummer, huh?

In a weird, twisted way, I get excited about these discoveries.  They’re the nails that are going to seal the coffin on these drugs, and maybe even Bayer and Johnson & Johnson.  I imagine these facts bursting into common consciousness with an expose in Time, Scientific American or The New Yorker.  I get excited about being right, about being at the forefront of this problem, about being able to tell people, “I told you so” when they realize that quinolone toxicity is a huge problem that is adversely affecting the lives of millions of people.  Irrefutably showing the danger of these drugs is key to getting their use curbed, to stopping the atrocity of people being maimed by prescription antibiotics.  It’s also the key to justice – once the damage pathway for these drugs is shown, those who have been hurt by them can get compensated for their pain and suffering.

My ego gets wrapped up in fantasies of taking down Bayer and J&J.  I have grandiose notions of saving the world from these nasty, evil drugs that are maiming and killing innocent people.  I want people to connect the dots, to see what I see; that fluoroquinolone toxicity is connected with all autoimmune diseases, Fibromyalgia, Chronic Fatigue Syndrome, Allergies, Dietary Intolerances, Depression and Anxiety, Insomnia, Gulf War Syndrome and even Autism Spectrum Disorders.  I want to be validated by recognition.  I want the world to change.

In wanting validation and change in the world, I have lost track of the purpose of this blog.  The purpose of this blog is not to save the world.  It is not to bring down Bayer or Johnson & Johnson.  It is not to be right.  The purpose of this blog is to give hope for healing to those adversely affected by fluoroquinolone antibiotics.  It is, not

I apologize for scaring you guys.  I apologize for pointing out the cellular damage that these drugs inflict.  I don’t think that the damage done is irreparable.  I think that most people heal from Fluoroquinolone Toxicity.  I think that most people move on to live full, happy, healthy lives.  I think that DNA is constantly patching and repairing itself.  I think that the body is constantly fighting to neutralize toxins and that even if our enzymes aren’t replaceable, we have enough of them to function or else we’d be dead.  I think that there is hope.  I think that there is healing.

That is why I created this web site.  To let people know that healing is possible.  To tell stories of healing so that those who are scared can realize that there is a light at the end of the tunnel, that they should have hope because this too shall pass.

So I’m sorry for highlighting scary information.  I’m sorry that the focus of many of these posts has been freak-out material, not hopeful, healing material.  I really want you all to be hopeful.  I want you to heal and hope is healing.  It is, I promise.

I can’t promise to be 100% hopeful 100% of the time.  I think that bringing research about the adverse effects of these drugs to the fore is important.  I think that it’s important to try to change the world and to try to stop these drugs from being prescribed inappropriately.  I’ll just promise to try to remember that this site is about supporting people through a difficult time, letting them know that things do get better with time and letting them know that hope is necessary and that healing is possible.

I’m not a Scientist.  I’m not a Chemist or a Toxicologist or a Geneticist.  I’m actually quite annoyed that people with these titles aren’t putting together the implications of these various studies and shouting about them, and thus there is a void.  I’m trying to fill that void by connecting the dots to the best of my abilities, but analyzing these studies is not my area of expertise.  My area of expertise is healing from FQ toxicity.  It’s my area of expertise because it’s what I have done.  I can personally testify that healing is possible because I have healed.  So have the other people who have shared their stories on  We have been scared, we have been hurt and we have healed.  Healing is possible.  It is possible for you too.  Have hope.


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Conflicting Study Results: Do DNA Breaks Hold Answers?

conflicting results

There is a lot of conflicting information about fluoroquinolone antibiotics (Cipro, Levaquin, Avelox, Floxin and a few others) noted in scientific journals.  One study will conclude one thing about how fluoroquinolones effect human cells and another study will reach the opposite conclusion.  It’s frustrating for everyone involved and it leads to the conclusion, that is also noted in most journal articles about fluoroquinolones, that, “Despite their widespread application, the exact mechanism of action of the quinolones is not fully understood.” (1)  Despite the fact that the exact mechanism of action of fluoroquinolones is unknown, shouldn’t some of the details of their effects on human cells be known?  Shouldn’t there be some clarity in how these drugs affect cells, if not how they work or sometimes don’t work?  Basic, verifiable, answers are sought, but they remain elusive.  Some interesting, and possibly useful, information may be found in examining why clear answers are so difficult to obtain.

Shouldn’t it be testable whether fluoroquinolones increase or decrease levels of Reactive Oxygen Species (ROS)?  Shouldn’t the question of whether fluoroquinolones increase or decrease cellular inflammation be verifiable?  Shouldn’t Scientists know whether fluoroquinolones activate or inhibit t-cell gene expression?  These things can be studied in laboratories.  Answering these questions doesn’t require long-term studies, surveys that are subject to interpretation or vague definitions.  They should be answerable questions and the answers should be clear.  It’s science, not philosophy.  The answers should be black or white, yes or no, not shades of grey.

Yet with each of these questions there are multiple conflicting reports.  No one seems to be able to consistently verify what happens to human cells when they are exposed to fluoroquinolones.  Some studies done by well-run institutions and published in reputable journals say that fluoroquinolones decrease ROS, reduce inflammation and inhibit t-cell gene expression (2).  Other articles in equally well-respected journals say the opposite (3, 4, 5, 6).  So which is true?  Does the arrow go up or down?  I’m sure that answering these questions isn’t easy, but they should be answerable and the answers should be the same each time an experiment is done, right?

So why are there differing answers?  Why can’t Scientists, many of whom are undoubtedly brilliant and capable, figure this out?  A couple of possible answers are that one group of Scientists’ methods are wrong, or that cells react differently to fluoroquinolones with each exposure.  Both possibilities are fascinating on some level.  If the methodologies of one group of Scientists produce an anti-inflammatory response within cells, but the methodologies of another group of Scientists produce an inflammatory response within cells, perhaps the difference in methodologies holds the key to limiting an inflammatory response in living humans.  A cure, or an antidote to the inflammation that is definitely experienced by some people having an adverse reaction to fluoroquinolones, may be revealed from the study methodologies in which an anti-inflammatory response was induced/observed.

An even more interesting possibility is that how cells react to fluoroquinolones depends on which strand of DNA the quinolone molecules attach to.  Studies have found that fluoroquinolones form a poisonous adduct to DNA (7, 8).  Perhaps the reaction of the cell in response to exposure to fluoroquinolones depends on which DNA strands are broken, where they’re broken and where the quinolone molecule attaches to the DNA.  It is plausible that there are some places where DNA could be broken and adducted to that would create an inflammatory response and there are other places where DNA could be broken and adducted to that would create an anti-inflammatory response.  I have neither the tools nor the expertise to test this hypothesis, but from the perspective of someone who has been studying adverse reactions to fluoroquinolones for the past 2 years, the notion that fluoroquinolones break and attach to DNA makes sense of many perplexing aspects about fluoroquinolone toxicity.  If we assume that DNA breaks and quinolone adduction to DNA is behind adverse reactions to fluoroquinolones, the following questions may have the following answers:

Why are some people adversely affected by fluoroquinolones while others aren’t?  Potential answer – some people have important strands of DNA affected while other people have unimportant strands of DNA affected.  And/Or, some people have DNA affected that triggers and inflammatory response and the over-production of ROS, while others don’t because their DNA is broken in less consequential spots.

Why could I handle Cipro for 3 prescriptions but the 4th prescription hurt me?  Potential answer – the Cipro affected inconsequential strands of DNA the first 3 times it was administered, but it damaged an important strand of DNA the 4th time it was administered.

Why did I experience a delayed adverse reaction to Levaquin?  Potential answer – it takes time for damaged DNA to replicate.

Why can’t anyone seem to figure out how these drugs work?  Potential answer – because the human genome is not fully mapped out and most Researchers aren’t looking at how fluoroquinolones affect DNA.

I’m not a Scientist.  I certainly could be wrong about the above hypothesis.  But I do find it both frustrating and interesting that Scientists, who are undoubtedly smarter than I am, can’t seem to figure out some basic facts about how fluoroquinolones work.  I think that there are some answers in their inability to find clear answers.  I suspect that the answers lie in quinolone adducts to DNA.  Perhaps someone with the tools to determine whether I’m right or wrong will design an experiment (that is consistently verifiable) to determine the effects of fluoroquinolones on DNA, and to determine whether or not DNA damage results in differing effects of the drugs.


  1. Inorganic Chemistry, “New uses for old drugs: attempts to convert quinolone antibacterials into potential anticancer agents containing ruthenium.
  2. The Journal of Immunology, “Mitochondrial Reactive Oxygen Species Control T Cell Activation by Regulating IL-2 and IL-4 Expression:  Mechanism of Ciprofloxacin Mediated Immunosuppression
  3. The Tohoku Journal of Experimental Medicine, “Fluoroquinolone Induced Tendinopathy: Etiology and Preventative Measures
  4. Nepal Medical College Journal, “Genotoxic and cytotoxic effects of antibacterial drug, ciprofloxacin, on human lymphocytes in vitro”
  5. Journal of Young Pharmacists, “Oxidative Stress Induced by Fluoroquinolones on Treatment for Complicated Urinary Tract Infections in Indian Patients
  6. Science Translational Medicine, “Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells
  7. The Journal of Biological Chemistry, “The Mechanism of Inhibition of Topoisomerase IV by Quinolone Antibacterials.”
  8. Proceedings of the National Academy of Sciences of the United States, Biochemistry, “Quinolone Binding to DNA Mediated by Magnesium Ions”


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Article Breakdown – “Mitochondrial Reactive Oxygen Species Control T Cell Activation by Regulating IL-2 and IL-4 Expression: Mechanism of Ciprofloxacin-Mediated Immunosuppression”


I’ve read this article 14 times. I think that I understand it. It’s not an easy article to read. Actually, it’s a beast. I’m going to go over what I think are the interesting points of the article in this post. I’m also going to go over something that I think the researchers got wrong, and the implications of their false (IMO) conclusion.

Here is the article –

Mitochondrial Reactive Oxygen Species Control T Cell Activation by Regulating IL-2 and IL-4 Expression: Mechanism of Ciprofloxacin-Mediated Immunosuppression

The Journal of Immunology, 2010, 184: 4827–4841.

Marcin M. Kamin´ ski,* Sven W. Sauer,† Claus-Detlev Klemke,‡ Dorothee Su¨ ss,*

Ju¨rgen G. Okun,† Peter H. Krammer,* and Karsten Gu¨low*

There is a lot of phenomenal information in the article, but I’m going to go over what I think they got wrong first. The researchers found that Ciprofloxacin had an immunosuppresive effect on T-cells, inhibited the production of ROS (Reactive Oxygen Species) and were anti-inflammatory. I don’t think that this is correct. Some of the results discussed in the paper, that I will go over later in this post, note that the effect of Ciprofloxacin on T-cells is one of activation of immune responses, not suppression. More on that later. As for the production of ROS, there are multiple peer-reviewed articles that note that fluoroquinolones (Ciprofloxacin and others) increase the production of ROS. Here are a few –

There are hundreds more.

I have no reason to doubt the intelligence, motives or methods of the Researchers who conducted this study, so why did they get a result that is the opposite result from most other Researchers? I’m not sure of the answer, but I think that it may have something to do with the fact that the cells that they studied were cultured in uridine. Supplementation of uridine, as well as consuming foods that have uridine in them, have seemed to help Floxies. Because of this, I wonder if uridine counteracts the production of ROS, and thus the results of the study were skewed. There may be a completely different answer for why the researchers who wrote the study that I’m reviewing concluded that ROS decreases with Ciprofloxacin, and all other researchers who have looked at the topic note that fluoroquinolones increase ROS production, but I think that the uridine direction is an interesting path. It leads to acyl glucuronidation and other headache inducing topics.

Anyhow, they got that wrong (as shown by the multiple articles that state the FQs increase ROS, not decrease it, not because I say so), so all conclusions based on the premise that fluoroquinolones decrease ROS or oxidative stress, should be disregarded. However, they still said some really interesting stuff about the effects of Ciprofloxacin on the cell.

Before I go into the good stuff from the article, I’m going to express my annoyance over the following paragraph:

Ciprofloxacin, as well as other members of the fluoroquinolone group of antibiotics, is characterized by immunomodulatory properties of an unknown mechanism. The effects of ciprofloxacin on T cell activation-induced gene expression remain vague. Numerous conflicting reports stated that ciprofloxacin activates or inhibits T cell activation-induced gene expression (e.g., for IFN-g, TNF-a, IL-2, and IL-4) (11–14).”

If a drug has immunomodulatory properties, perhaps it’s a good idea to figure out the mechanism. If more than 20 million prescriptions of these drugs are going to be given out each year in the U.S. Alone, perhaps it is a good idea to figure out the mechanism for how they effect the human immune system.

The effects of Ciprofloxacin on gene expression may be vague, but researchers recently found that another topoisomerase interrupter, Topotecan, triggered the expression of Autism related genes. So “vague” has consequences and they may not be pleasant ones.

“Conflicting reports?” Welcome to my world. But it really bothers me that Scientists can’t determine the direction of the arrow. It’s not a judgment call. It’s not a matter of opinion. It should be a matter of fact. How does Ciprofloxacin effect T-cell activation-induced gene expression? This should be a testable question.

Now onto the highlights:

Interestingly, as an inhibitor of bacterial topoisomerase II and an inducer of DNA double-strand breaks, ciprofloxacin was also shown to deplete the mitochondrial DNA (mtDNA) content, thus leading to mitochondrial dysfunction and retarded cellular growth (15–17).”

Why is this stuff on the market? Oh yeah, because the FDA systematically ignores the effects of drugs on mitochondria. Here is an article about how this is the case for many drugs:

In this article, we show that prolonged ciprofloxacin treatment of preactivated human T cells leads to a loss of mtDNA content. This was accompanied by impaired activity of the mtDNA-encoded mitochondrial enzymes, such as complex I, whereas the activities of the nuclear-encoded mitochondrial enzymes, complex II (succinate dehydrogenase) and citrate synthase, were unaffected.”

I’m pretty sure that loss of mitochondrial DNA (mtDNA) content is bad.

Because complex I is central to energy production in the cell, its malfunction results in a wide range of neuromuscular diseases.” ( Does the finding that Ciprofloxacin impairs complex 1 mean that Ciprofloxacin can cause neuromuscular diseases? I’m pretty sure that most Floxies would sadly say, “It sure does!”

Per, “Complex I (NADH-ubiquinone oxidoreductase) catalyzes the transfer of electrons from NADH to ubiquinone (coenzyme Q) in the first step of the mitochondrial respiratory chain, resulting in the translocation of protons across the inner mitochondrial membrane.” Basically, this is an explanation as to how glutathione is massively depleted by fluoroqinolones (FQs). The FQs impair mitochondrial enzyme complex 1 which is responsible for the production of ubiqunone (coenzyme Q) which is responsible for the production of glutathione. This finding is also consistent with an increased production of ROS, not a decrease in ROS. Antioxidant production is inhibited because Complex 1 is inhibited – therefore an increase in ROS would make sense. 

Thus, the current study demonstrates for the first time that mitochondrial complex I-derived ROS control T cell activation.”

Does it mean that mitochondrial complex 1 damage has something to do with autoimmune diseases? It certainly means that it’s REALLY IMPORTANT that it be correctly determined whether Ciprofloxacin (and other fluoroquinolones) increase or decrease ROS production. As I noted above, all other studies that I found said that ROS increases with administration of fluoroquinolones.

Ciprofloxacin treatment was shown to exert various effects on activation- induced gene expression in T cells (10). Stimulatory effects of immediate ciprofloxacin treatment (incubation time up to 72 h) on basal expression of IL-2, TNF-a, or IFN-g in mitogen-activated T cells have been reported (11, 12, 24).”

Stimulating the expression of IL-2, TNF-a and IFN-g is really bad news. Basically, if those are stimulated, an autoimmune-disease, or at least an autoimmune-disease-like state, will ensue. IL-2 is a protein signaling molecule found in the immune system – especially white blood cells. TNF-a is Tumor Necrosis Factor (a) and it also regulates immune system cells. It should be noted that drugs that are used to fight autoimmune diseases are TNF inhibitors. Enbrel and Humira work by suppressing the expression of TNF. If Ciprofloxacin (and other fluoroquinolones) increase the expression of TNF, well, they will induce an autoimmune-disease-like reaction, if not an actual autoimmune disease. IFN-g is interferon gamma, it’s a protein signal that is critical for the operation of the immune system. Again, over-stimulating it is probably a bad idea – unless an autoimmune disease is the goal.

To be fair, it should be noted that the Researchers who authored this particular study did not find that Ciprofloxacin had a stimulatory effect on T-cells. Rather, they found that, “Ciprofloxacin treatment led to a moderate increase in basal IL-2 and -4 expression levels in PHA-preactivated T cells (Fig. 1A). However, prolonged ciprofloxacin treatment clearly inhibited anti-CD3–induced IL-2 and -4 expression in a dose-dependent manner (Fig. 1B).”

They also found that:

Ciprofloxacin treatment induces mtDNA loss, impairs mitochondrial function, and inhibits cellular growth in cultured preactivated human T cells.” (Italicization and emphasis added by them.)

What are the consequences of mtDNA loss? What are the consequences of impairment of mitochondrial function? What are the consequences of inhibiting cellular growth in human t-cells? These are questions that should be asked. The questions should be asked both for the subject human that has consumed the damaging drug and intergenerationally. After all, we are talking about DNA.

In addition, ciprofloxacin induced mtDNA depletion in cultured PHA-preactivated T cells by up to 50%, as estimated by real-time PCR analysis (Fig. 1E). Moreover, mtDNA loss resulted in an impairment of mitochondrial function. This is reflected by significantly decreased activity of the mtDNA-encoded respiratory complex I (Fig. 2A).”

This is a partial answer to the questions about the consequences of mtDNA depletion. What are the consequences of impairing mitochondrial function? What are the consequences of decreasing activity of the mtDNA encoded respiratory complex 1? (Again, I question the result of “decreasing” the activity – it might increase it – there are so many conflicting reports that it’s just obnoxious.)

Genes located on mtDNA encode crucial components of the mitochondrial ETC, such as complex I, III, and IV and ATP synthase. Thus,the loss of mtDNA results in a decreased activity of the ETC (25).”

ETC is the electron transport chain – the process through which mitochondria create energy. Decreasing mtDNA and the activity of the ETC doesn’t seem like a very good idea. What are the consequences of doing so? It doesn’t seem like an unreasonable question to ask.

This indicates that the IL-2 and -4 promoters depend on the simultaneous presence of the increased cytosolic Ca2+ concentration and the PMA-induced oxidative signal. Selective blocking of ROS (with the antioxidant NAC) and the Ca2+ influx (with the intracellular Ca2+ chelator BAPTA-AM) (Fig. 4A, 4C) led to a significant inhibition of IL-2 and -4 promoter activities (Fig. 4B, 4D).”

If one assumes that Ciprofloxacin is a promoter of IL-2 and IL-4 (the opposite of the conclusion of the Researchers, it should be noted, – but I really think that they got the direction of the arrow as to the effect of fluoroquinolones on immune system cells wrong – and my thinking this is backed up by other studies), does this mean that a combination of too much Ca2+ (calcium) and ROS (oxidative signal) within our bodies was part of the equation that made us have the reaction that we had (getting Floxed)? If so, would a combination of NAC as an inhibitor of ROS, combined with a calcium chelator be a cure if applied early on?

I also interpreted this as meaning that Floxies should avoid calcium, but I’m not sure about that.

The immunomodulatory properties of ciprofloxacin and other drugs of the fluoroquinolone group are well documented (10). Most of the in vitro studies showed stimulatory effects of immediate or short-term (up to 72 h) ciprofloxacin treatment on basal gene expression in peripheral mitogen-preactivated human T cells (11, 12, 24). However, several in vitro and in vivo studies suggested that ciprofloxacin has inhibitory properties toward T cell activation (10, 13, 14, 28). In addition, in vitro experiments demonstrated that prolonged ciprofloxacin treatment retards cellular growth (25). This cytostatic effect is mediated by inhibition of the putative mitochondrial topoisomerase II in proliferating cells, resulting in a gradual mtDNA loss and energy shortage (16, 25). Our previous work showed that the mitochondria-generated oxidative signal, in the form of H2O2, is indispensable for T cell activation induced expression of CD95L, a crucial AICD mediator (9). Thus, it is important to clarify whether ciprofloxacin-induced mitochondrial dysfunction could account for differential effects of ciprofloxacin on activation-induced gene expression in T cells.”

This paragraph is both interesting and infuriating because it is abundantly clear that too little is known about these drugs.

The last sentence in the paragraph is interesting. It makes me wonder, do the effects of Ciprofloxacin and other fluoroquinolones depend on which genes are activated/depressed and how t-cell gene expression is influenced (and it’s influenced differently in different people)? Perhaps in some cases/people, genes that inhibit the immune system are expressed, but in other cases/people, genes that stimulate the immune system are expressed. Fluoroquinolones adduct to DNA ( Maybe where the quinolone molecule inserts itself into the DNA makes the difference between inhibition and stimulation of the immune system. That could also be an explanation as to why there are such dramatically differing results from study to study. These drugs don’t influence all cells in the same way – making scientific experimentation and conclusions difficult. But if these drugs were looked at from the perspective of being DNA adducts, perhaps the mysterious discrepancies in results could be explained.

Our previous work demonstrated that in the case of CD95L expression, the IP3/Iono induced Ca2+ signal is complemented by a DAG/PMA-induced H2O2 signal. The combination of a mitochondria-generated H2O2 signal with a simultaneous Ca2+ influx into the cytosol constitutes the minimal requirement for induction of CD95L expression (8).”

CD95L is a transmembrane protein that belongs to the TNF family and induces apoptosis – programmed cell death.

Fluoroquinolones have been repeatedly shown to induce apoptosis. This paragraph again makes me think that calcium is an important part of the equation of Floxing. Perhaps it is part of what makes the apoptosis occur.

However, the ability of ciprofloxacin to induce delayed-type hypersensitivity via direct TCR triggering (51) may pose difficulties to the topical application of ciprofloxacin to alleviate skin inflammation.”

The acknowledgement of “delayed-type hypersensitivity via direct TCR (t-cell receptor) triggering” is important.

Applying Ciprofloxacin to the skin in order to reduce inflammation is a dumb idea for multiple reasons, one of which being that the microbiome on the skin is really important and disturbing it by killing all the bacteria on the skin is a really bad idea. Also, an adverse reaction to the Ciprofloxacin can induce more inflammation.

Furthermore, it was demonstrated that the malfunctioning of complex I leads to excessive generation of ROS (54). Thus, it seems interesting that Leber hereditary optic neuropathy, caused by deficient function of mitochondrial respiratory complex I, is often associated with T cell-mediated autoimmune multiple sclerosis-like syndrome (55).”

Cipro leads to the malfunctioning of complex 1 which leads to excessive generation of ROS.

Perhaps Floxies should ask their Rheumatologists if they have T-cell-mediated autoimmune multiple sclerosis-like syndrome.

This article has some really interesting points, that’s why I’m dissecting it, but the internal inconsistency within the article is annoying to say the least. Which direction do the arrows go? Does Cipro lead to an increase in ROS or not? Answer – of course it does. But this article concludes otherwise, despite statements like the direct quote above.

In addition, recent epidemiologic studies on a cohort of patients with mitochondrial disorders showed a high statistical association between these pathologies and lymphoid malignancies (56).”

Insert profanity here.

Written by me for another post that has yet to be published, “Destruction of mitochondrial DNA can result in mass apoptosis. When this occurs, an autoimmune-disease-like reaction can occur (14). However, if cell damage occurs but the cell does not die, but rather replicates the DNA errors, cancer can result (30, 31). Additionally, drugs that inhibit CYP450 liver enzymes leave people more susceptible to cancer-causing pathogens (32) and fluoroquinolones inhibit CYP450 enzymes (8, 33). How ironic, isn’t it? Cancer can result from DNA damaging drugs that, when used in doses that cause apoptosis, can be chemotherapeutic (and have all of the drawbacks of chemotherapy drugs).”

To explore how mitochondrial damage effects cells, the researchers compared the effects of Ciprofloxacin to the effects of Rotenone (Rot), a pesticide, insecticide and piscicide. That should at least imply something.

I am not a Scientist. I am not an expert in mitochondria, cellular function, autoimmune diseases or anything else. However, I have experienced being floxed and I have been doing research on the topic of fluoroquinolone toxicity for the past 2 years. I’m sure that doesn’t count for much, but I think that I’m right in my assessment of the article reviewed above. (Of course I do, I wouldn’t have written what I wrote if I didn’t think I was right – but I could still be wrong – it has happened.) I encourage you to read the article yourself – preferably multiple times because it really is a beast of an article. I hope that this post clarified things and that it didn’t make you glaze over completely.

Fluoroquinolones are damaging human mitochondria. Though I disagree with the researchers who authored this study about the effects of fluoroquinolones on ROS and inflammation, they do note much of what fluoroquinolones can do to mitochondria and mtDNA. The consequences of damaging mtDNA are yet to be determined. I hope that they’re not too catastrophic.

Thank you for reading Floxie Hope!  I hope that all who read Floxie Hope gain insight, support, understanding and, most of all, HOPE.  If you would like to support Floxie Hope, all contributions will be greatly appreciated!  Click HERE to contribute to Floxie Hope.  Thank you!

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When Investigating Fluoroquinolone Reactions, Move beyond the ER

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If you’re looking at the number of trips to the ER that result from fluoroquinolones in order to determine how safe they are, YOU’RE LOOKING AT THE WRONG DATA POINT!  Here is an essay about the topic of ER visits and how they relate to determining the safety of fluoroquinolones.

As always, thank you for reading it!

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